Asteraceae Dermatitis: Everyday Plants With Allergenic Potential

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Asteraceae Dermatitis: Everyday Plants With Allergenic Potential

The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
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Dr. Wallace is from the Medical College of Georgia, Augusta. Dr. Elston is from the Department of Dermatology & Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors have no relevant financial disclosures to report.

Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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Dr. Wallace is from the Medical College of Georgia, Augusta. Dr. Elston is from the Department of Dermatology & Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors have no relevant financial disclosures to report.

Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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Dr. Wallace is from the Medical College of Georgia, Augusta. Dr. Elston is from the Department of Dermatology & Dermatologic Surgery, Medical University of South Carolina, Charleston.

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Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
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Practice Points

  • Asteraceae dermatitis can occur from direct contact with plants of the Asteraceae family; through airborne pollen; or from exposure to topical medications, cooking products, and cosmetics.
  • Patient education on primary prevention, especially protective clothing, is crucial, as these plants are ubiquitous outdoors and have diverse phenotypes.
  • Management of mild Asteraceae dermatitis consists primarily of topical corticosteroids and calcineurin inhibitors, while systemic corticosteroids and other immunosuppressive agents are utilized for severe or recalcitrant cases.
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Atopic Dermatitis: Upadacitinib Effectiveness Maintained Through 76 weeks Among Adolescents

Article Type
Changed
Mon, 10/28/2024 - 12:09

 

TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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Study Compares Punch Excision vs. Core Excision for Recalcitrant Keloids

Article Type
Changed
Mon, 10/28/2024 - 12:03

Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

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Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

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Bipartisan Bill to Provide Free Gun Lockboxes to Veterans

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About 7 of every 10 veterans who die by suicide involve the use of a firearm. A reason for this high rate is access, as half of veterans report owning ≥ 1 personal firearms. Of those individuals, more than half report storing firearms loaded and/or unsecured and one-third of veterans who store their firearms loaded and unlocked do not own a lockbox or safe. 

Suicide death prevention has improved as firearms have become more difficult to obtain. That’s why Navy veteran Rep. Chris Deluzio (D-PA), former FBI Special Agent and federal prosecutor Rep. Brian Fitzpatrick (R-PA), and Rep. Greg Landsman (D-OH) have teamed up to introduce the Saving Our Veterans Lives Act of 2024. Under the proposed act, any veteran would be able to get a free lockbox from the US Department of Veterans Affairs (VA).

Suicidal crises can be brief. According to the VA, if a person experiencing a suicidal crisis can’t access the method they planned to use, they generally do not seek out other lethal means. Lockboxes are a way of “putting space between thought and trigger,” the VA said.

The VA Suicide Prevention Program distributes free firearm cable locks to any veteran who requests one. However, many veterans favor lockboxes and safes to secure their guns. A VA pilot program offers free lockboxes to veterans enrolled in the Veterans Health Administration who are at an elevated risk for suicide. The program is set to launch in late 2024 and is a collaboration between the Rocky Mountain Mental Illness Research, Education, and Clinical Center for Suicide Prevention, VA National Prosthetics Service, and VA Office of Suicide Prevention.

The proposed bill would make the lockboxes (which typically cost between $25 and $350) free to any veteran, regardless of VA enrollment status or diagnosis. It ensures “sufficient funding for many tens of thousands of lockboxes to be distributed.” The bill would also direct the VA to create a public education campaign on the availability of lockboxes and the importance of secure firearm storage in suicide prevention.

“The alarming and tragic reality is that our veterans face a suicide rate 57% higher than that of civilians,” Rep. Fitzpatrick said. “This commonsense, bipartisan initiative is more than a solution—it's a lifeline.”

The representatives report that the bill has been endorsed by an “unprecedented” number of organizations, including the National Shooting Sports Foundation, Disabled American Veterans, The American Legion, GIFFORDS, Everytown for Gun Safety, Brady, American Psychological Association, American Foundation for Suicide Prevention, and Association of VA Psychologist Leaders.

“Did you know that in some cases only 10 minutes elapse between an individual having suicidal ideation and acting?” American Legion National Commander James LaCoursiere said in the representatives’ press release. “The Saving Our Veterans Lives Act is an important part of preventing suicide as it will provide veterans with the information and means to securely store their firearms to prevent suicide, while still protecting their Second Amendment rights. The Legion commends Rep. Deluzio and his team for bringing this bill forward and for their continued dedication to the welfare of our nation’s veterans.” 

"I hear colleagues all the time talk about veteran suicide," Rep. Deluzio said in an interview with Military.com. "It is a problem in my community. It's a problem across the country. Let's take action. This is a chance where we can do it that I think can cut through the politics that normally divide us on these [gun] issues. And I think the coalition supporting the bill tells you, we've got a path to pass it."

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About 7 of every 10 veterans who die by suicide involve the use of a firearm. A reason for this high rate is access, as half of veterans report owning ≥ 1 personal firearms. Of those individuals, more than half report storing firearms loaded and/or unsecured and one-third of veterans who store their firearms loaded and unlocked do not own a lockbox or safe. 

Suicide death prevention has improved as firearms have become more difficult to obtain. That’s why Navy veteran Rep. Chris Deluzio (D-PA), former FBI Special Agent and federal prosecutor Rep. Brian Fitzpatrick (R-PA), and Rep. Greg Landsman (D-OH) have teamed up to introduce the Saving Our Veterans Lives Act of 2024. Under the proposed act, any veteran would be able to get a free lockbox from the US Department of Veterans Affairs (VA).

Suicidal crises can be brief. According to the VA, if a person experiencing a suicidal crisis can’t access the method they planned to use, they generally do not seek out other lethal means. Lockboxes are a way of “putting space between thought and trigger,” the VA said.

The VA Suicide Prevention Program distributes free firearm cable locks to any veteran who requests one. However, many veterans favor lockboxes and safes to secure their guns. A VA pilot program offers free lockboxes to veterans enrolled in the Veterans Health Administration who are at an elevated risk for suicide. The program is set to launch in late 2024 and is a collaboration between the Rocky Mountain Mental Illness Research, Education, and Clinical Center for Suicide Prevention, VA National Prosthetics Service, and VA Office of Suicide Prevention.

The proposed bill would make the lockboxes (which typically cost between $25 and $350) free to any veteran, regardless of VA enrollment status or diagnosis. It ensures “sufficient funding for many tens of thousands of lockboxes to be distributed.” The bill would also direct the VA to create a public education campaign on the availability of lockboxes and the importance of secure firearm storage in suicide prevention.

“The alarming and tragic reality is that our veterans face a suicide rate 57% higher than that of civilians,” Rep. Fitzpatrick said. “This commonsense, bipartisan initiative is more than a solution—it's a lifeline.”

The representatives report that the bill has been endorsed by an “unprecedented” number of organizations, including the National Shooting Sports Foundation, Disabled American Veterans, The American Legion, GIFFORDS, Everytown for Gun Safety, Brady, American Psychological Association, American Foundation for Suicide Prevention, and Association of VA Psychologist Leaders.

“Did you know that in some cases only 10 minutes elapse between an individual having suicidal ideation and acting?” American Legion National Commander James LaCoursiere said in the representatives’ press release. “The Saving Our Veterans Lives Act is an important part of preventing suicide as it will provide veterans with the information and means to securely store their firearms to prevent suicide, while still protecting their Second Amendment rights. The Legion commends Rep. Deluzio and his team for bringing this bill forward and for their continued dedication to the welfare of our nation’s veterans.” 

"I hear colleagues all the time talk about veteran suicide," Rep. Deluzio said in an interview with Military.com. "It is a problem in my community. It's a problem across the country. Let's take action. This is a chance where we can do it that I think can cut through the politics that normally divide us on these [gun] issues. And I think the coalition supporting the bill tells you, we've got a path to pass it."

About 7 of every 10 veterans who die by suicide involve the use of a firearm. A reason for this high rate is access, as half of veterans report owning ≥ 1 personal firearms. Of those individuals, more than half report storing firearms loaded and/or unsecured and one-third of veterans who store their firearms loaded and unlocked do not own a lockbox or safe. 

Suicide death prevention has improved as firearms have become more difficult to obtain. That’s why Navy veteran Rep. Chris Deluzio (D-PA), former FBI Special Agent and federal prosecutor Rep. Brian Fitzpatrick (R-PA), and Rep. Greg Landsman (D-OH) have teamed up to introduce the Saving Our Veterans Lives Act of 2024. Under the proposed act, any veteran would be able to get a free lockbox from the US Department of Veterans Affairs (VA).

Suicidal crises can be brief. According to the VA, if a person experiencing a suicidal crisis can’t access the method they planned to use, they generally do not seek out other lethal means. Lockboxes are a way of “putting space between thought and trigger,” the VA said.

The VA Suicide Prevention Program distributes free firearm cable locks to any veteran who requests one. However, many veterans favor lockboxes and safes to secure their guns. A VA pilot program offers free lockboxes to veterans enrolled in the Veterans Health Administration who are at an elevated risk for suicide. The program is set to launch in late 2024 and is a collaboration between the Rocky Mountain Mental Illness Research, Education, and Clinical Center for Suicide Prevention, VA National Prosthetics Service, and VA Office of Suicide Prevention.

The proposed bill would make the lockboxes (which typically cost between $25 and $350) free to any veteran, regardless of VA enrollment status or diagnosis. It ensures “sufficient funding for many tens of thousands of lockboxes to be distributed.” The bill would also direct the VA to create a public education campaign on the availability of lockboxes and the importance of secure firearm storage in suicide prevention.

“The alarming and tragic reality is that our veterans face a suicide rate 57% higher than that of civilians,” Rep. Fitzpatrick said. “This commonsense, bipartisan initiative is more than a solution—it's a lifeline.”

The representatives report that the bill has been endorsed by an “unprecedented” number of organizations, including the National Shooting Sports Foundation, Disabled American Veterans, The American Legion, GIFFORDS, Everytown for Gun Safety, Brady, American Psychological Association, American Foundation for Suicide Prevention, and Association of VA Psychologist Leaders.

“Did you know that in some cases only 10 minutes elapse between an individual having suicidal ideation and acting?” American Legion National Commander James LaCoursiere said in the representatives’ press release. “The Saving Our Veterans Lives Act is an important part of preventing suicide as it will provide veterans with the information and means to securely store their firearms to prevent suicide, while still protecting their Second Amendment rights. The Legion commends Rep. Deluzio and his team for bringing this bill forward and for their continued dedication to the welfare of our nation’s veterans.” 

"I hear colleagues all the time talk about veteran suicide," Rep. Deluzio said in an interview with Military.com. "It is a problem in my community. It's a problem across the country. Let's take action. This is a chance where we can do it that I think can cut through the politics that normally divide us on these [gun] issues. And I think the coalition supporting the bill tells you, we've got a path to pass it."

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Air Pollution Exposure Linked to Higher Breast Cancer Risk

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TOPLINE: 

A recent study found that long-term exposure to fine particulate matter ≤ 2.5 μm (PM2.5) is associated with an increased risk for breast cancer, with the highest risk observed among White women.

METHODOLOGY:

  • Studies have suggested that exposure to air pollution — specifically PM2.5 — may increase the risk for breast cancer, but data are largely in populations of White women.
  • The current analysis explored the potential risk among a more racially and ethnically diverse group.
  • The study included 58,358 women (median age, 60.4 years at enrollment) from the California Cancer Registry, followed over an average of 19.3 years. Overall, 35% were African American, 39% were Latino, 15% were White, and 10% were Japanese American.
  • Researchers measured PM2.5 exposure using satellite-based data and geocoded addresses. Other pollutants, such as PM10, NO2, NOX, and CO, were also tracked using Environmental Protection Agency data.

TAKEAWAY:

  • A total of 3524 invasive breast cancer cases were diagnosed over an average follow-up period of 19.3 years. PM2.5 exposure was associated with a 28% increased risk for breast cancer overall (hazard ratio [HR], 1.28; 95% CI, 1.08-1.51).
  • When looking at risk by racial/ethnic group, the association between PM2.5 exposure and breast cancer risk was strongest among White women (HR, 1.67). PM2.5 exposure was also associated with a higher risk for breast cancer among African American women (HR, 1.14; 95% CI, 0.89-1.46) and Latino women (HR, 1.34; 95% CI, 0.94-1.92), but the associations were not significant.
  • Overall breast cancer incidence was also positively associated with exposure to NO2, NOX, and CO (HRs, 1.09-1.11), but the associations were not significant. A meta-analysis of this study and ten other cohorts estimated a 5% increased breast cancer incidence per 10-unit increase in PM2.5 (HR, 1.05).

IN PRACTICE:

“Collective findings suggest that PM2.5 exposure should be considered a risk factor for breast cancer, and curtailing air pollution exposures at the population level using regulatory strategies should be a priority,” the authors concluded.

SOURCE:

The study, led by Anna H. Wu, PhD, MPH, Keck School of Medicine, University of Southern California, Los Angeles, was published online in the Journal of Clinical Oncology.

LIMITATIONS:

The study did not include data on nonresidential exposures or residential history before cohort entry, which limited the assessment of earlier exposures. The study also lacked information on specific sources of PM emissions, as well as an explanation for why White women had the highest breast cancer risk compared with other racial/ethnic groups.

DISCLOSURES:

The study was supported by grants from the Health Effects Air Pollution Foundation, the National Cancer Institute, USC Environmental Exposures, Host Factors, and Human Disease, and the California Air Resource Board. One author disclosed being an associate editor for the Journal of Clinical Oncology. No other potential conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE: 

A recent study found that long-term exposure to fine particulate matter ≤ 2.5 μm (PM2.5) is associated with an increased risk for breast cancer, with the highest risk observed among White women.

METHODOLOGY:

  • Studies have suggested that exposure to air pollution — specifically PM2.5 — may increase the risk for breast cancer, but data are largely in populations of White women.
  • The current analysis explored the potential risk among a more racially and ethnically diverse group.
  • The study included 58,358 women (median age, 60.4 years at enrollment) from the California Cancer Registry, followed over an average of 19.3 years. Overall, 35% were African American, 39% were Latino, 15% were White, and 10% were Japanese American.
  • Researchers measured PM2.5 exposure using satellite-based data and geocoded addresses. Other pollutants, such as PM10, NO2, NOX, and CO, were also tracked using Environmental Protection Agency data.

TAKEAWAY:

  • A total of 3524 invasive breast cancer cases were diagnosed over an average follow-up period of 19.3 years. PM2.5 exposure was associated with a 28% increased risk for breast cancer overall (hazard ratio [HR], 1.28; 95% CI, 1.08-1.51).
  • When looking at risk by racial/ethnic group, the association between PM2.5 exposure and breast cancer risk was strongest among White women (HR, 1.67). PM2.5 exposure was also associated with a higher risk for breast cancer among African American women (HR, 1.14; 95% CI, 0.89-1.46) and Latino women (HR, 1.34; 95% CI, 0.94-1.92), but the associations were not significant.
  • Overall breast cancer incidence was also positively associated with exposure to NO2, NOX, and CO (HRs, 1.09-1.11), but the associations were not significant. A meta-analysis of this study and ten other cohorts estimated a 5% increased breast cancer incidence per 10-unit increase in PM2.5 (HR, 1.05).

IN PRACTICE:

“Collective findings suggest that PM2.5 exposure should be considered a risk factor for breast cancer, and curtailing air pollution exposures at the population level using regulatory strategies should be a priority,” the authors concluded.

SOURCE:

The study, led by Anna H. Wu, PhD, MPH, Keck School of Medicine, University of Southern California, Los Angeles, was published online in the Journal of Clinical Oncology.

LIMITATIONS:

The study did not include data on nonresidential exposures or residential history before cohort entry, which limited the assessment of earlier exposures. The study also lacked information on specific sources of PM emissions, as well as an explanation for why White women had the highest breast cancer risk compared with other racial/ethnic groups.

DISCLOSURES:

The study was supported by grants from the Health Effects Air Pollution Foundation, the National Cancer Institute, USC Environmental Exposures, Host Factors, and Human Disease, and the California Air Resource Board. One author disclosed being an associate editor for the Journal of Clinical Oncology. No other potential conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE: 

A recent study found that long-term exposure to fine particulate matter ≤ 2.5 μm (PM2.5) is associated with an increased risk for breast cancer, with the highest risk observed among White women.

METHODOLOGY:

  • Studies have suggested that exposure to air pollution — specifically PM2.5 — may increase the risk for breast cancer, but data are largely in populations of White women.
  • The current analysis explored the potential risk among a more racially and ethnically diverse group.
  • The study included 58,358 women (median age, 60.4 years at enrollment) from the California Cancer Registry, followed over an average of 19.3 years. Overall, 35% were African American, 39% were Latino, 15% were White, and 10% were Japanese American.
  • Researchers measured PM2.5 exposure using satellite-based data and geocoded addresses. Other pollutants, such as PM10, NO2, NOX, and CO, were also tracked using Environmental Protection Agency data.

TAKEAWAY:

  • A total of 3524 invasive breast cancer cases were diagnosed over an average follow-up period of 19.3 years. PM2.5 exposure was associated with a 28% increased risk for breast cancer overall (hazard ratio [HR], 1.28; 95% CI, 1.08-1.51).
  • When looking at risk by racial/ethnic group, the association between PM2.5 exposure and breast cancer risk was strongest among White women (HR, 1.67). PM2.5 exposure was also associated with a higher risk for breast cancer among African American women (HR, 1.14; 95% CI, 0.89-1.46) and Latino women (HR, 1.34; 95% CI, 0.94-1.92), but the associations were not significant.
  • Overall breast cancer incidence was also positively associated with exposure to NO2, NOX, and CO (HRs, 1.09-1.11), but the associations were not significant. A meta-analysis of this study and ten other cohorts estimated a 5% increased breast cancer incidence per 10-unit increase in PM2.5 (HR, 1.05).

IN PRACTICE:

“Collective findings suggest that PM2.5 exposure should be considered a risk factor for breast cancer, and curtailing air pollution exposures at the population level using regulatory strategies should be a priority,” the authors concluded.

SOURCE:

The study, led by Anna H. Wu, PhD, MPH, Keck School of Medicine, University of Southern California, Los Angeles, was published online in the Journal of Clinical Oncology.

LIMITATIONS:

The study did not include data on nonresidential exposures or residential history before cohort entry, which limited the assessment of earlier exposures. The study also lacked information on specific sources of PM emissions, as well as an explanation for why White women had the highest breast cancer risk compared with other racial/ethnic groups.

DISCLOSURES:

The study was supported by grants from the Health Effects Air Pollution Foundation, the National Cancer Institute, USC Environmental Exposures, Host Factors, and Human Disease, and the California Air Resource Board. One author disclosed being an associate editor for the Journal of Clinical Oncology. No other potential conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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FDA Approves OnabotulinumtoxinA for Improving Platysma Bands

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The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

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The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

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Neurologists Lack Awareness of Steroid Toxicity

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There is a lack of understanding among neuromuscular specialists on how to balance the risks for and benefits of corticosteroids when treating patients with generalized myasthenia gravis (gMG) and chronic inflammatory demyelinating polyneuropathy (CIDP), results of a US survey showed.

For both MG and CIDP specialists, uncertainty around corticosteroid dosing, duration, and toxicity underscores the need for more guidance, the investigators noted. Over 85% of respondents indicated that a tool for systematically monitoring corticosteroid toxicity would be valuable.

The results indicate “a lack of knowledge by this pool of neurologists about the guidelines and what they contain,” said study investigator Gil Wolfe, MD, professor of neurology at the Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, in New York.

Clearer guidance on how to administer corticosteroids and manage toxicities in patients with gMG and CIDP “would be welcomed by neurologists and have potential for benefit to patient care,” the team noted.

The findings were presented at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Lack of Knowledge

Although guidelines for both CIDP and gMG recommend corticosteroids as first-line treatment and emphasize using the lowest effective dose to control symptoms, they do not include specific recommendations on dosing, duration, or toxicity monitoring, the researchers noted.

Despite this, a large proportion of survey respondents reported using guidelines to make clinical decisions on monitoring toxicity, with up to a third actually endorsing a guideline that doesn’t exist.

The cross-sectional, online survey was deployed in November and December 2023 and included 200 US neurologists. Of these, 99 answered questions on CIDP, and 101 answered similar questions on gMG.

To participate in the survey, respondents had to be board-certified neurologists, practicing for at least 2 years post-residency, and have treated or consulted on at least three patients with CIDP or 10 patients with gMG in the past year who were on a corticosteroid dose of at least 10 mg daily for 1 month or more.

CIDP respondents had been practicing a mean of 18.1 years since residency and were board certified in neuromuscular (20%), electrodiagnostic medicine/clinical neurophysiology (21%), and pediatric neurology (8%). Two thirds of them accepted referrals from other neurologists.

The gMG respondents had been practicing a mean of 20.5 years since residency and were board certified in neuromuscular (45%), electrodiagnostic medicine/clinical neurophysiology (35%), and pediatric neurology (17%). A total of 72% accepted referrals from other neurologists.

Respondents estimated that about 60% of their patients with gMG and 58% of patients with CIDP were being treated with corticosteroids, with gMG and CIDP respondents reporting a mean of 26.4 and 15.6 patients, respectively, meeting the study’s dosing criteria.
 

Appropriate Dosing

When asked what chronic, long-term (≥ 6 months) corticosteroid dose they considered safe in terms of minimizing adverse events, 43% of CIDP respondents and 51% of gMG respondents considered corticosteroid doses of 10 mg/d or less (prednisone equivalent) well tolerated; additionally, 32% and 31%, respectively, considered 20-40 mg/d well tolerated. Moreover, they said only about half of their patients would be able to taper to less than 10 mg/d in less than 6 months.

“Studies suggest safety is not seen until patients are on doses at 5 mg/d or less,” Wolfe said. “There is not enough appreciation that doses at levels we once considered safe really do pose significant risk,” he added.

“With the increasing number of treatment options in MG and to a lesser extent in CIDP, we need to do all we can to use corticosteroids as judiciously as possible and be aware of side effects our patients may not even report unless we make a pointed effort to ask about them.”

Familiarity with corticosteroid toxicities was more common among gMG respondents, of whom 77% reported being very/extremely familiar, than among 55% of CIDP respondents. Appetite/weight gain was reported among the most common adverse effects (AEs) associated with long-term CS use (reported by 68% of CIDP and 58% of gMG respondents). Other common AEs reported were insulin resistance (53% of CIDP and 50% of gMG respondents), decreased bone density (47% and 48%, respectively), immunosuppression (37% and 45%, respectively). Mood and behavioral change were noted by 56% of CIDP and 37% of gMG respondents, particularly mood swings, irritability, mania, and sleep disorders.

When asked how they balanced the risk for and benefit of corticosteroids, more than 80% of CIDP specialists reported personally monitoring for corticosteroid-related toxicity, and 42% reported they collaborated with the patient’s primary care provider. However, fewer than 10% reported ordering lab tests. Among neurologists treating gMG, 84% said they typically monitor corticosteroid toxicity independently, while 41% reported doing so in collaboration with primary care providers.

Two thirds of CIDP respondents and 53% of gMG respondents reported using guidelines to make clinical decisions on monitoring toxicity, and 34% of gMG respondents actually endorsed using the Guideline for Systematic Surveillance of Steroid Safety, which does not exist.
 

‘A Big Issue’ in Neurology

Commenting on the results, Said R. Beydoun, MD, professor and division chief, Neuromuscular Medicine, Department of Neurology at Keck Medicine of University of Southern California, Los Angeles, said steroid toxicity is “a big issue” in neurology.

These patients can be on chronic therapy, and they aren’t really monitored for osteoporosis or other complications, he said, adding that neurologists aren’t always taking the necessary precautions to prevent steroid toxicity.

Beydoun estimated that about half of neurologists are not adequately familiar with balancing the efficacy of corticosteroids versus in toxicity.

“Objective improvement, either on the functional scale or the muscle impairment scale — that’s really response treatment. Whereas adverse effects of a treatment are something separate. The patient may be improving but also maybe developing other complications from the treatment,” he said.

Also commenting, Ghazala Hayat, MD, professor of neurology and director of neuromuscular and clinical neurophysiology services at Saint Louis University in St. Louis, said there is a clear need for more education.

“I always say prednisone is our best friend initially, and then it becomes the worst enemy. If you don’t see lots of neuromuscular patients, you might not know even how to recognize toxicity or how to taper. Or the opposite to that, if you taper too quickly, patients relapse.”

The study was funded by argenx. Wolfe reported serving on advisory boards for Alexion, argenx, UCB, and Johnson & Johnson. Neelam Goyal, MD, is a consultant/advisor for Alexion, argenx, Amgen, Janssen, Lycia Therapeutics, and UCB and has received grant support from argenx. Beydoun reported receiving research support and consulting and speaking fees from Healey Center, Amylyx, AB Science, Sanofi, Janssen, Genentech, Regeneron, UCB, Abcuro argenx, Alnylam, AstraZeneca, Amylyx, CSL Behring, Grifols, Takeda, Octapharma, UCB, and Janssen. Hayat reported speaker and advisory roles with argenx, Alexion, and MTPA.
 

A version of this article appeared on Medscape.com.

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There is a lack of understanding among neuromuscular specialists on how to balance the risks for and benefits of corticosteroids when treating patients with generalized myasthenia gravis (gMG) and chronic inflammatory demyelinating polyneuropathy (CIDP), results of a US survey showed.

For both MG and CIDP specialists, uncertainty around corticosteroid dosing, duration, and toxicity underscores the need for more guidance, the investigators noted. Over 85% of respondents indicated that a tool for systematically monitoring corticosteroid toxicity would be valuable.

The results indicate “a lack of knowledge by this pool of neurologists about the guidelines and what they contain,” said study investigator Gil Wolfe, MD, professor of neurology at the Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, in New York.

Clearer guidance on how to administer corticosteroids and manage toxicities in patients with gMG and CIDP “would be welcomed by neurologists and have potential for benefit to patient care,” the team noted.

The findings were presented at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Lack of Knowledge

Although guidelines for both CIDP and gMG recommend corticosteroids as first-line treatment and emphasize using the lowest effective dose to control symptoms, they do not include specific recommendations on dosing, duration, or toxicity monitoring, the researchers noted.

Despite this, a large proportion of survey respondents reported using guidelines to make clinical decisions on monitoring toxicity, with up to a third actually endorsing a guideline that doesn’t exist.

The cross-sectional, online survey was deployed in November and December 2023 and included 200 US neurologists. Of these, 99 answered questions on CIDP, and 101 answered similar questions on gMG.

To participate in the survey, respondents had to be board-certified neurologists, practicing for at least 2 years post-residency, and have treated or consulted on at least three patients with CIDP or 10 patients with gMG in the past year who were on a corticosteroid dose of at least 10 mg daily for 1 month or more.

CIDP respondents had been practicing a mean of 18.1 years since residency and were board certified in neuromuscular (20%), electrodiagnostic medicine/clinical neurophysiology (21%), and pediatric neurology (8%). Two thirds of them accepted referrals from other neurologists.

The gMG respondents had been practicing a mean of 20.5 years since residency and were board certified in neuromuscular (45%), electrodiagnostic medicine/clinical neurophysiology (35%), and pediatric neurology (17%). A total of 72% accepted referrals from other neurologists.

Respondents estimated that about 60% of their patients with gMG and 58% of patients with CIDP were being treated with corticosteroids, with gMG and CIDP respondents reporting a mean of 26.4 and 15.6 patients, respectively, meeting the study’s dosing criteria.
 

Appropriate Dosing

When asked what chronic, long-term (≥ 6 months) corticosteroid dose they considered safe in terms of minimizing adverse events, 43% of CIDP respondents and 51% of gMG respondents considered corticosteroid doses of 10 mg/d or less (prednisone equivalent) well tolerated; additionally, 32% and 31%, respectively, considered 20-40 mg/d well tolerated. Moreover, they said only about half of their patients would be able to taper to less than 10 mg/d in less than 6 months.

“Studies suggest safety is not seen until patients are on doses at 5 mg/d or less,” Wolfe said. “There is not enough appreciation that doses at levels we once considered safe really do pose significant risk,” he added.

“With the increasing number of treatment options in MG and to a lesser extent in CIDP, we need to do all we can to use corticosteroids as judiciously as possible and be aware of side effects our patients may not even report unless we make a pointed effort to ask about them.”

Familiarity with corticosteroid toxicities was more common among gMG respondents, of whom 77% reported being very/extremely familiar, than among 55% of CIDP respondents. Appetite/weight gain was reported among the most common adverse effects (AEs) associated with long-term CS use (reported by 68% of CIDP and 58% of gMG respondents). Other common AEs reported were insulin resistance (53% of CIDP and 50% of gMG respondents), decreased bone density (47% and 48%, respectively), immunosuppression (37% and 45%, respectively). Mood and behavioral change were noted by 56% of CIDP and 37% of gMG respondents, particularly mood swings, irritability, mania, and sleep disorders.

When asked how they balanced the risk for and benefit of corticosteroids, more than 80% of CIDP specialists reported personally monitoring for corticosteroid-related toxicity, and 42% reported they collaborated with the patient’s primary care provider. However, fewer than 10% reported ordering lab tests. Among neurologists treating gMG, 84% said they typically monitor corticosteroid toxicity independently, while 41% reported doing so in collaboration with primary care providers.

Two thirds of CIDP respondents and 53% of gMG respondents reported using guidelines to make clinical decisions on monitoring toxicity, and 34% of gMG respondents actually endorsed using the Guideline for Systematic Surveillance of Steroid Safety, which does not exist.
 

‘A Big Issue’ in Neurology

Commenting on the results, Said R. Beydoun, MD, professor and division chief, Neuromuscular Medicine, Department of Neurology at Keck Medicine of University of Southern California, Los Angeles, said steroid toxicity is “a big issue” in neurology.

These patients can be on chronic therapy, and they aren’t really monitored for osteoporosis or other complications, he said, adding that neurologists aren’t always taking the necessary precautions to prevent steroid toxicity.

Beydoun estimated that about half of neurologists are not adequately familiar with balancing the efficacy of corticosteroids versus in toxicity.

“Objective improvement, either on the functional scale or the muscle impairment scale — that’s really response treatment. Whereas adverse effects of a treatment are something separate. The patient may be improving but also maybe developing other complications from the treatment,” he said.

Also commenting, Ghazala Hayat, MD, professor of neurology and director of neuromuscular and clinical neurophysiology services at Saint Louis University in St. Louis, said there is a clear need for more education.

“I always say prednisone is our best friend initially, and then it becomes the worst enemy. If you don’t see lots of neuromuscular patients, you might not know even how to recognize toxicity or how to taper. Or the opposite to that, if you taper too quickly, patients relapse.”

The study was funded by argenx. Wolfe reported serving on advisory boards for Alexion, argenx, UCB, and Johnson & Johnson. Neelam Goyal, MD, is a consultant/advisor for Alexion, argenx, Amgen, Janssen, Lycia Therapeutics, and UCB and has received grant support from argenx. Beydoun reported receiving research support and consulting and speaking fees from Healey Center, Amylyx, AB Science, Sanofi, Janssen, Genentech, Regeneron, UCB, Abcuro argenx, Alnylam, AstraZeneca, Amylyx, CSL Behring, Grifols, Takeda, Octapharma, UCB, and Janssen. Hayat reported speaker and advisory roles with argenx, Alexion, and MTPA.
 

A version of this article appeared on Medscape.com.

There is a lack of understanding among neuromuscular specialists on how to balance the risks for and benefits of corticosteroids when treating patients with generalized myasthenia gravis (gMG) and chronic inflammatory demyelinating polyneuropathy (CIDP), results of a US survey showed.

For both MG and CIDP specialists, uncertainty around corticosteroid dosing, duration, and toxicity underscores the need for more guidance, the investigators noted. Over 85% of respondents indicated that a tool for systematically monitoring corticosteroid toxicity would be valuable.

The results indicate “a lack of knowledge by this pool of neurologists about the guidelines and what they contain,” said study investigator Gil Wolfe, MD, professor of neurology at the Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, in New York.

Clearer guidance on how to administer corticosteroids and manage toxicities in patients with gMG and CIDP “would be welcomed by neurologists and have potential for benefit to patient care,” the team noted.

The findings were presented at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Lack of Knowledge

Although guidelines for both CIDP and gMG recommend corticosteroids as first-line treatment and emphasize using the lowest effective dose to control symptoms, they do not include specific recommendations on dosing, duration, or toxicity monitoring, the researchers noted.

Despite this, a large proportion of survey respondents reported using guidelines to make clinical decisions on monitoring toxicity, with up to a third actually endorsing a guideline that doesn’t exist.

The cross-sectional, online survey was deployed in November and December 2023 and included 200 US neurologists. Of these, 99 answered questions on CIDP, and 101 answered similar questions on gMG.

To participate in the survey, respondents had to be board-certified neurologists, practicing for at least 2 years post-residency, and have treated or consulted on at least three patients with CIDP or 10 patients with gMG in the past year who were on a corticosteroid dose of at least 10 mg daily for 1 month or more.

CIDP respondents had been practicing a mean of 18.1 years since residency and were board certified in neuromuscular (20%), electrodiagnostic medicine/clinical neurophysiology (21%), and pediatric neurology (8%). Two thirds of them accepted referrals from other neurologists.

The gMG respondents had been practicing a mean of 20.5 years since residency and were board certified in neuromuscular (45%), electrodiagnostic medicine/clinical neurophysiology (35%), and pediatric neurology (17%). A total of 72% accepted referrals from other neurologists.

Respondents estimated that about 60% of their patients with gMG and 58% of patients with CIDP were being treated with corticosteroids, with gMG and CIDP respondents reporting a mean of 26.4 and 15.6 patients, respectively, meeting the study’s dosing criteria.
 

Appropriate Dosing

When asked what chronic, long-term (≥ 6 months) corticosteroid dose they considered safe in terms of minimizing adverse events, 43% of CIDP respondents and 51% of gMG respondents considered corticosteroid doses of 10 mg/d or less (prednisone equivalent) well tolerated; additionally, 32% and 31%, respectively, considered 20-40 mg/d well tolerated. Moreover, they said only about half of their patients would be able to taper to less than 10 mg/d in less than 6 months.

“Studies suggest safety is not seen until patients are on doses at 5 mg/d or less,” Wolfe said. “There is not enough appreciation that doses at levels we once considered safe really do pose significant risk,” he added.

“With the increasing number of treatment options in MG and to a lesser extent in CIDP, we need to do all we can to use corticosteroids as judiciously as possible and be aware of side effects our patients may not even report unless we make a pointed effort to ask about them.”

Familiarity with corticosteroid toxicities was more common among gMG respondents, of whom 77% reported being very/extremely familiar, than among 55% of CIDP respondents. Appetite/weight gain was reported among the most common adverse effects (AEs) associated with long-term CS use (reported by 68% of CIDP and 58% of gMG respondents). Other common AEs reported were insulin resistance (53% of CIDP and 50% of gMG respondents), decreased bone density (47% and 48%, respectively), immunosuppression (37% and 45%, respectively). Mood and behavioral change were noted by 56% of CIDP and 37% of gMG respondents, particularly mood swings, irritability, mania, and sleep disorders.

When asked how they balanced the risk for and benefit of corticosteroids, more than 80% of CIDP specialists reported personally monitoring for corticosteroid-related toxicity, and 42% reported they collaborated with the patient’s primary care provider. However, fewer than 10% reported ordering lab tests. Among neurologists treating gMG, 84% said they typically monitor corticosteroid toxicity independently, while 41% reported doing so in collaboration with primary care providers.

Two thirds of CIDP respondents and 53% of gMG respondents reported using guidelines to make clinical decisions on monitoring toxicity, and 34% of gMG respondents actually endorsed using the Guideline for Systematic Surveillance of Steroid Safety, which does not exist.
 

‘A Big Issue’ in Neurology

Commenting on the results, Said R. Beydoun, MD, professor and division chief, Neuromuscular Medicine, Department of Neurology at Keck Medicine of University of Southern California, Los Angeles, said steroid toxicity is “a big issue” in neurology.

These patients can be on chronic therapy, and they aren’t really monitored for osteoporosis or other complications, he said, adding that neurologists aren’t always taking the necessary precautions to prevent steroid toxicity.

Beydoun estimated that about half of neurologists are not adequately familiar with balancing the efficacy of corticosteroids versus in toxicity.

“Objective improvement, either on the functional scale or the muscle impairment scale — that’s really response treatment. Whereas adverse effects of a treatment are something separate. The patient may be improving but also maybe developing other complications from the treatment,” he said.

Also commenting, Ghazala Hayat, MD, professor of neurology and director of neuromuscular and clinical neurophysiology services at Saint Louis University in St. Louis, said there is a clear need for more education.

“I always say prednisone is our best friend initially, and then it becomes the worst enemy. If you don’t see lots of neuromuscular patients, you might not know even how to recognize toxicity or how to taper. Or the opposite to that, if you taper too quickly, patients relapse.”

The study was funded by argenx. Wolfe reported serving on advisory boards for Alexion, argenx, UCB, and Johnson & Johnson. Neelam Goyal, MD, is a consultant/advisor for Alexion, argenx, Amgen, Janssen, Lycia Therapeutics, and UCB and has received grant support from argenx. Beydoun reported receiving research support and consulting and speaking fees from Healey Center, Amylyx, AB Science, Sanofi, Janssen, Genentech, Regeneron, UCB, Abcuro argenx, Alnylam, AstraZeneca, Amylyx, CSL Behring, Grifols, Takeda, Octapharma, UCB, and Janssen. Hayat reported speaker and advisory roles with argenx, Alexion, and MTPA.
 

A version of this article appeared on Medscape.com.

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Veterans Affairs Hailed as a ‘Bright Spot’ in ALS Care

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Teamwork and transdisciplinary collaboration create an effective system of care for amyotrophic lateral sclerosis (ALS), ensuring improved health both for patients and clinicians alike, said one expert.

In a plenary address at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024, Ileana Howard, MD, medical co-director of the ALS Center of Excellence at VA Puget Sound in Seattle, said the recently released National Academies report “Living with ALS” cited the Veterans Administration as “a bright spot in the landscape of ALS care due to its interdisciplinary, holistic, and proactive approach to care.”

Since the early 2000s and the publication of several studies linking active military service with ALS, the US Department of Veterans Affairs (VA) has opened an ALS registry, a tissue and brain biobank, and in 2008, granted 100% presumptive service connection to any individual who served more than 90 days of active duty and was later diagnosed with ALS, she said.

“We now serve approximately 4000 veterans with ALS across the system, and we count 47 full interdisciplinary clinics within VA across the nation, with ALS coordinators designated for all 170 VA facilities, regardless of whether they had an ALS clinic or not, to serve as a navigator for patients and their families, to identify the closest ALS clinic that could meet their needs.” 
 

Multidisciplinary vs Interdisciplinary

Howard emphasized that transdisciplinary collaboration is essential for maintaining an effective system. She pointed out that the term “multidisciplinary” is outdated, referring to teams that work independently but in parallel on the same issue.

In contrast, interdisciplinary teams integrate their assessments into a cohesive plan of care, whereas transdisciplinary teams take it further by combining both their assessments and care plans, allowing for greater intentional overlap.

The VA’s ALS handbook lists approximately 20 essential clinicians for a VA ALS clinic, including recreation therapists, assistive technology specialists, and veteran benefit service officers to assist with disability benefits application, among others, she said.

Essential to this collaboration is “role release,” which deliberately blurs the boundaries between disciplines. “The future of our specialty hinges on effective and selfless collaboration,” she said.

Howard encouraged ALS healthcare providers to move away from outdated terminology rooted in hierarchical team models and to break down silos that no longer benefit either the patients or the care teams.

She noted that while teamwork can enhance patient outcomes and overall health, it has also been associated with better health among healthcare providers. It’s well-known, she said, that neurologists and physiatrists are among the specialties with the highest burnout rates, and ALS teams, in particular, experience significant stress and burnout.
 

Better Together

recent Canadian study on resiliency and burnout in ALS clinics surveyed a wide range of practitioners within ALS centers and found respondents drew resiliency through relationships with patients and colleagues, and that there was a strongly expressed desire for increased resources, team building/debriefing, and formal training in emotional exhaustion and burnout.

“A consistent theme was the lack of adequate allied health support (nursing, social work, occupational therapy) to address the complex needs of patients,” said the report’s senior author Kerri Lynn Schellenberg, MD, medical director of the ALS/Motor Neuron Diseases clinic and associate professor at the University of Saskatchewan College of Medicine in Saskatoon, Saskatchewan, Canada.

“The majority of participants felt they would benefit from more consistent team building exercises and debriefing,” noted the authors.

Schellenberg agreed, emphasizing that care teams perform best when there is mutual appreciation and support among members. By learning from one another and reaching consensus together, the care plan benefits from the collective expertise of the team. “We are stronger together,” she said.

Howard and Schellenberg reported no disclosures.
 

A version of this article appeared on Medscape.com.

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Teamwork and transdisciplinary collaboration create an effective system of care for amyotrophic lateral sclerosis (ALS), ensuring improved health both for patients and clinicians alike, said one expert.

In a plenary address at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024, Ileana Howard, MD, medical co-director of the ALS Center of Excellence at VA Puget Sound in Seattle, said the recently released National Academies report “Living with ALS” cited the Veterans Administration as “a bright spot in the landscape of ALS care due to its interdisciplinary, holistic, and proactive approach to care.”

Since the early 2000s and the publication of several studies linking active military service with ALS, the US Department of Veterans Affairs (VA) has opened an ALS registry, a tissue and brain biobank, and in 2008, granted 100% presumptive service connection to any individual who served more than 90 days of active duty and was later diagnosed with ALS, she said.

“We now serve approximately 4000 veterans with ALS across the system, and we count 47 full interdisciplinary clinics within VA across the nation, with ALS coordinators designated for all 170 VA facilities, regardless of whether they had an ALS clinic or not, to serve as a navigator for patients and their families, to identify the closest ALS clinic that could meet their needs.” 
 

Multidisciplinary vs Interdisciplinary

Howard emphasized that transdisciplinary collaboration is essential for maintaining an effective system. She pointed out that the term “multidisciplinary” is outdated, referring to teams that work independently but in parallel on the same issue.

In contrast, interdisciplinary teams integrate their assessments into a cohesive plan of care, whereas transdisciplinary teams take it further by combining both their assessments and care plans, allowing for greater intentional overlap.

The VA’s ALS handbook lists approximately 20 essential clinicians for a VA ALS clinic, including recreation therapists, assistive technology specialists, and veteran benefit service officers to assist with disability benefits application, among others, she said.

Essential to this collaboration is “role release,” which deliberately blurs the boundaries between disciplines. “The future of our specialty hinges on effective and selfless collaboration,” she said.

Howard encouraged ALS healthcare providers to move away from outdated terminology rooted in hierarchical team models and to break down silos that no longer benefit either the patients or the care teams.

She noted that while teamwork can enhance patient outcomes and overall health, it has also been associated with better health among healthcare providers. It’s well-known, she said, that neurologists and physiatrists are among the specialties with the highest burnout rates, and ALS teams, in particular, experience significant stress and burnout.
 

Better Together

recent Canadian study on resiliency and burnout in ALS clinics surveyed a wide range of practitioners within ALS centers and found respondents drew resiliency through relationships with patients and colleagues, and that there was a strongly expressed desire for increased resources, team building/debriefing, and formal training in emotional exhaustion and burnout.

“A consistent theme was the lack of adequate allied health support (nursing, social work, occupational therapy) to address the complex needs of patients,” said the report’s senior author Kerri Lynn Schellenberg, MD, medical director of the ALS/Motor Neuron Diseases clinic and associate professor at the University of Saskatchewan College of Medicine in Saskatoon, Saskatchewan, Canada.

“The majority of participants felt they would benefit from more consistent team building exercises and debriefing,” noted the authors.

Schellenberg agreed, emphasizing that care teams perform best when there is mutual appreciation and support among members. By learning from one another and reaching consensus together, the care plan benefits from the collective expertise of the team. “We are stronger together,” she said.

Howard and Schellenberg reported no disclosures.
 

A version of this article appeared on Medscape.com.

Teamwork and transdisciplinary collaboration create an effective system of care for amyotrophic lateral sclerosis (ALS), ensuring improved health both for patients and clinicians alike, said one expert.

In a plenary address at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024, Ileana Howard, MD, medical co-director of the ALS Center of Excellence at VA Puget Sound in Seattle, said the recently released National Academies report “Living with ALS” cited the Veterans Administration as “a bright spot in the landscape of ALS care due to its interdisciplinary, holistic, and proactive approach to care.”

Since the early 2000s and the publication of several studies linking active military service with ALS, the US Department of Veterans Affairs (VA) has opened an ALS registry, a tissue and brain biobank, and in 2008, granted 100% presumptive service connection to any individual who served more than 90 days of active duty and was later diagnosed with ALS, she said.

“We now serve approximately 4000 veterans with ALS across the system, and we count 47 full interdisciplinary clinics within VA across the nation, with ALS coordinators designated for all 170 VA facilities, regardless of whether they had an ALS clinic or not, to serve as a navigator for patients and their families, to identify the closest ALS clinic that could meet their needs.” 
 

Multidisciplinary vs Interdisciplinary

Howard emphasized that transdisciplinary collaboration is essential for maintaining an effective system. She pointed out that the term “multidisciplinary” is outdated, referring to teams that work independently but in parallel on the same issue.

In contrast, interdisciplinary teams integrate their assessments into a cohesive plan of care, whereas transdisciplinary teams take it further by combining both their assessments and care plans, allowing for greater intentional overlap.

The VA’s ALS handbook lists approximately 20 essential clinicians for a VA ALS clinic, including recreation therapists, assistive technology specialists, and veteran benefit service officers to assist with disability benefits application, among others, she said.

Essential to this collaboration is “role release,” which deliberately blurs the boundaries between disciplines. “The future of our specialty hinges on effective and selfless collaboration,” she said.

Howard encouraged ALS healthcare providers to move away from outdated terminology rooted in hierarchical team models and to break down silos that no longer benefit either the patients or the care teams.

She noted that while teamwork can enhance patient outcomes and overall health, it has also been associated with better health among healthcare providers. It’s well-known, she said, that neurologists and physiatrists are among the specialties with the highest burnout rates, and ALS teams, in particular, experience significant stress and burnout.
 

Better Together

recent Canadian study on resiliency and burnout in ALS clinics surveyed a wide range of practitioners within ALS centers and found respondents drew resiliency through relationships with patients and colleagues, and that there was a strongly expressed desire for increased resources, team building/debriefing, and formal training in emotional exhaustion and burnout.

“A consistent theme was the lack of adequate allied health support (nursing, social work, occupational therapy) to address the complex needs of patients,” said the report’s senior author Kerri Lynn Schellenberg, MD, medical director of the ALS/Motor Neuron Diseases clinic and associate professor at the University of Saskatchewan College of Medicine in Saskatoon, Saskatchewan, Canada.

“The majority of participants felt they would benefit from more consistent team building exercises and debriefing,” noted the authors.

Schellenberg agreed, emphasizing that care teams perform best when there is mutual appreciation and support among members. By learning from one another and reaching consensus together, the care plan benefits from the collective expertise of the team. “We are stronger together,” she said.

Howard and Schellenberg reported no disclosures.
 

A version of this article appeared on Medscape.com.

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Digital Tool May Help Neurologists Assess Steroid Toxicity

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A digital tool to help neurologists assess steroid toxicity in patients with myasthenia gravis (MG) demonstrated sensitivity in distinguishing between different doses and durations of steroid exposure in a retrospective, real-world study.

The Glucocorticoid Toxicity Index-Metabolic Domains (GTI-MD), an abbreviated version of the GTI (Steritas), used weighted, standardized clinical outcome assessments to calculate steroid toxicity using a de-identified electronic health record (EHR) dataset.

“The results of our study indicate that patients with MG who initiated steroids demonstrated evidence of steroid toxicity in as little as 90 days after initial exposure, which was significant for patients with 20+ mg at index with repeated use,” noted study investigators, led by Neelam Goyal, MD, clinical professor of neurology and neurological sciences at Stanford University School of Medicine in Palo Alto, California.

The findings were presented at American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Rapid Evidence of Toxicity

The GTI uses nine health domains to calculate steroid toxicity scores, and the GTI-MD, which has been shown to be closely correlated, uses four domains collected routinely in clinical practice: Body mass index (BMI), blood pressure, glucose tolerance, and lipid metabolism.

The study used the Optum EHR dataset to identify 682 adult patients with MG, mean age of 70 years, 38% women, with at least two confirmed diagnoses of MG between 30 and 730 days apart and information on steroid utilization.

Patients were divided into two groups: Steroid initiators (SI; n = 377) were those whose steroid use was already in progress at the index date, whereas steroid-naive (SN) patients (n = 305) began their steroid use at the index date. Among the SI group, 30% were on doses greater than 20 mg/d and 22% were on lower doses. Among the SN group, 22% were on doses greater than 20 mg/d and 26% were on lower doses.

As expected, mean GTI-MD scores measured 90 days after the index date were higher in the SI group than in the SN group, indicating a higher level of steroid toxicity in the SI group. This was measured with two subscores of the GTI-MD: The Cumulative Worsening Score (22.6 vs 18.7; P = .007) and the Aggregate Improvement Score (4.9 vs 1.9; P = .27), the latter incorporating resolved toxicities resulting from the introduction of steroid-sparing agents.

The authors commented that scores were higher in the SN group than expected, “which could be explained by age, previous steroid exposure, comorbidities, and side effects from other medications.” However, they concluded that the findings suggest utility of the tool retrospectively, with EHR data.
 

Clinical Application

The GTI and related measurements are proprietary tools and therefore not readily available to all clinicians, noted Marie Beaudin, MD, another neurologist at Stanford University School of Medicine, who was not involved in the research.

In a separate, observational, ongoing study, Beaudin and Goyal’s team are examining the use of the tool prospectively for following the steroid toxicity burden in 50 patients with MG and correlating it with MG outcomes measured using the MG-Activities of Daily Living, MG Composite, and MG-Quality of Life 15R validated scales, as well as the adverse event unit.

“The objective of this study is to quantify the burden of toxicity that our patients are having from glucocorticoids, see how sensitive to change the scale is as their dosage of prednisone changes, and explore the correlations between the score and their disease outcome measures,” Beaudin said.

Unlike the abbreviated GTI-MD, the GTI measures nine domains: Bone mineral density, BMI, lipid metabolism, blood pressure, glucose tolerance, myopathy, skin toxicity, neuropsychiatric symptoms, and infections.

The score involves actively prompting and examining the patient, making it quite comprehensive. Beaudin said the study has revealed interesting insights into how patients report their side effects. When asked broadly about steroid-related side effects, many patients mention issues like weight or skin issues.

However, she noted, when prompted specifically about symptoms like insomnia, irritability, depression, or cognitive changes, there was an unexpected increase in positive responses, as patients are often unaware these could be side effects. This suggests the study may capture a greater burden than originally anticipated, said Beaudin.

She added that the long-term utility of the GTI score might be to help clinicians predict steroid toxicity and guide management.

“Then we would get more aggressive in trying to wean or taper patients. But these are often complicated cases because as soon as we taper, the disease flares. It’s a difficult decision whether to reduce the dosage of prednisone because toxicity burden is high, when disease burden is high too, and that’s where other medications can come into play.”

For example, she said, for insurance coverage, a high steroid toxicity score could justify the need to initiate more expensive steroid-sparing agents.

Both studies were funded by argenx. Goyal reported that she has consulted and received grant support from argenx, UCB, Alexion, and Janssen argenx. Beaudin is supported by a McLaughlin Scholarship from Laval University, Quebec, Canada.
 

A version of this article appeared on Medscape.com.

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A digital tool to help neurologists assess steroid toxicity in patients with myasthenia gravis (MG) demonstrated sensitivity in distinguishing between different doses and durations of steroid exposure in a retrospective, real-world study.

The Glucocorticoid Toxicity Index-Metabolic Domains (GTI-MD), an abbreviated version of the GTI (Steritas), used weighted, standardized clinical outcome assessments to calculate steroid toxicity using a de-identified electronic health record (EHR) dataset.

“The results of our study indicate that patients with MG who initiated steroids demonstrated evidence of steroid toxicity in as little as 90 days after initial exposure, which was significant for patients with 20+ mg at index with repeated use,” noted study investigators, led by Neelam Goyal, MD, clinical professor of neurology and neurological sciences at Stanford University School of Medicine in Palo Alto, California.

The findings were presented at American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Rapid Evidence of Toxicity

The GTI uses nine health domains to calculate steroid toxicity scores, and the GTI-MD, which has been shown to be closely correlated, uses four domains collected routinely in clinical practice: Body mass index (BMI), blood pressure, glucose tolerance, and lipid metabolism.

The study used the Optum EHR dataset to identify 682 adult patients with MG, mean age of 70 years, 38% women, with at least two confirmed diagnoses of MG between 30 and 730 days apart and information on steroid utilization.

Patients were divided into two groups: Steroid initiators (SI; n = 377) were those whose steroid use was already in progress at the index date, whereas steroid-naive (SN) patients (n = 305) began their steroid use at the index date. Among the SI group, 30% were on doses greater than 20 mg/d and 22% were on lower doses. Among the SN group, 22% were on doses greater than 20 mg/d and 26% were on lower doses.

As expected, mean GTI-MD scores measured 90 days after the index date were higher in the SI group than in the SN group, indicating a higher level of steroid toxicity in the SI group. This was measured with two subscores of the GTI-MD: The Cumulative Worsening Score (22.6 vs 18.7; P = .007) and the Aggregate Improvement Score (4.9 vs 1.9; P = .27), the latter incorporating resolved toxicities resulting from the introduction of steroid-sparing agents.

The authors commented that scores were higher in the SN group than expected, “which could be explained by age, previous steroid exposure, comorbidities, and side effects from other medications.” However, they concluded that the findings suggest utility of the tool retrospectively, with EHR data.
 

Clinical Application

The GTI and related measurements are proprietary tools and therefore not readily available to all clinicians, noted Marie Beaudin, MD, another neurologist at Stanford University School of Medicine, who was not involved in the research.

In a separate, observational, ongoing study, Beaudin and Goyal’s team are examining the use of the tool prospectively for following the steroid toxicity burden in 50 patients with MG and correlating it with MG outcomes measured using the MG-Activities of Daily Living, MG Composite, and MG-Quality of Life 15R validated scales, as well as the adverse event unit.

“The objective of this study is to quantify the burden of toxicity that our patients are having from glucocorticoids, see how sensitive to change the scale is as their dosage of prednisone changes, and explore the correlations between the score and their disease outcome measures,” Beaudin said.

Unlike the abbreviated GTI-MD, the GTI measures nine domains: Bone mineral density, BMI, lipid metabolism, blood pressure, glucose tolerance, myopathy, skin toxicity, neuropsychiatric symptoms, and infections.

The score involves actively prompting and examining the patient, making it quite comprehensive. Beaudin said the study has revealed interesting insights into how patients report their side effects. When asked broadly about steroid-related side effects, many patients mention issues like weight or skin issues.

However, she noted, when prompted specifically about symptoms like insomnia, irritability, depression, or cognitive changes, there was an unexpected increase in positive responses, as patients are often unaware these could be side effects. This suggests the study may capture a greater burden than originally anticipated, said Beaudin.

She added that the long-term utility of the GTI score might be to help clinicians predict steroid toxicity and guide management.

“Then we would get more aggressive in trying to wean or taper patients. But these are often complicated cases because as soon as we taper, the disease flares. It’s a difficult decision whether to reduce the dosage of prednisone because toxicity burden is high, when disease burden is high too, and that’s where other medications can come into play.”

For example, she said, for insurance coverage, a high steroid toxicity score could justify the need to initiate more expensive steroid-sparing agents.

Both studies were funded by argenx. Goyal reported that she has consulted and received grant support from argenx, UCB, Alexion, and Janssen argenx. Beaudin is supported by a McLaughlin Scholarship from Laval University, Quebec, Canada.
 

A version of this article appeared on Medscape.com.

A digital tool to help neurologists assess steroid toxicity in patients with myasthenia gravis (MG) demonstrated sensitivity in distinguishing between different doses and durations of steroid exposure in a retrospective, real-world study.

The Glucocorticoid Toxicity Index-Metabolic Domains (GTI-MD), an abbreviated version of the GTI (Steritas), used weighted, standardized clinical outcome assessments to calculate steroid toxicity using a de-identified electronic health record (EHR) dataset.

“The results of our study indicate that patients with MG who initiated steroids demonstrated evidence of steroid toxicity in as little as 90 days after initial exposure, which was significant for patients with 20+ mg at index with repeated use,” noted study investigators, led by Neelam Goyal, MD, clinical professor of neurology and neurological sciences at Stanford University School of Medicine in Palo Alto, California.

The findings were presented at American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) 2024.
 

Rapid Evidence of Toxicity

The GTI uses nine health domains to calculate steroid toxicity scores, and the GTI-MD, which has been shown to be closely correlated, uses four domains collected routinely in clinical practice: Body mass index (BMI), blood pressure, glucose tolerance, and lipid metabolism.

The study used the Optum EHR dataset to identify 682 adult patients with MG, mean age of 70 years, 38% women, with at least two confirmed diagnoses of MG between 30 and 730 days apart and information on steroid utilization.

Patients were divided into two groups: Steroid initiators (SI; n = 377) were those whose steroid use was already in progress at the index date, whereas steroid-naive (SN) patients (n = 305) began their steroid use at the index date. Among the SI group, 30% were on doses greater than 20 mg/d and 22% were on lower doses. Among the SN group, 22% were on doses greater than 20 mg/d and 26% were on lower doses.

As expected, mean GTI-MD scores measured 90 days after the index date were higher in the SI group than in the SN group, indicating a higher level of steroid toxicity in the SI group. This was measured with two subscores of the GTI-MD: The Cumulative Worsening Score (22.6 vs 18.7; P = .007) and the Aggregate Improvement Score (4.9 vs 1.9; P = .27), the latter incorporating resolved toxicities resulting from the introduction of steroid-sparing agents.

The authors commented that scores were higher in the SN group than expected, “which could be explained by age, previous steroid exposure, comorbidities, and side effects from other medications.” However, they concluded that the findings suggest utility of the tool retrospectively, with EHR data.
 

Clinical Application

The GTI and related measurements are proprietary tools and therefore not readily available to all clinicians, noted Marie Beaudin, MD, another neurologist at Stanford University School of Medicine, who was not involved in the research.

In a separate, observational, ongoing study, Beaudin and Goyal’s team are examining the use of the tool prospectively for following the steroid toxicity burden in 50 patients with MG and correlating it with MG outcomes measured using the MG-Activities of Daily Living, MG Composite, and MG-Quality of Life 15R validated scales, as well as the adverse event unit.

“The objective of this study is to quantify the burden of toxicity that our patients are having from glucocorticoids, see how sensitive to change the scale is as their dosage of prednisone changes, and explore the correlations between the score and their disease outcome measures,” Beaudin said.

Unlike the abbreviated GTI-MD, the GTI measures nine domains: Bone mineral density, BMI, lipid metabolism, blood pressure, glucose tolerance, myopathy, skin toxicity, neuropsychiatric symptoms, and infections.

The score involves actively prompting and examining the patient, making it quite comprehensive. Beaudin said the study has revealed interesting insights into how patients report their side effects. When asked broadly about steroid-related side effects, many patients mention issues like weight or skin issues.

However, she noted, when prompted specifically about symptoms like insomnia, irritability, depression, or cognitive changes, there was an unexpected increase in positive responses, as patients are often unaware these could be side effects. This suggests the study may capture a greater burden than originally anticipated, said Beaudin.

She added that the long-term utility of the GTI score might be to help clinicians predict steroid toxicity and guide management.

“Then we would get more aggressive in trying to wean or taper patients. But these are often complicated cases because as soon as we taper, the disease flares. It’s a difficult decision whether to reduce the dosage of prednisone because toxicity burden is high, when disease burden is high too, and that’s where other medications can come into play.”

For example, she said, for insurance coverage, a high steroid toxicity score could justify the need to initiate more expensive steroid-sparing agents.

Both studies were funded by argenx. Goyal reported that she has consulted and received grant support from argenx, UCB, Alexion, and Janssen argenx. Beaudin is supported by a McLaughlin Scholarship from Laval University, Quebec, Canada.
 

A version of this article appeared on Medscape.com.

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Click on the link below to access the entire supplement. 

 

 

  • Case Studies in Continuous Glucose Monitoring
  • Detection and Diagnosis of Early Symptomatic 
    Alzheimer’s Disease in Primary Care
  • Elevating the Importance of Asthma Care in the United States
  • Hypercortisolism is More Common Than You Think – 
    Here’s How to Find It
  • Improving COPD Management at Transitions of Care
  • Improving Patient-Centric COPD Management 
  • The Role of Finerenone in Optimizing Cardiovascular-
    Kidney-Metabolic Health: Everything PCPs Should Know
  • What Primary Care Clinicians Need to Know About Once-Weekly Insulins

This supplement offers the opportunity to earn a total of 3 continuing medical education (CME) credits. Credit is awarded for the successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.

Click here to read the 2024 Hot Topics in Primary Care

 

 

Hot Topics in Primary Care 2024 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.

Click on the link below to access the entire supplement. 

 

 

  • Case Studies in Continuous Glucose Monitoring
  • Detection and Diagnosis of Early Symptomatic 
    Alzheimer’s Disease in Primary Care
  • Elevating the Importance of Asthma Care in the United States
  • Hypercortisolism is More Common Than You Think – 
    Here’s How to Find It
  • Improving COPD Management at Transitions of Care
  • Improving Patient-Centric COPD Management 
  • The Role of Finerenone in Optimizing Cardiovascular-
    Kidney-Metabolic Health: Everything PCPs Should Know
  • What Primary Care Clinicians Need to Know About Once-Weekly Insulins

This supplement offers the opportunity to earn a total of 3 continuing medical education (CME) credits. Credit is awarded for the successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.

Click here to read the 2024 Hot Topics in Primary Care

 

 

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