Mrs. A, age 68, has a 40-year history of schizoaffective disorder with comorbid anxiety disorder not otherwise specified, type 2 diabetes mellitus, and hypertension. She takes furosemide, 40 mg/d, lisinopril, 20 mg/d, and metformin, 2,000 mg/d, for hypertension and diabetes; lorazepam, 1.5 mg/d, and paroxetine, 40 mg/d, for anxiety; and quetiapine extended release, 800 mg/d, for psychotic features and mood dysregulation with schizoaffective disorder. Mrs. A’s husband died 5 years ago and she lives alone in a senior care facility. Mrs. A uses a weekly pill reminder box because her residential facility does not monitor medication adherence. She sees her psychiatrist once a month and her primary care provider every 3 months. She has no history of illicit drug, alcohol, or tobacco use.

Two weeks ago, Mrs. A was found leaning against the wall in a hallway, complaining of dizziness and disorientation, and unable to find her way back to her apartment. In the emergency department, her serum potassium is low (3.0 mEq/L; normal range: 3.5 to 5.0), fasting glucose is elevated (110 mg/dL; range: 65 to 99), and ECG reveals a prolonged QTc interval of 530 milliseconds. Before this episode, Mrs. A had been medically stable without mood or psychotic symptoms, although her daughter reported medication self-administration was becoming difficult.

Exposure to psychotropics carries a risk of QTc prolongation. The QT interval is an ECG measure of ventricular depolarization and repolarization. The QTc designation indicates a correction for heart rate with increasing heart rate correlating with a shorter QT interval. Readings of 440 milliseconds are considered normal.¹ QTc prolongation is defined as >450 milliseconds for men and >470 milliseconds for women.² An increase in the QT interval is a predictor of serious cardiac events.³

Antidepressants and antipsychotics have been associated with QTc prolongation. When identifying agents that could disrupt cardiac conduction, clinicians need to consider whether the drug’s molecular structure, receptor affinity, or pharmacologic effects are most critical.² Although these may be important, patient-specific variables that increase the risk of QTc prolongation may have greater impact. These include:

• age >65
• female sex
• electrolyte imbalances (specifically low serum potassium and magnesium levels)
• high or toxic serum levels of the suspected drug
• preexisting cardiovascular impairment, such as bradycardia.^4,5

Other risk factors include concurrent use of an agent with similar cardiovascular effects or one that competes for metabolism (either enzymatic or at the binding site), physiologic limitations such as renal insufficiency, and medication changes that may increase or decrease psychotropic clearance.^4,6 Geriatric patients with dementia have an increased risk for cardiovascular-related death.^7,8

Antidepressants

Among tricyclic antidepressants, most reports of QTc prolongation involve amitriptyline and maprotiline.⁹ Risk factors include demographics (eg, female sex, age), personal or family history (congenital long QT syndrome, cardiovascular disease), and concurrent conditions or drug use, particularly those associated with QTc prolongation.³ Desipramine and nortriptyline also have been identified as high-risk agents.¹⁰

QTc prolongation has been reported with all selective serotonin reuptake inhibitors at plasma concentrations above the therapeutic level.¹¹ Fluoxetine-associated QTc prolongation was limited to cases of overdose or when additional risk factors were reported.⁴ QTc prolongation from psychotropics could increase the risk of torsades de pointes, according to an analysis of the FDA Adverse Event Reporting System.¹² In 2011, the FDA reported an increased risk of abnormal heart rhythms—including QTc prolongation—with citalopram doses >40 mg/d.¹³ Although cases of QTc prolongation with paroxetine have not been reported,¹¹ the Arizona Center for Education and Research on Therapeutics lists paroxetine with other agents that may increase the risk for QTc prolongation with concurrent use of medications that may prolong QTc interval.¹⁴ Venlafaxine doses >300 mg/d may require additional cardiac monitoring.^5,12 Data from venlafaxine poisoning case reports found a positive correlation between dose and QTc prolongation.¹⁵ In a review of toxicology database information, Wenzel-Seifert et al⁴ found extended QT interval with citalopram, fluoxetine, and venlafaxine at toxic doses or in the presence of additional risk factors such as sex, older age, or personal or family history of congenital long QT syndrome or cardiovascular disease.

Antipsychotics

Case reports, case series, and research trials have evaluated the risk of QTc prolongation with antipsychotics (Table).^1,2,4,16,17 The first-generation antipsychotics thioridazine,^4,16,18 mesoridazine,^16,18 chlorpromazine,¹⁹ and haloperidol³ warrant cardiac monitoring. The QTc prolongation effects of thioridazine and its active metabolite mesoridazine are well-documented and thioridazine-mediated QTc prolongation increases are dose-dependent.^4,18 ECG monitoring is recommended with IV haloperidol, which is used for delirium in adults.²⁰ QTc prolongation has been associated with long-term ziprasidone use more often than with risperidone, olanzapine, or quetiapine.¹⁹ Ziprasidone prolongs the QTc interval an average of 20 milliseconds,²¹ which could represent a clinically significant change. QTc prolongation for iloperidone is comparable to ziprasidone and haloperidol.²² There is some evidence that aripiprazole may shorten, rather than prolong, the QTc interval.^4,17

Cardiovascular adverse effects associated with clozapine—including QTc prolongation—are dose-dependent.³ Olanzapine prolongs QTc interval, although the mean change is less than with other agents unless other variables were present, such as:

• concomitant use of medications that may prolong QTc interval (ie, amantadine, hydroxyzine, or tamoxifen²)
• preexisting cardiovascular conduction disorders
• higher doses (>40 mg/d).^3,23

In 17 case reports of cardiac changes associated with quetiapine use, doses ranged from 100 mg/d²⁴ to an overdose of 36 g/d.²⁵ Only 1 patient death was reported secondary to overdose and preexisting dysrhythmia and hypertension.²⁶ QTc prolongation associated with risperidone was minor¹ based on oral doses in the normal therapeutic range and incidences of overdose.¹⁰ Paliperidone²⁷ and lurasidone²⁸ are associated with clinically insignificant QTc prolongation. Changes in QTc interval were positively correlated with asenapine dose, although at the highest dose of 40 mg/d, the increase was <5 milliseconds.²⁹

Mrs. A presents with a number of risk factors for QTc prolongation, including older age, female sex, and psychiatric and medical comorbidities that require medication. A pill count revealed that she was taking more than the prescribed daily doses of her medications. During the interview, Mrs. A said that if she missed her medication time, she would take them when she remembered. If she could not remember if she took her pills, she would take them again. Her physicians will explore strategies to increase medication adherence.

Table

Examples of QTc prolongation associated with select antipsychotics^a

Related Resources

• De Hert M, Detraux J, van Winkel R, et al. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat Rev Endocrinol. 2011;8(2):114-126.
• Vieweg WV, Wood MA, Fernandez A, et al. Proarrhythmic risk with antipsychotic and antidepressant drugs: implications in the elderly. Drugs Aging. 2009;26(12):997-1012.
• Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.

Drug Brand Names

• Amantadine • Symmetrel
• Amitriptyline • Elavil
• Aripiprazole • Abilify
• Asenapine • Saphris
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Clozapine • Clozaril
• Desipramine • Norpramin
• Fluoxetine • Prozac
• Furosemide • Lasix
• Haloperidol • Haldol
• Hydroxyzine • Atarax, Vistaril
• Iloperidone • Fanapt
• Lisinopril • Prinivil, Zestril
• Lorazepam • Ativan
• Lurasidone • Latuda
• Maprotiline • Ludiomil
• Mesoridazine • Serentil
• Metformin • Glucophage
• Nortriptyline • Pamelor
• Olanzapine • Zyprexa
• Paliperidone • Invega
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Tamoxifen • Nolvadex, Soltamox
• Thioridazine • Mellaril
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. No similar work by the authors is under review or in press. No funding was requested or received in conjunction with this manuscript.

Mrs. A, age 68, has a 40-year history of schizoaffective disorder with comorbid anxiety disorder not otherwise specified, type 2 diabetes mellitus, and hypertension. She takes furosemide, 40 mg/d, lisinopril, 20 mg/d, and metformin, 2,000 mg/d, for hypertension and diabetes; lorazepam, 1.5 mg/d, and paroxetine, 40 mg/d, for anxiety; and quetiapine extended release, 800 mg/d, for psychotic features and mood dysregulation with schizoaffective disorder. Mrs. A’s husband died 5 years ago and she lives alone in a senior care facility. Mrs. A uses a weekly pill reminder box because her residential facility does not monitor medication adherence. She sees her psychiatrist once a month and her primary care provider every 3 months. She has no history of illicit drug, alcohol, or tobacco use.

Two weeks ago, Mrs. A was found leaning against the wall in a hallway, complaining of dizziness and disorientation, and unable to find her way back to her apartment. In the emergency department, her serum potassium is low (3.0 mEq/L; normal range: 3.5 to 5.0), fasting glucose is elevated (110 mg/dL; range: 65 to 99), and ECG reveals a prolonged QTc interval of 530 milliseconds. Before this episode, Mrs. A had been medically stable without mood or psychotic symptoms, although her daughter reported medication self-administration was becoming difficult.

Exposure to psychotropics carries a risk of QTc prolongation. The QT interval is an ECG measure of ventricular depolarization and repolarization. The QTc designation indicates a correction for heart rate with increasing heart rate correlating with a shorter QT interval. Readings of 440 milliseconds are considered normal.¹ QTc prolongation is defined as >450 milliseconds for men and >470 milliseconds for women.² An increase in the QT interval is a predictor of serious cardiac events.³

Antidepressants and antipsychotics have been associated with QTc prolongation. When identifying agents that could disrupt cardiac conduction, clinicians need to consider whether the drug’s molecular structure, receptor affinity, or pharmacologic effects are most critical.² Although these may be important, patient-specific variables that increase the risk of QTc prolongation may have greater impact. These include:

• age >65
• female sex
• electrolyte imbalances (specifically low serum potassium and magnesium levels)
• high or toxic serum levels of the suspected drug
• preexisting cardiovascular impairment, such as bradycardia.^4,5

Other risk factors include concurrent use of an agent with similar cardiovascular effects or one that competes for metabolism (either enzymatic or at the binding site), physiologic limitations such as renal insufficiency, and medication changes that may increase or decrease psychotropic clearance.^4,6 Geriatric patients with dementia have an increased risk for cardiovascular-related death.^7,8

Antidepressants

Among tricyclic antidepressants, most reports of QTc prolongation involve amitriptyline and maprotiline.⁹ Risk factors include demographics (eg, female sex, age), personal or family history (congenital long QT syndrome, cardiovascular disease), and concurrent conditions or drug use, particularly those associated with QTc prolongation.³ Desipramine and nortriptyline also have been identified as high-risk agents.¹⁰

QTc prolongation has been reported with all selective serotonin reuptake inhibitors at plasma concentrations above the therapeutic level.¹¹ Fluoxetine-associated QTc prolongation was limited to cases of overdose or when additional risk factors were reported.⁴ QTc prolongation from psychotropics could increase the risk of torsades de pointes, according to an analysis of the FDA Adverse Event Reporting System.¹² In 2011, the FDA reported an increased risk of abnormal heart rhythms—including QTc prolongation—with citalopram doses >40 mg/d.¹³ Although cases of QTc prolongation with paroxetine have not been reported,¹¹ the Arizona Center for Education and Research on Therapeutics lists paroxetine with other agents that may increase the risk for QTc prolongation with concurrent use of medications that may prolong QTc interval.¹⁴ Venlafaxine doses >300 mg/d may require additional cardiac monitoring.^5,12 Data from venlafaxine poisoning case reports found a positive correlation between dose and QTc prolongation.¹⁵ In a review of toxicology database information, Wenzel-Seifert et al⁴ found extended QT interval with citalopram, fluoxetine, and venlafaxine at toxic doses or in the presence of additional risk factors such as sex, older age, or personal or family history of congenital long QT syndrome or cardiovascular disease.

Antipsychotics

Case reports, case series, and research trials have evaluated the risk of QTc prolongation with antipsychotics (Table).^1,2,4,16,17 The first-generation antipsychotics thioridazine,^4,16,18 mesoridazine,^16,18 chlorpromazine,¹⁹ and haloperidol³ warrant cardiac monitoring. The QTc prolongation effects of thioridazine and its active metabolite mesoridazine are well-documented and thioridazine-mediated QTc prolongation increases are dose-dependent.^4,18 ECG monitoring is recommended with IV haloperidol, which is used for delirium in adults.²⁰ QTc prolongation has been associated with long-term ziprasidone use more often than with risperidone, olanzapine, or quetiapine.¹⁹ Ziprasidone prolongs the QTc interval an average of 20 milliseconds,²¹ which could represent a clinically significant change. QTc prolongation for iloperidone is comparable to ziprasidone and haloperidol.²² There is some evidence that aripiprazole may shorten, rather than prolong, the QTc interval.^4,17

Cardiovascular adverse effects associated with clozapine—including QTc prolongation—are dose-dependent.³ Olanzapine prolongs QTc interval, although the mean change is less than with other agents unless other variables were present, such as:

• concomitant use of medications that may prolong QTc interval (ie, amantadine, hydroxyzine, or tamoxifen²)
• preexisting cardiovascular conduction disorders
• higher doses (>40 mg/d).^3,23

In 17 case reports of cardiac changes associated with quetiapine use, doses ranged from 100 mg/d²⁴ to an overdose of 36 g/d.²⁵ Only 1 patient death was reported secondary to overdose and preexisting dysrhythmia and hypertension.²⁶ QTc prolongation associated with risperidone was minor¹ based on oral doses in the normal therapeutic range and incidences of overdose.¹⁰ Paliperidone²⁷ and lurasidone²⁸ are associated with clinically insignificant QTc prolongation. Changes in QTc interval were positively correlated with asenapine dose, although at the highest dose of 40 mg/d, the increase was <5 milliseconds.²⁹

Mrs. A presents with a number of risk factors for QTc prolongation, including older age, female sex, and psychiatric and medical comorbidities that require medication. A pill count revealed that she was taking more than the prescribed daily doses of her medications. During the interview, Mrs. A said that if she missed her medication time, she would take them when she remembered. If she could not remember if she took her pills, she would take them again. Her physicians will explore strategies to increase medication adherence.

Table

Examples of QTc prolongation associated with select antipsychotics^a

Related Resources

• De Hert M, Detraux J, van Winkel R, et al. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat Rev Endocrinol. 2011;8(2):114-126.
• Vieweg WV, Wood MA, Fernandez A, et al. Proarrhythmic risk with antipsychotic and antidepressant drugs: implications in the elderly. Drugs Aging. 2009;26(12):997-1012.
• Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.

Drug Brand Names

• Amantadine • Symmetrel
• Amitriptyline • Elavil
• Aripiprazole • Abilify
• Asenapine • Saphris
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Clozapine • Clozaril
• Desipramine • Norpramin
• Fluoxetine • Prozac
• Furosemide • Lasix
• Haloperidol • Haldol
• Hydroxyzine • Atarax, Vistaril
• Iloperidone • Fanapt
• Lisinopril • Prinivil, Zestril
• Lorazepam • Ativan
• Lurasidone • Latuda
• Maprotiline • Ludiomil
• Mesoridazine • Serentil
• Metformin • Glucophage
• Nortriptyline • Pamelor
• Olanzapine • Zyprexa
• Paliperidone • Invega
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Tamoxifen • Nolvadex, Soltamox
• Thioridazine • Mellaril
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. No similar work by the authors is under review or in press. No funding was requested or received in conjunction with this manuscript.

Mrs. A, age 68, has a 40-year history of schizoaffective disorder with comorbid anxiety disorder not otherwise specified, type 2 diabetes mellitus, and hypertension. She takes furosemide, 40 mg/d, lisinopril, 20 mg/d, and metformin, 2,000 mg/d, for hypertension and diabetes; lorazepam, 1.5 mg/d, and paroxetine, 40 mg/d, for anxiety; and quetiapine extended release, 800 mg/d, for psychotic features and mood dysregulation with schizoaffective disorder. Mrs. A’s husband died 5 years ago and she lives alone in a senior care facility. Mrs. A uses a weekly pill reminder box because her residential facility does not monitor medication adherence. She sees her psychiatrist once a month and her primary care provider every 3 months. She has no history of illicit drug, alcohol, or tobacco use.

Two weeks ago, Mrs. A was found leaning against the wall in a hallway, complaining of dizziness and disorientation, and unable to find her way back to her apartment. In the emergency department, her serum potassium is low (3.0 mEq/L; normal range: 3.5 to 5.0), fasting glucose is elevated (110 mg/dL; range: 65 to 99), and ECG reveals a prolonged QTc interval of 530 milliseconds. Before this episode, Mrs. A had been medically stable without mood or psychotic symptoms, although her daughter reported medication self-administration was becoming difficult.

Exposure to psychotropics carries a risk of QTc prolongation. The QT interval is an ECG measure of ventricular depolarization and repolarization. The QTc designation indicates a correction for heart rate with increasing heart rate correlating with a shorter QT interval. Readings of 440 milliseconds are considered normal.¹ QTc prolongation is defined as >450 milliseconds for men and >470 milliseconds for women.² An increase in the QT interval is a predictor of serious cardiac events.³

Antidepressants and antipsychotics have been associated with QTc prolongation. When identifying agents that could disrupt cardiac conduction, clinicians need to consider whether the drug’s molecular structure, receptor affinity, or pharmacologic effects are most critical.² Although these may be important, patient-specific variables that increase the risk of QTc prolongation may have greater impact. These include:

• age >65
• female sex
• electrolyte imbalances (specifically low serum potassium and magnesium levels)
• high or toxic serum levels of the suspected drug
• preexisting cardiovascular impairment, such as bradycardia.^4,5

Other risk factors include concurrent use of an agent with similar cardiovascular effects or one that competes for metabolism (either enzymatic or at the binding site), physiologic limitations such as renal insufficiency, and medication changes that may increase or decrease psychotropic clearance.^4,6 Geriatric patients with dementia have an increased risk for cardiovascular-related death.^7,8

Antidepressants

Among tricyclic antidepressants, most reports of QTc prolongation involve amitriptyline and maprotiline.⁹ Risk factors include demographics (eg, female sex, age), personal or family history (congenital long QT syndrome, cardiovascular disease), and concurrent conditions or drug use, particularly those associated with QTc prolongation.³ Desipramine and nortriptyline also have been identified as high-risk agents.¹⁰

QTc prolongation has been reported with all selective serotonin reuptake inhibitors at plasma concentrations above the therapeutic level.¹¹ Fluoxetine-associated QTc prolongation was limited to cases of overdose or when additional risk factors were reported.⁴ QTc prolongation from psychotropics could increase the risk of torsades de pointes, according to an analysis of the FDA Adverse Event Reporting System.¹² In 2011, the FDA reported an increased risk of abnormal heart rhythms—including QTc prolongation—with citalopram doses >40 mg/d.¹³ Although cases of QTc prolongation with paroxetine have not been reported,¹¹ the Arizona Center for Education and Research on Therapeutics lists paroxetine with other agents that may increase the risk for QTc prolongation with concurrent use of medications that may prolong QTc interval.¹⁴ Venlafaxine doses >300 mg/d may require additional cardiac monitoring.^5,12 Data from venlafaxine poisoning case reports found a positive correlation between dose and QTc prolongation.¹⁵ In a review of toxicology database information, Wenzel-Seifert et al⁴ found extended QT interval with citalopram, fluoxetine, and venlafaxine at toxic doses or in the presence of additional risk factors such as sex, older age, or personal or family history of congenital long QT syndrome or cardiovascular disease.

Antipsychotics

Case reports, case series, and research trials have evaluated the risk of QTc prolongation with antipsychotics (Table).^1,2,4,16,17 The first-generation antipsychotics thioridazine,^4,16,18 mesoridazine,^16,18 chlorpromazine,¹⁹ and haloperidol³ warrant cardiac monitoring. The QTc prolongation effects of thioridazine and its active metabolite mesoridazine are well-documented and thioridazine-mediated QTc prolongation increases are dose-dependent.^4,18 ECG monitoring is recommended with IV haloperidol, which is used for delirium in adults.²⁰ QTc prolongation has been associated with long-term ziprasidone use more often than with risperidone, olanzapine, or quetiapine.¹⁹ Ziprasidone prolongs the QTc interval an average of 20 milliseconds,²¹ which could represent a clinically significant change. QTc prolongation for iloperidone is comparable to ziprasidone and haloperidol.²² There is some evidence that aripiprazole may shorten, rather than prolong, the QTc interval.^4,17

Cardiovascular adverse effects associated with clozapine—including QTc prolongation—are dose-dependent.³ Olanzapine prolongs QTc interval, although the mean change is less than with other agents unless other variables were present, such as:

• concomitant use of medications that may prolong QTc interval (ie, amantadine, hydroxyzine, or tamoxifen²)
• preexisting cardiovascular conduction disorders
• higher doses (>40 mg/d).^3,23

In 17 case reports of cardiac changes associated with quetiapine use, doses ranged from 100 mg/d²⁴ to an overdose of 36 g/d.²⁵ Only 1 patient death was reported secondary to overdose and preexisting dysrhythmia and hypertension.²⁶ QTc prolongation associated with risperidone was minor¹ based on oral doses in the normal therapeutic range and incidences of overdose.¹⁰ Paliperidone²⁷ and lurasidone²⁸ are associated with clinically insignificant QTc prolongation. Changes in QTc interval were positively correlated with asenapine dose, although at the highest dose of 40 mg/d, the increase was <5 milliseconds.²⁹

Mrs. A presents with a number of risk factors for QTc prolongation, including older age, female sex, and psychiatric and medical comorbidities that require medication. A pill count revealed that she was taking more than the prescribed daily doses of her medications. During the interview, Mrs. A said that if she missed her medication time, she would take them when she remembered. If she could not remember if she took her pills, she would take them again. Her physicians will explore strategies to increase medication adherence.

Table

Examples of QTc prolongation associated with select antipsychotics^a

Related Resources

• De Hert M, Detraux J, van Winkel R, et al. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat Rev Endocrinol. 2011;8(2):114-126.
• Vieweg WV, Wood MA, Fernandez A, et al. Proarrhythmic risk with antipsychotic and antidepressant drugs: implications in the elderly. Drugs Aging. 2009;26(12):997-1012.
• Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.

Drug Brand Names

• Amantadine • Symmetrel
• Amitriptyline • Elavil
• Aripiprazole • Abilify
• Asenapine • Saphris
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Clozapine • Clozaril
• Desipramine • Norpramin
• Fluoxetine • Prozac
• Furosemide • Lasix
• Haloperidol • Haldol
• Hydroxyzine • Atarax, Vistaril
• Iloperidone • Fanapt
• Lisinopril • Prinivil, Zestril
• Lorazepam • Ativan
• Lurasidone • Latuda
• Maprotiline • Ludiomil
• Mesoridazine • Serentil
• Metformin • Glucophage
• Nortriptyline • Pamelor
• Olanzapine • Zyprexa
• Paliperidone • Invega
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Tamoxifen • Nolvadex, Soltamox
• Thioridazine • Mellaril
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. No similar work by the authors is under review or in press. No funding was requested or received in conjunction with this manuscript.

In 2006, the FDA issued a warning of the risk of potentially fatal serotonin syndrome when 5-hydroxytryptamine receptor agonist antimigraine medications (triptans) and selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRI) are coprescribed.¹ As a result, most drug interaction programs trigger a serotonin syndrome warning when triptans are prescribed with an SSRI or SNRI.² However, many patients with depression or anxiety also suffer from migraines and require treatment with both triptans and an SSRI or SNRI.^3,4 Kalaydjian et al⁴ found the incidence of major depression and generalized anxiety disorder were approximately 3 times greater in patients with migraines than in those without migraines. Should we avoid coprescribing triptans and SSRIs or SNRIs?

What is serotonin syndrome?

Serotonin syndrome is an adverse drug reaction that results from excessive serotonin stimulation. There are 2 sets of validated diagnostic criteria: the Sternbach Criteria and the Hunter Serotonin Toxicity Criteria; the latter is considered more stringent.^3,5-7 Symptoms of serotonin syndrome include mental status changes, autonomic hyperactivity, and neuromuscular changes such as muscle rigidity.^5-7 Typical manifestations of serotonin syndrome on physical exam include spontaneous and/or inducible clonus, agitation, diaphoresis, tremor, hyperreflexia, hypertonia, and temperature >38°C.⁶ In severe cases, serotonin syndrome can lead to seizures, coma, and death. Management includes supportive treatment, discontinuing the offending agents, controlling agitation with medications such as benzodiazepines, and possibly administering cyproheptadine, a 5HT2A antagonist.⁸ Most cases resolve within 24 hours of discontinuing the offending agents or appropriate treatment.⁵

What did the FDA say?

The 2006 FDA warning initially was based on 27 reports of serotonin syndrome in patients receiving triptans and SSRIs or SNRIs; this was later expanded to include 29 patients.^1,9 No patients died but 13 required hospitalization and 2 had life-threatening symptoms. However, most cases lacked data necessary to diagnose serotonin syndrome.⁹ Further, reviews of the available clinical information have suggested that in some cases, clinicians did not rule out other disorders as required by diagnostic criteria, while others were viral in nature or resolved despite ongoing treatment with the presumed offending agents.^9-11

Some clinicians met the FDA’s assessment with skepticism. Only 10 of the 29 cases met the Sternbach criteria of serotonin syndrome and none met the more rigorous Hunter criteria. Additionally, the theoretical basis has been questioned.^9-11 Available evidence indicates that serotonin syndrome requires activation of 5HT2A receptors and a possible limited role of 5HT1A.^9-12 However, triptans are agonists at the 5HT1B/1D/1F receptor subtypes, with weak affinity for 5HT1A receptors and no activity at the 5HT2 receptors.^13,14 Additionally, triptan medications are used as needed, not as standing treatments, with parameters limiting the maximum dose, dosing interval, and frequency of use. In clinical practice, it appears that these dosing guidelines are being followed: Tepper et al¹⁵ found the typical female patient experiences 1 to 2 migraines per month; on average, patients use 1.2 to 1.8 triptan tablets per month.

Our opinion

We believe it is reasonable to coprescribe SSRIs or SNRIs with triptans because:

• data indicate that many patients are treated with a combination of triptans and SSRIs or SNRIs but the number of reported cases of serotonin syndrome is extremely limited
• the nature of serotonin syndrome cases reported in the literature is questionable
• the interaction is biologically implausible
• triptans remain in the body for a limited time
• triptans are used infrequently.^5-11

This view is supported by the most recent American Headache Society position paper,¹¹ which states that inadequate data are available to assess the risk but current evidence does not support limiting use of triptans with SSRIs and SNRIs.

How we deal with the warning in clinical practice. In practice we are alerted to this interaction by notification in our e-prescribing systems, by pharmacists calling with concerns about dispensing an SSRI or SNRI for a patient already receiving a triptan, and during patient visits that involve prescribing an SSRI or SNRI.

Although it is relatively easy to override a drug interaction warning in our e-prescribing system, we discuss the issue with pharmacists and patients. We provide information about the signs and symptoms of serotonin syndrome and its potential dangerousness. We note that serotonin syndrome is a theoretical concern, but highly unlikely with this combination of medications because of their pharmacologic properties. We explain the parameters of triptan use, recommend that our patients use triptans for migraines when needed, and reassure patients we are available to answer questions. When a patient uses triptans more than twice monthly, we consider discussing this usage with the patient and the treating physician.

Related Resource

• Sclar DA, Robison LM, Castillo LV, et al. Concomitant use of triptan, and SSRI or SNRI after the US Food and Drug Administration alert on serotonin syndrome. Headache. 2012. www.headachejournal.org/SpringboardWebApp/userfiles/headache/file/sclar.pdf.

Drug Brand Name

• Cyproheptadine • Perinctin

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

In 2006, the FDA issued a warning of the risk of potentially fatal serotonin syndrome when 5-hydroxytryptamine receptor agonist antimigraine medications (triptans) and selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRI) are coprescribed.¹ As a result, most drug interaction programs trigger a serotonin syndrome warning when triptans are prescribed with an SSRI or SNRI.² However, many patients with depression or anxiety also suffer from migraines and require treatment with both triptans and an SSRI or SNRI.^3,4 Kalaydjian et al⁴ found the incidence of major depression and generalized anxiety disorder were approximately 3 times greater in patients with migraines than in those without migraines. Should we avoid coprescribing triptans and SSRIs or SNRIs?

What is serotonin syndrome?

Serotonin syndrome is an adverse drug reaction that results from excessive serotonin stimulation. There are 2 sets of validated diagnostic criteria: the Sternbach Criteria and the Hunter Serotonin Toxicity Criteria; the latter is considered more stringent.^3,5-7 Symptoms of serotonin syndrome include mental status changes, autonomic hyperactivity, and neuromuscular changes such as muscle rigidity.^5-7 Typical manifestations of serotonin syndrome on physical exam include spontaneous and/or inducible clonus, agitation, diaphoresis, tremor, hyperreflexia, hypertonia, and temperature >38°C.⁶ In severe cases, serotonin syndrome can lead to seizures, coma, and death. Management includes supportive treatment, discontinuing the offending agents, controlling agitation with medications such as benzodiazepines, and possibly administering cyproheptadine, a 5HT2A antagonist.⁸ Most cases resolve within 24 hours of discontinuing the offending agents or appropriate treatment.⁵

What did the FDA say?

The 2006 FDA warning initially was based on 27 reports of serotonin syndrome in patients receiving triptans and SSRIs or SNRIs; this was later expanded to include 29 patients.^1,9 No patients died but 13 required hospitalization and 2 had life-threatening symptoms. However, most cases lacked data necessary to diagnose serotonin syndrome.⁹ Further, reviews of the available clinical information have suggested that in some cases, clinicians did not rule out other disorders as required by diagnostic criteria, while others were viral in nature or resolved despite ongoing treatment with the presumed offending agents.^9-11

Some clinicians met the FDA’s assessment with skepticism. Only 10 of the 29 cases met the Sternbach criteria of serotonin syndrome and none met the more rigorous Hunter criteria. Additionally, the theoretical basis has been questioned.^9-11 Available evidence indicates that serotonin syndrome requires activation of 5HT2A receptors and a possible limited role of 5HT1A.^9-12 However, triptans are agonists at the 5HT1B/1D/1F receptor subtypes, with weak affinity for 5HT1A receptors and no activity at the 5HT2 receptors.^13,14 Additionally, triptan medications are used as needed, not as standing treatments, with parameters limiting the maximum dose, dosing interval, and frequency of use. In clinical practice, it appears that these dosing guidelines are being followed: Tepper et al¹⁵ found the typical female patient experiences 1 to 2 migraines per month; on average, patients use 1.2 to 1.8 triptan tablets per month.

Our opinion

We believe it is reasonable to coprescribe SSRIs or SNRIs with triptans because:

• data indicate that many patients are treated with a combination of triptans and SSRIs or SNRIs but the number of reported cases of serotonin syndrome is extremely limited
• the nature of serotonin syndrome cases reported in the literature is questionable
• the interaction is biologically implausible
• triptans remain in the body for a limited time
• triptans are used infrequently.^5-11

This view is supported by the most recent American Headache Society position paper,¹¹ which states that inadequate data are available to assess the risk but current evidence does not support limiting use of triptans with SSRIs and SNRIs.

How we deal with the warning in clinical practice. In practice we are alerted to this interaction by notification in our e-prescribing systems, by pharmacists calling with concerns about dispensing an SSRI or SNRI for a patient already receiving a triptan, and during patient visits that involve prescribing an SSRI or SNRI.

Although it is relatively easy to override a drug interaction warning in our e-prescribing system, we discuss the issue with pharmacists and patients. We provide information about the signs and symptoms of serotonin syndrome and its potential dangerousness. We note that serotonin syndrome is a theoretical concern, but highly unlikely with this combination of medications because of their pharmacologic properties. We explain the parameters of triptan use, recommend that our patients use triptans for migraines when needed, and reassure patients we are available to answer questions. When a patient uses triptans more than twice monthly, we consider discussing this usage with the patient and the treating physician.

Related Resource

• Sclar DA, Robison LM, Castillo LV, et al. Concomitant use of triptan, and SSRI or SNRI after the US Food and Drug Administration alert on serotonin syndrome. Headache. 2012. www.headachejournal.org/SpringboardWebApp/userfiles/headache/file/sclar.pdf.

Drug Brand Name

• Cyproheptadine • Perinctin

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

In 2006, the FDA issued a warning of the risk of potentially fatal serotonin syndrome when 5-hydroxytryptamine receptor agonist antimigraine medications (triptans) and selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRI) are coprescribed.¹ As a result, most drug interaction programs trigger a serotonin syndrome warning when triptans are prescribed with an SSRI or SNRI.² However, many patients with depression or anxiety also suffer from migraines and require treatment with both triptans and an SSRI or SNRI.^3,4 Kalaydjian et al⁴ found the incidence of major depression and generalized anxiety disorder were approximately 3 times greater in patients with migraines than in those without migraines. Should we avoid coprescribing triptans and SSRIs or SNRIs?

What is serotonin syndrome?

Serotonin syndrome is an adverse drug reaction that results from excessive serotonin stimulation. There are 2 sets of validated diagnostic criteria: the Sternbach Criteria and the Hunter Serotonin Toxicity Criteria; the latter is considered more stringent.^3,5-7 Symptoms of serotonin syndrome include mental status changes, autonomic hyperactivity, and neuromuscular changes such as muscle rigidity.^5-7 Typical manifestations of serotonin syndrome on physical exam include spontaneous and/or inducible clonus, agitation, diaphoresis, tremor, hyperreflexia, hypertonia, and temperature >38°C.⁶ In severe cases, serotonin syndrome can lead to seizures, coma, and death. Management includes supportive treatment, discontinuing the offending agents, controlling agitation with medications such as benzodiazepines, and possibly administering cyproheptadine, a 5HT2A antagonist.⁸ Most cases resolve within 24 hours of discontinuing the offending agents or appropriate treatment.⁵

What did the FDA say?

The 2006 FDA warning initially was based on 27 reports of serotonin syndrome in patients receiving triptans and SSRIs or SNRIs; this was later expanded to include 29 patients.^1,9 No patients died but 13 required hospitalization and 2 had life-threatening symptoms. However, most cases lacked data necessary to diagnose serotonin syndrome.⁹ Further, reviews of the available clinical information have suggested that in some cases, clinicians did not rule out other disorders as required by diagnostic criteria, while others were viral in nature or resolved despite ongoing treatment with the presumed offending agents.^9-11

Some clinicians met the FDA’s assessment with skepticism. Only 10 of the 29 cases met the Sternbach criteria of serotonin syndrome and none met the more rigorous Hunter criteria. Additionally, the theoretical basis has been questioned.^9-11 Available evidence indicates that serotonin syndrome requires activation of 5HT2A receptors and a possible limited role of 5HT1A.^9-12 However, triptans are agonists at the 5HT1B/1D/1F receptor subtypes, with weak affinity for 5HT1A receptors and no activity at the 5HT2 receptors.^13,14 Additionally, triptan medications are used as needed, not as standing treatments, with parameters limiting the maximum dose, dosing interval, and frequency of use. In clinical practice, it appears that these dosing guidelines are being followed: Tepper et al¹⁵ found the typical female patient experiences 1 to 2 migraines per month; on average, patients use 1.2 to 1.8 triptan tablets per month.

Our opinion

We believe it is reasonable to coprescribe SSRIs or SNRIs with triptans because:

• data indicate that many patients are treated with a combination of triptans and SSRIs or SNRIs but the number of reported cases of serotonin syndrome is extremely limited
• the nature of serotonin syndrome cases reported in the literature is questionable
• the interaction is biologically implausible
• triptans remain in the body for a limited time
• triptans are used infrequently.^5-11

This view is supported by the most recent American Headache Society position paper,¹¹ which states that inadequate data are available to assess the risk but current evidence does not support limiting use of triptans with SSRIs and SNRIs.

How we deal with the warning in clinical practice. In practice we are alerted to this interaction by notification in our e-prescribing systems, by pharmacists calling with concerns about dispensing an SSRI or SNRI for a patient already receiving a triptan, and during patient visits that involve prescribing an SSRI or SNRI.

Although it is relatively easy to override a drug interaction warning in our e-prescribing system, we discuss the issue with pharmacists and patients. We provide information about the signs and symptoms of serotonin syndrome and its potential dangerousness. We note that serotonin syndrome is a theoretical concern, but highly unlikely with this combination of medications because of their pharmacologic properties. We explain the parameters of triptan use, recommend that our patients use triptans for migraines when needed, and reassure patients we are available to answer questions. When a patient uses triptans more than twice monthly, we consider discussing this usage with the patient and the treating physician.

Related Resource

• Sclar DA, Robison LM, Castillo LV, et al. Concomitant use of triptan, and SSRI or SNRI after the US Food and Drug Administration alert on serotonin syndrome. Headache. 2012. www.headachejournal.org/SpringboardWebApp/userfiles/headache/file/sclar.pdf.

Drug Brand Name

• Cyproheptadine • Perinctin

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Patients receiving treatment with epidermal growth factor receptor inhibitors often experience dermatological toxicities. The majority of patients develop skin rash, and may also experience adverse nail and periungual alterations. EGFR inhibitors have become part of the standard of care for several solid tumors, including metastatic colorectal cancer, cancers of the head and neck, and non small-cell lung cancer, thus adequate management of these side effects is necessary to ensure patient compliance to therapy, as well as to maximize patient comfort and quality of life. This review presents a protocol our center optimized to successfully manage cetuximab-associated acneiform rash and nail toxicities.

Click on the PDF icon at the top of this introduction to read the full article.

Patients receiving treatment with epidermal growth factor receptor inhibitors often experience dermatological toxicities. The majority of patients develop skin rash, and may also experience adverse nail and periungual alterations. EGFR inhibitors have become part of the standard of care for several solid tumors, including metastatic colorectal cancer, cancers of the head and neck, and non small-cell lung cancer, thus adequate management of these side effects is necessary to ensure patient compliance to therapy, as well as to maximize patient comfort and quality of life. This review presents a protocol our center optimized to successfully manage cetuximab-associated acneiform rash and nail toxicities.

Click on the PDF icon at the top of this introduction to read the full article.

Patients receiving treatment with epidermal growth factor receptor inhibitors often experience dermatological toxicities. The majority of patients develop skin rash, and may also experience adverse nail and periungual alterations. EGFR inhibitors have become part of the standard of care for several solid tumors, including metastatic colorectal cancer, cancers of the head and neck, and non small-cell lung cancer, thus adequate management of these side effects is necessary to ensure patient compliance to therapy, as well as to maximize patient comfort and quality of life. This review presents a protocol our center optimized to successfully manage cetuximab-associated acneiform rash and nail toxicities.

Click on the PDF icon at the top of this introduction to read the full article.

Hypertension is the force of blood pushing against the walls of the arteries. It is measured as systolic pressure when the heart beats and pumps blood and as diastolic pressure in the arteries when the heart rests between beats. There are 4 stages in blood pressure classification—normal, prehypertension, stage 1, and stage 2. Hypertension affects approximately 50 million people in the United States and 1 billion people worldwide. People who are normotensive at age 55 years have a 90% chance of developing hypertension in their lifetime. Starting with a blood pressure of 115/75 mmHg, the risk of cardiovascular death doubles with each 20/10 mmHg increment...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Hypertension is the force of blood pushing against the walls of the arteries. It is measured as systolic pressure when the heart beats and pumps blood and as diastolic pressure in the arteries when the heart rests between beats. There are 4 stages in blood pressure classification—normal, prehypertension, stage 1, and stage 2. Hypertension affects approximately 50 million people in the United States and 1 billion people worldwide. People who are normotensive at age 55 years have a 90% chance of developing hypertension in their lifetime. Starting with a blood pressure of 115/75 mmHg, the risk of cardiovascular death doubles with each 20/10 mmHg increment...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Hypertension is the force of blood pushing against the walls of the arteries. It is measured as systolic pressure when the heart beats and pumps blood and as diastolic pressure in the arteries when the heart rests between beats. There are 4 stages in blood pressure classification—normal, prehypertension, stage 1, and stage 2. Hypertension affects approximately 50 million people in the United States and 1 billion people worldwide. People who are normotensive at age 55 years have a 90% chance of developing hypertension in their lifetime. Starting with a blood pressure of 115/75 mmHg, the risk of cardiovascular death doubles with each 20/10 mmHg increment...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Patients with glioblastoma and other high-grade gliomas have poor outcomes and are challenging to treat. The relative rarity of these tumors has made large-scale, practice-changing trials difficult to accomplish and has led to the formation of large multinational organizations that focus on neuro-oncology. This has resulted in the rapid completion of several large trials that in some cases have set new standards of care that can offer increased progression-free and overall survivals for some patients. The incorporation of correlative tissue studies in these trials has led to the identification of prognostic and predictive genetic markers that demonstrate the heterogeneity of these tumors and will assist in developing individualized treatment strategies as research continues to uncover new therapeutic targets. This review of recently completed and in-progress phase 3 trials in high-grade gliomas highlights the developments and future directions in the treatment of these tumors...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Patients with glioblastoma and other high-grade gliomas have poor outcomes and are challenging to treat. The relative rarity of these tumors has made large-scale, practice-changing trials difficult to accomplish and has led to the formation of large multinational organizations that focus on neuro-oncology. This has resulted in the rapid completion of several large trials that in some cases have set new standards of care that can offer increased progression-free and overall survivals for some patients. The incorporation of correlative tissue studies in these trials has led to the identification of prognostic and predictive genetic markers that demonstrate the heterogeneity of these tumors and will assist in developing individualized treatment strategies as research continues to uncover new therapeutic targets. This review of recently completed and in-progress phase 3 trials in high-grade gliomas highlights the developments and future directions in the treatment of these tumors...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Patients with glioblastoma and other high-grade gliomas have poor outcomes and are challenging to treat. The relative rarity of these tumors has made large-scale, practice-changing trials difficult to accomplish and has led to the formation of large multinational organizations that focus on neuro-oncology. This has resulted in the rapid completion of several large trials that in some cases have set new standards of care that can offer increased progression-free and overall survivals for some patients. The incorporation of correlative tissue studies in these trials has led to the identification of prognostic and predictive genetic markers that demonstrate the heterogeneity of these tumors and will assist in developing individualized treatment strategies as research continues to uncover new therapeutic targets. This review of recently completed and in-progress phase 3 trials in high-grade gliomas highlights the developments and future directions in the treatment of these tumors...

*For PDFs of the full article and related Commentary, click on the links to the left of this introduction.

Adalimumab, a subcutaneously administered tumor necrosis factor blocker, has been approved for treating adults with moderately to severely active ulcerative colitis who have not had an adequate response with conventional treatments, the Food and Drug Administration announced on Sept. 28.

The safety and effectiveness of adalimumab for this patient population was established in two clinical studies of 908 patients with moderately to severely active ulcerative colitis (UC).

Adalimumab, marketed as Humira by Abbott Laboratories, was first approved for treating rheumatoid arthritis in 2002, followed by psoriatic arthritis in 2005, ankylosing spondylitis in 2006, Crohn’s disease in 2007, and plaque psoriasis and juvenile idiopathic arthritis in 2008.

Adalimumab is the second TNF blocker to be approved for ulcerative colitis; infliximab (Remicade), an intravenous TNF blocker, was previously approved for treating UC.

Clinical remission rates in the two studies were significantly greater among patients treated with infliximab than among those who received placebo: In an 8-week study, which did not include patients who had previously been treated with a TNF blocker, the clinical remission rate at 8 weeks was 18.5% among those on adalimumab vs. 9.2% in those on placebo, a 9.3% difference. In the second study, which followed patients for 1 year and included some who had been treated with infliximab, the clinical remission rate at 8 weeks was 16.5% among those on adalimumab, vs. 9.3% among those on placebo, a 7.2% difference.

At a meeting on Aug. 28 held to review these data, the majority of the FDA’s Gastrointestinal Drugs Advisory Committee agreed that these differences represented clinically meaningful benefits and supported approval of adalimumab for this indication. Panelists cited the need for more treatments for UC and for a subcutaneous TNF blocker for these patients, as well as its potential steroid-sparing effects.

In the studies, no new side effects were identified, the agency said. The FDA statement points out that the effectiveness of adalimumab "has not been established in patients with ulcerative colitis who have lost response to or were intolerant to TNF blockers."

The approved dosing regimen for adalimumab is a starting dose of 160 mg, followed by a second dose of 80 mg 2 weeks later and then a maintenance dose of 40 mg every other week. "The drug should only continue to be used in patients who have shown evidence of clinical remission by 8 weeks of therapy," according to the FDA statement.

Adalimumab is the first self-administered biologic treatment for ulcerative colitis to be approved.

Adalimumab, a subcutaneously administered tumor necrosis factor blocker, has been approved for treating adults with moderately to severely active ulcerative colitis who have not had an adequate response with conventional treatments, the Food and Drug Administration announced on Sept. 28.

The safety and effectiveness of adalimumab for this patient population was established in two clinical studies of 908 patients with moderately to severely active ulcerative colitis (UC).

Adalimumab, marketed as Humira by Abbott Laboratories, was first approved for treating rheumatoid arthritis in 2002, followed by psoriatic arthritis in 2005, ankylosing spondylitis in 2006, Crohn’s disease in 2007, and plaque psoriasis and juvenile idiopathic arthritis in 2008.

Adalimumab is the second TNF blocker to be approved for ulcerative colitis; infliximab (Remicade), an intravenous TNF blocker, was previously approved for treating UC.

Clinical remission rates in the two studies were significantly greater among patients treated with infliximab than among those who received placebo: In an 8-week study, which did not include patients who had previously been treated with a TNF blocker, the clinical remission rate at 8 weeks was 18.5% among those on adalimumab vs. 9.2% in those on placebo, a 9.3% difference. In the second study, which followed patients for 1 year and included some who had been treated with infliximab, the clinical remission rate at 8 weeks was 16.5% among those on adalimumab, vs. 9.3% among those on placebo, a 7.2% difference.

At a meeting on Aug. 28 held to review these data, the majority of the FDA’s Gastrointestinal Drugs Advisory Committee agreed that these differences represented clinically meaningful benefits and supported approval of adalimumab for this indication. Panelists cited the need for more treatments for UC and for a subcutaneous TNF blocker for these patients, as well as its potential steroid-sparing effects.

In the studies, no new side effects were identified, the agency said. The FDA statement points out that the effectiveness of adalimumab "has not been established in patients with ulcerative colitis who have lost response to or were intolerant to TNF blockers."

The approved dosing regimen for adalimumab is a starting dose of 160 mg, followed by a second dose of 80 mg 2 weeks later and then a maintenance dose of 40 mg every other week. "The drug should only continue to be used in patients who have shown evidence of clinical remission by 8 weeks of therapy," according to the FDA statement.

Adalimumab is the first self-administered biologic treatment for ulcerative colitis to be approved.

Adalimumab, a subcutaneously administered tumor necrosis factor blocker, has been approved for treating adults with moderately to severely active ulcerative colitis who have not had an adequate response with conventional treatments, the Food and Drug Administration announced on Sept. 28.

The safety and effectiveness of adalimumab for this patient population was established in two clinical studies of 908 patients with moderately to severely active ulcerative colitis (UC).

Adalimumab, marketed as Humira by Abbott Laboratories, was first approved for treating rheumatoid arthritis in 2002, followed by psoriatic arthritis in 2005, ankylosing spondylitis in 2006, Crohn’s disease in 2007, and plaque psoriasis and juvenile idiopathic arthritis in 2008.

Adalimumab is the second TNF blocker to be approved for ulcerative colitis; infliximab (Remicade), an intravenous TNF blocker, was previously approved for treating UC.

Clinical remission rates in the two studies were significantly greater among patients treated with infliximab than among those who received placebo: In an 8-week study, which did not include patients who had previously been treated with a TNF blocker, the clinical remission rate at 8 weeks was 18.5% among those on adalimumab vs. 9.2% in those on placebo, a 9.3% difference. In the second study, which followed patients for 1 year and included some who had been treated with infliximab, the clinical remission rate at 8 weeks was 16.5% among those on adalimumab, vs. 9.3% among those on placebo, a 7.2% difference.

At a meeting on Aug. 28 held to review these data, the majority of the FDA’s Gastrointestinal Drugs Advisory Committee agreed that these differences represented clinically meaningful benefits and supported approval of adalimumab for this indication. Panelists cited the need for more treatments for UC and for a subcutaneous TNF blocker for these patients, as well as its potential steroid-sparing effects.

In the studies, no new side effects were identified, the agency said. The FDA statement points out that the effectiveness of adalimumab "has not been established in patients with ulcerative colitis who have lost response to or were intolerant to TNF blockers."

The approved dosing regimen for adalimumab is a starting dose of 160 mg, followed by a second dose of 80 mg 2 weeks later and then a maintenance dose of 40 mg every other week. "The drug should only continue to be used in patients who have shown evidence of clinical remission by 8 weeks of therapy," according to the FDA statement.

Adalimumab is the first self-administered biologic treatment for ulcerative colitis to be approved.

The first guidelines on the management of gout from the American College of Rheumatology recommend new ways of using old drugs and changes in prophylaxis strategies, among other things.

The two-part guidelines, published online Sept. 28, should help speed up effective treatment of gout and get physicians to treat patients to a target urate level of less than 6 mg/dL in order to improve symptoms, Dr. John D. FitzGerald said in an interview.

"There has been a fair amount of recent movement on gout medications" including new alternatives to allopurinol and colchicine and new data on how to use those traditional drugs in safer ways, said Dr. FitzGerald, acting chief of the rheumatology division at the University of California, Los Angeles. "It’s a fair number of changes for medications that people had been using for decades."

The documents update previous guidelines from medical organizations in Europe, the Netherlands, and Japan. The new guidelines will be published in October 2012 by the journal Arthritis Care & Research.

Part 1 of the American College of Rheumatology (ACR) guidelines covers nonpharmacologic and pharmacologic approaches to managing hyperuricemia (Arthritis Care Res. 2012;64:1431-46 [doi:10.1002/acr.21772]).

Part 2 addresses prophylaxis and treatment for acute gouty arthritis (Arthritis Care Res. 2012;64:1447-61 [doi.wiley.com/10.1002/acr.21773]).

Dr. FitzGerald and two other co-leaders of the project, Dr. Dinesh Khanna of the University of Michigan, Ann Arbor and Dr. Robert Terkeltaub of the University of California, San Diego, reviewed the medical literature on gout from the 1950s to the present and drew up nine clinical case scenarios commonly seen in practice. A task force panel comprising seven rheumatologists, two primary care physicians, a nephrologist, and a patient representative used the scenarios to create consensus recommendations.

Among the recommendations, for example, on the use of allopurinol is to start at a low dose of 100 mg/day (instead of the common practice of starting with 300 mg/day), or even lower for patients with chronic kidney disease, and then gradually titrate upward every 2-5 weeks. That recommendation supports previous statements from the Food and Drug Administration and the European League Against Rheumatism.

Also, allopurinol therapy should be actively managed and patients followed to make sure the uric acid target is achieved. "You can’t just give a prescription and say your job is done," though some recent studies suggest that many physicians do just that, Dr. FitzGerald said. "The corollary would be if someone gave blood pressure medication and then didn’t follow the patient’s blood pressure. That wouldn’t be seen as good medicine."

Maintenance doses of allopurinol to prevent acute gout attacks can exceed 300 mg even in patients with chronic kidney disease provided there is adequate patient education and monitoring.

A new recommendation drops the starting dose of oral colchicine for acute gout attacks to a loading dose of 1.2 mg, followed by 0.6 mg an hour later, and then starting prophylaxis 12 hours later at dosing of 0.6 mg once or twice daily.

"We used to give up to eight tablets a day," Dr. FitzGerald said. "That is dropped down to three to four tablets at the start of an attacks, because of findings that more colchicine didn’t really help outcomes" and that smaller doses are safer. The authors called this recommendation from ACR "a paradigm shift" that’s in accordance with Food and Drug Administration-approved label language.

Other highlights of the new ACR recommendations include sections on screening for HLA-B*5801 in patients at high risk of severe adverse reaction to allopurinol, combination therapy when target urate levels are not achieved, medication options including new drugs, and more.

Although the reports are titled "Guidelines," the text makes clear that they are expert recommendations and that clinicians are expected to take active roles in choosing the best management strategies for their particular patients. The authors were "very concerned" that the guidelines not be used by third-party payers to restrict access to medications or to promote one drug over another if there isn’t clear evidence to support it, Dr. FitzGerald said.

The methodology of the project precluded evaluations of costs and cost effectiveness, instead focusing on efficacy. So, for example, the guidelines say that allopurinol and febuxostat can be used equivalently in some circumstances, but clinicians need to consider all other aspects of these options including cost, patient preference, and more.

The ACR plans to update the guidelines as new data become available. The task force panel did create specific indications for use of imaging studies because results should be available in the next few years from studies on the use of high-resolution ultrasound and dual-energy CT for patients with gout.

In the United States, gout affects an estimated 4% of adults – more than 8 million people.

"I’m most excited and hopeful about trying to get this out to internal medicine and family practice doctors," Dr. FitzGerald said. "They see more gout than rheumatologists."

Dr. FitzGerald reported having no financial disclosures. Some members of the task force reported financial associations with multiple pharmaceutical companies but, by design, a majority of task force members had no perceived potential conflicts of interest. 

The first guidelines on the management of gout from the American College of Rheumatology recommend new ways of using old drugs and changes in prophylaxis strategies, among other things.

The two-part guidelines, published online Sept. 28, should help speed up effective treatment of gout and get physicians to treat patients to a target urate level of less than 6 mg/dL in order to improve symptoms, Dr. John D. FitzGerald said in an interview.

"There has been a fair amount of recent movement on gout medications" including new alternatives to allopurinol and colchicine and new data on how to use those traditional drugs in safer ways, said Dr. FitzGerald, acting chief of the rheumatology division at the University of California, Los Angeles. "It’s a fair number of changes for medications that people had been using for decades."

The documents update previous guidelines from medical organizations in Europe, the Netherlands, and Japan. The new guidelines will be published in October 2012 by the journal Arthritis Care & Research.

Part 1 of the American College of Rheumatology (ACR) guidelines covers nonpharmacologic and pharmacologic approaches to managing hyperuricemia (Arthritis Care Res. 2012;64:1431-46 [doi:10.1002/acr.21772]).

Part 2 addresses prophylaxis and treatment for acute gouty arthritis (Arthritis Care Res. 2012;64:1447-61 [doi.wiley.com/10.1002/acr.21773]).

Dr. FitzGerald and two other co-leaders of the project, Dr. Dinesh Khanna of the University of Michigan, Ann Arbor and Dr. Robert Terkeltaub of the University of California, San Diego, reviewed the medical literature on gout from the 1950s to the present and drew up nine clinical case scenarios commonly seen in practice. A task force panel comprising seven rheumatologists, two primary care physicians, a nephrologist, and a patient representative used the scenarios to create consensus recommendations.

Among the recommendations, for example, on the use of allopurinol is to start at a low dose of 100 mg/day (instead of the common practice of starting with 300 mg/day), or even lower for patients with chronic kidney disease, and then gradually titrate upward every 2-5 weeks. That recommendation supports previous statements from the Food and Drug Administration and the European League Against Rheumatism.

Also, allopurinol therapy should be actively managed and patients followed to make sure the uric acid target is achieved. "You can’t just give a prescription and say your job is done," though some recent studies suggest that many physicians do just that, Dr. FitzGerald said. "The corollary would be if someone gave blood pressure medication and then didn’t follow the patient’s blood pressure. That wouldn’t be seen as good medicine."

Maintenance doses of allopurinol to prevent acute gout attacks can exceed 300 mg even in patients with chronic kidney disease provided there is adequate patient education and monitoring.

A new recommendation drops the starting dose of oral colchicine for acute gout attacks to a loading dose of 1.2 mg, followed by 0.6 mg an hour later, and then starting prophylaxis 12 hours later at dosing of 0.6 mg once or twice daily.

"We used to give up to eight tablets a day," Dr. FitzGerald said. "That is dropped down to three to four tablets at the start of an attacks, because of findings that more colchicine didn’t really help outcomes" and that smaller doses are safer. The authors called this recommendation from ACR "a paradigm shift" that’s in accordance with Food and Drug Administration-approved label language.

Other highlights of the new ACR recommendations include sections on screening for HLA-B*5801 in patients at high risk of severe adverse reaction to allopurinol, combination therapy when target urate levels are not achieved, medication options including new drugs, and more.

Although the reports are titled "Guidelines," the text makes clear that they are expert recommendations and that clinicians are expected to take active roles in choosing the best management strategies for their particular patients. The authors were "very concerned" that the guidelines not be used by third-party payers to restrict access to medications or to promote one drug over another if there isn’t clear evidence to support it, Dr. FitzGerald said.

The methodology of the project precluded evaluations of costs and cost effectiveness, instead focusing on efficacy. So, for example, the guidelines say that allopurinol and febuxostat can be used equivalently in some circumstances, but clinicians need to consider all other aspects of these options including cost, patient preference, and more.

The ACR plans to update the guidelines as new data become available. The task force panel did create specific indications for use of imaging studies because results should be available in the next few years from studies on the use of high-resolution ultrasound and dual-energy CT for patients with gout.

In the United States, gout affects an estimated 4% of adults – more than 8 million people.

"I’m most excited and hopeful about trying to get this out to internal medicine and family practice doctors," Dr. FitzGerald said. "They see more gout than rheumatologists."

Dr. FitzGerald reported having no financial disclosures. Some members of the task force reported financial associations with multiple pharmaceutical companies but, by design, a majority of task force members had no perceived potential conflicts of interest. 

The first guidelines on the management of gout from the American College of Rheumatology recommend new ways of using old drugs and changes in prophylaxis strategies, among other things.

The two-part guidelines, published online Sept. 28, should help speed up effective treatment of gout and get physicians to treat patients to a target urate level of less than 6 mg/dL in order to improve symptoms, Dr. John D. FitzGerald said in an interview.

"There has been a fair amount of recent movement on gout medications" including new alternatives to allopurinol and colchicine and new data on how to use those traditional drugs in safer ways, said Dr. FitzGerald, acting chief of the rheumatology division at the University of California, Los Angeles. "It’s a fair number of changes for medications that people had been using for decades."

The documents update previous guidelines from medical organizations in Europe, the Netherlands, and Japan. The new guidelines will be published in October 2012 by the journal Arthritis Care & Research.

Part 1 of the American College of Rheumatology (ACR) guidelines covers nonpharmacologic and pharmacologic approaches to managing hyperuricemia (Arthritis Care Res. 2012;64:1431-46 [doi:10.1002/acr.21772]).

Part 2 addresses prophylaxis and treatment for acute gouty arthritis (Arthritis Care Res. 2012;64:1447-61 [doi.wiley.com/10.1002/acr.21773]).

Dr. FitzGerald and two other co-leaders of the project, Dr. Dinesh Khanna of the University of Michigan, Ann Arbor and Dr. Robert Terkeltaub of the University of California, San Diego, reviewed the medical literature on gout from the 1950s to the present and drew up nine clinical case scenarios commonly seen in practice. A task force panel comprising seven rheumatologists, two primary care physicians, a nephrologist, and a patient representative used the scenarios to create consensus recommendations.

Among the recommendations, for example, on the use of allopurinol is to start at a low dose of 100 mg/day (instead of the common practice of starting with 300 mg/day), or even lower for patients with chronic kidney disease, and then gradually titrate upward every 2-5 weeks. That recommendation supports previous statements from the Food and Drug Administration and the European League Against Rheumatism.

Also, allopurinol therapy should be actively managed and patients followed to make sure the uric acid target is achieved. "You can’t just give a prescription and say your job is done," though some recent studies suggest that many physicians do just that, Dr. FitzGerald said. "The corollary would be if someone gave blood pressure medication and then didn’t follow the patient’s blood pressure. That wouldn’t be seen as good medicine."

Maintenance doses of allopurinol to prevent acute gout attacks can exceed 300 mg even in patients with chronic kidney disease provided there is adequate patient education and monitoring.

A new recommendation drops the starting dose of oral colchicine for acute gout attacks to a loading dose of 1.2 mg, followed by 0.6 mg an hour later, and then starting prophylaxis 12 hours later at dosing of 0.6 mg once or twice daily.

"We used to give up to eight tablets a day," Dr. FitzGerald said. "That is dropped down to three to four tablets at the start of an attacks, because of findings that more colchicine didn’t really help outcomes" and that smaller doses are safer. The authors called this recommendation from ACR "a paradigm shift" that’s in accordance with Food and Drug Administration-approved label language.

Other highlights of the new ACR recommendations include sections on screening for HLA-B*5801 in patients at high risk of severe adverse reaction to allopurinol, combination therapy when target urate levels are not achieved, medication options including new drugs, and more.

Although the reports are titled "Guidelines," the text makes clear that they are expert recommendations and that clinicians are expected to take active roles in choosing the best management strategies for their particular patients. The authors were "very concerned" that the guidelines not be used by third-party payers to restrict access to medications or to promote one drug over another if there isn’t clear evidence to support it, Dr. FitzGerald said.

The methodology of the project precluded evaluations of costs and cost effectiveness, instead focusing on efficacy. So, for example, the guidelines say that allopurinol and febuxostat can be used equivalently in some circumstances, but clinicians need to consider all other aspects of these options including cost, patient preference, and more.

The ACR plans to update the guidelines as new data become available. The task force panel did create specific indications for use of imaging studies because results should be available in the next few years from studies on the use of high-resolution ultrasound and dual-energy CT for patients with gout.

In the United States, gout affects an estimated 4% of adults – more than 8 million people.

"I’m most excited and hopeful about trying to get this out to internal medicine and family practice doctors," Dr. FitzGerald said. "They see more gout than rheumatologists."

Dr. FitzGerald reported having no financial disclosures. Some members of the task force reported financial associations with multiple pharmaceutical companies but, by design, a majority of task force members had no perceived potential conflicts of interest. 

ANSWER
The correct interpretation includes normal sinus rhythm, right bundle branch block, and left anterior fascicular block. Normal sinus rhythm is evidenced by a rate between 60 and 100 beats/min, with a corresponding P for every QRS and a QRS for every P.

Right bundle branch block is evidenced by a QRS duration > 120 ms, a terminal broad S wave in lead I, and an RSR’ complex in lead V₁. Left anterior fascicular block is evident from the finding that the S waves are greater than the R waves in leads II, III, and aVF.

The presence of a right ventricular block and left anterior fascicular block (bifascicular block) is consistent with a history of a VSD and/or surgical repair. The right and left bundles proceed from the atrioventricular node and bundle of His down the ventricular septum to the Purkinje fibers in the distal ventricular myocardium. Therefore, congenital anomalies of the ventricular septum, and/or surgical intervention within it, often affect conduction of the right and/or left bundle.

This patient’s symptoms were a result of his dilated aorta, and he underwent successful repair, with resolution of his symptoms.

ANSWER
The correct interpretation includes normal sinus rhythm, right bundle branch block, and left anterior fascicular block. Normal sinus rhythm is evidenced by a rate between 60 and 100 beats/min, with a corresponding P for every QRS and a QRS for every P.

Right bundle branch block is evidenced by a QRS duration > 120 ms, a terminal broad S wave in lead I, and an RSR’ complex in lead V₁. Left anterior fascicular block is evident from the finding that the S waves are greater than the R waves in leads II, III, and aVF.

The presence of a right ventricular block and left anterior fascicular block (bifascicular block) is consistent with a history of a VSD and/or surgical repair. The right and left bundles proceed from the atrioventricular node and bundle of His down the ventricular septum to the Purkinje fibers in the distal ventricular myocardium. Therefore, congenital anomalies of the ventricular septum, and/or surgical intervention within it, often affect conduction of the right and/or left bundle.

This patient’s symptoms were a result of his dilated aorta, and he underwent successful repair, with resolution of his symptoms.

ANSWER
The correct interpretation includes normal sinus rhythm, right bundle branch block, and left anterior fascicular block. Normal sinus rhythm is evidenced by a rate between 60 and 100 beats/min, with a corresponding P for every QRS and a QRS for every P.

Right bundle branch block is evidenced by a QRS duration > 120 ms, a terminal broad S wave in lead I, and an RSR’ complex in lead V₁. Left anterior fascicular block is evident from the finding that the S waves are greater than the R waves in leads II, III, and aVF.

The presence of a right ventricular block and left anterior fascicular block (bifascicular block) is consistent with a history of a VSD and/or surgical repair. The right and left bundles proceed from the atrioventricular node and bundle of His down the ventricular septum to the Purkinje fibers in the distal ventricular myocardium. Therefore, congenital anomalies of the ventricular septum, and/or surgical intervention within it, often affect conduction of the right and/or left bundle.

This patient’s symptoms were a result of his dilated aorta, and he underwent successful repair, with resolution of his symptoms.

ANSWER
The correct answer is petaloid seborrheic dermatitis (choice “d”), named for the flowerlike appearance of its polycyclic borders. Psoriasis (choice “a”) can present in this area, but tends to be scalier and usually involves multiple areas (eg, elbows, knees, and nails).

Rashes like this patient’s are often termed yeast infection (choice “b”). However, while a commensal yeast (Pityrosporum) can play a role in its formation, it appears that seborrhea represents an idiosyncratic reaction to increased numbers of this organism, rather than an actual infection.

Bowen’s disease (choice “c”) is a superficial squamous cell carcinoma, usually caused by overexposure to sunlight. Its lesions will be fixed, slowly growing larger with time, while seborrheic dermatitis will typically come and go. Biopsy is sometimes necessary to distinguish one from the other.

DISCUSSION
Seborrheic dermatitis (SD, aka seborrhea) is common, affecting up to 5% of the population. Dandruff is its usual manifestation, but it affects numerous other areas (as in this case), including the axillae, groin, beard, and genitals.

Presenting with scaling on an erythematous base, SD often flares and remits with the season (especially winter), with stress, and with increases in alcohol intake. Although it is usually mild, some cases can be severe. SD is associated with or accentuated by several other conditions, including Parkinson’s, stroke, and HIV. Severe SD in infants raises the possibility of Langerhans cell histiocytosis, especially when the presentation is atypical.

The diagnosis of SD can be difficult when it appears elsewhere than the scalp and face (eg, as an axillary or genital rash). Likewise, sternal petaloid SD is mystifying, unless other corroboratory manifestations are sought and found.

A few patients show signs of SD and psoriasis such that a definitive diagnosis cannot be made. Such overlap cases are sometimes termed sebopsoriasis. But psoriasis will usually exhibit signs not seen with SD, such as pitting of the nails, involvement of extensor surfaces of elbows and knees, and characteristic signs of psoriatic arthropathy in about 20% of cases. Pinpoint bleeding caused by peeling away scale, called the Auspitz sign, is seen with psoriasis and not with SD.

TREATMENT
This patient’s chest involvement responded rapidly to topical betamethasone foam, quickly tapered to avoid thinning the skin. Less powerful steroid creams, lotions, or gels (eg, triamcinolone 0.025%) can be used on other areas, such as ears and face. The daily use of an OTC dandruff shampoo (containing selenium sulfide, zinc pyrithione, tar, or ketoconazole) is an effective approach to controlling scalp involvement, but the product should be changed weekly.

Once the initial inflammation is controlled, topical antiyeast/antifungal preparations (eg, ketoconazole cream or any of the imidazoles, such as clotrimazole or oxiconazole) can be useful.

Finally, emphasis must be placed on educating the patient to expect control of the condition but not a cure.

ANSWER
The correct answer is petaloid seborrheic dermatitis (choice “d”), named for the flowerlike appearance of its polycyclic borders. Psoriasis (choice “a”) can present in this area, but tends to be scalier and usually involves multiple areas (eg, elbows, knees, and nails).

Rashes like this patient’s are often termed yeast infection (choice “b”). However, while a commensal yeast (Pityrosporum) can play a role in its formation, it appears that seborrhea represents an idiosyncratic reaction to increased numbers of this organism, rather than an actual infection.

Bowen’s disease (choice “c”) is a superficial squamous cell carcinoma, usually caused by overexposure to sunlight. Its lesions will be fixed, slowly growing larger with time, while seborrheic dermatitis will typically come and go. Biopsy is sometimes necessary to distinguish one from the other.

DISCUSSION
Seborrheic dermatitis (SD, aka seborrhea) is common, affecting up to 5% of the population. Dandruff is its usual manifestation, but it affects numerous other areas (as in this case), including the axillae, groin, beard, and genitals.

Presenting with scaling on an erythematous base, SD often flares and remits with the season (especially winter), with stress, and with increases in alcohol intake. Although it is usually mild, some cases can be severe. SD is associated with or accentuated by several other conditions, including Parkinson’s, stroke, and HIV. Severe SD in infants raises the possibility of Langerhans cell histiocytosis, especially when the presentation is atypical.

The diagnosis of SD can be difficult when it appears elsewhere than the scalp and face (eg, as an axillary or genital rash). Likewise, sternal petaloid SD is mystifying, unless other corroboratory manifestations are sought and found.

A few patients show signs of SD and psoriasis such that a definitive diagnosis cannot be made. Such overlap cases are sometimes termed sebopsoriasis. But psoriasis will usually exhibit signs not seen with SD, such as pitting of the nails, involvement of extensor surfaces of elbows and knees, and characteristic signs of psoriatic arthropathy in about 20% of cases. Pinpoint bleeding caused by peeling away scale, called the Auspitz sign, is seen with psoriasis and not with SD.

TREATMENT
This patient’s chest involvement responded rapidly to topical betamethasone foam, quickly tapered to avoid thinning the skin. Less powerful steroid creams, lotions, or gels (eg, triamcinolone 0.025%) can be used on other areas, such as ears and face. The daily use of an OTC dandruff shampoo (containing selenium sulfide, zinc pyrithione, tar, or ketoconazole) is an effective approach to controlling scalp involvement, but the product should be changed weekly.

Once the initial inflammation is controlled, topical antiyeast/antifungal preparations (eg, ketoconazole cream or any of the imidazoles, such as clotrimazole or oxiconazole) can be useful.

Finally, emphasis must be placed on educating the patient to expect control of the condition but not a cure.

ANSWER
The correct answer is petaloid seborrheic dermatitis (choice “d”), named for the flowerlike appearance of its polycyclic borders. Psoriasis (choice “a”) can present in this area, but tends to be scalier and usually involves multiple areas (eg, elbows, knees, and nails).

Rashes like this patient’s are often termed yeast infection (choice “b”). However, while a commensal yeast (Pityrosporum) can play a role in its formation, it appears that seborrhea represents an idiosyncratic reaction to increased numbers of this organism, rather than an actual infection.

Bowen’s disease (choice “c”) is a superficial squamous cell carcinoma, usually caused by overexposure to sunlight. Its lesions will be fixed, slowly growing larger with time, while seborrheic dermatitis will typically come and go. Biopsy is sometimes necessary to distinguish one from the other.

DISCUSSION
Seborrheic dermatitis (SD, aka seborrhea) is common, affecting up to 5% of the population. Dandruff is its usual manifestation, but it affects numerous other areas (as in this case), including the axillae, groin, beard, and genitals.

Presenting with scaling on an erythematous base, SD often flares and remits with the season (especially winter), with stress, and with increases in alcohol intake. Although it is usually mild, some cases can be severe. SD is associated with or accentuated by several other conditions, including Parkinson’s, stroke, and HIV. Severe SD in infants raises the possibility of Langerhans cell histiocytosis, especially when the presentation is atypical.

The diagnosis of SD can be difficult when it appears elsewhere than the scalp and face (eg, as an axillary or genital rash). Likewise, sternal petaloid SD is mystifying, unless other corroboratory manifestations are sought and found.

A few patients show signs of SD and psoriasis such that a definitive diagnosis cannot be made. Such overlap cases are sometimes termed sebopsoriasis. But psoriasis will usually exhibit signs not seen with SD, such as pitting of the nails, involvement of extensor surfaces of elbows and knees, and characteristic signs of psoriatic arthropathy in about 20% of cases. Pinpoint bleeding caused by peeling away scale, called the Auspitz sign, is seen with psoriasis and not with SD.

TREATMENT
This patient’s chest involvement responded rapidly to topical betamethasone foam, quickly tapered to avoid thinning the skin. Less powerful steroid creams, lotions, or gels (eg, triamcinolone 0.025%) can be used on other areas, such as ears and face. The daily use of an OTC dandruff shampoo (containing selenium sulfide, zinc pyrithione, tar, or ketoconazole) is an effective approach to controlling scalp involvement, but the product should be changed weekly.

Once the initial inflammation is controlled, topical antiyeast/antifungal preparations (eg, ketoconazole cream or any of the imidazoles, such as clotrimazole or oxiconazole) can be useful.

Finally, emphasis must be placed on educating the patient to expect control of the condition but not a cure.