Case Reports

Erythema Induratum of Bazin Presenting as Peripheral Neuropathy

Author and Disclosure Information



The absence of M tuberculosis organisms in skin lesions has led some to doubt the causal relationship between M tuberculosis and EIB.7 However, the advent of polymerase chain reaction (PCR) and specific DNA primers for M tuberculosis has allowed for the detection of M tuberculosis DNA in biopsy specimens, which has further established the relationship between tuberculosis and EIB.5 Some authors have suggested that the absence of mycobacteria in EIB and other tuberculid lesions may be due to small numbers of bacilli in the lesions or early destruction of mycobacteria organisms before biopsy.8,9 These authors consider cutaneous tuberculosis and tuberculids as diseases on the same spectrum, with tuberculids representing one extreme in which there are few mycobacteria organisms present in the lesions.


Erythema induratum commonly affects middle-aged women and presents with recurrent crops of tender nodules on the lower extremities.10-13 Nodules often are most commonly found on the lower calves but also can present on the arms, thighs, feet, or buttocks.10 Our patient’s presentation was atypical in that lesions were distributed on the pretibial area of the legs and dorsal aspect of the feet. Obesity and venous insufficiency of the lower extremities are believed to be predisposing factors to the development of EIB nodules.2 The nodules develop over several weeks and heal over several months with possible ulceration and hyperpigmented scarring.10,11 Ulcerated nodules often are irregular and shallow with an overlying crust and a bluish border.11,13 Nodules often are precipitated by cold weather or venostasis.1,11,12

Silva et al14 reported a case of EIB on the lower legs associated with a burning sensation on the feet and paresthesia; all known causes of peripheral neuropathy were excluded by a comprehensive laboratory workup. The burning sensation on the feet resolved after several weeks of antituberculosis therapy. Our patient also presented with a burning sensation on the feet that remarkably improved after 6 months of antituberculosis therapy. Peripheral neuropathy could have been a consequence of diabetes mellitus in our patient, though neuronal damage also could be a consequence of hypersensitivity to tuberculosis antigens. Silva et al14 proposed that macrophages activated by M tuberculosis antigens produce lytic enzymes that can cause tissue necrosis and nerve damage if released into surrounding tissue.


The diagnosis of EIB is made based on clinical presentation, evidence of prior or current tuberculosis infection, histopathologic findings, and response to antituberculosis therapy.15 Evidence of active or latent tuberculosis infection typically is gathered by patient history, chest radiograph, tuberculin skin tests, interferon-releasing assays, and PCR of skin biopsies. Tuberculin skin tests in patients with EIB result in reactive induration that is typically more than 20 mm.8 In vitro T-lymphocyte proliferation assays in response to PPD have further supported the suggestion that there is a markedly enhanced T-lymphocyte response to M tuberculosis antigens in patients with EIB.16

IFN-γ release assays have provided useful methods for the detection of latent tuberculosis infection.17 The IGRA is effective when the tuberculin skin test yields a suspected false-negative or in the context of prior bacille Calmette-Guérin vaccination.17 IFN-γ release assays also may be preferred to tuberculin skin tests because it provides less discomfort to the patient in the event of a positive hypersensitive reaction to the PPD.

Before the advent of IGRAs, PCR was used to detect M tuberculosis DNA in skin biopsies and to confirm the diagnosis of EIB. Some researchers believe PCR can be an important tool for confirming a diagnosis of EIB, especially in cases and countries where results from the Mantoux test do not have great value.15,18 A PCR assay for detecting 
M tuberculosis DNA in blood and urine samples also was found helpful in confirming a diagnosis of EIB when skin biopsies were unavailable.8,19 However, PCR has been shown to have low sensitivity for the diagnosis of EIB because of its ability to detect M tuberculosis DNA ranging from 
0% to 77% of skin biopsy specimens.20,21 Therefore, a negative PCR for the detection of M tuberculosis DNA in nodules does not exclude a diagnosis of erythema induratum.


The mainstay of EIB treatment is a multidrug antituberculosis regimen.5,8,10-12 Our patient was successfully treated with rifampin and isoniazid and a repeat IGRA was used as a laboratory marker of response to therapy. Single-drug therapy with isoniazid has been shown to result in greater likelihood of EIB relapse in comparison to multidrug regimens.22 Other treatments include potassium iodide and gold, but they are not well-studied.23-25 Treatment of venous insufficiency with bed rest and nonsteroidal anti-inflammatory drugs for pain also may be helpful.2 In cases of nodular vasulitis that are not associated with tuberculosis infection, treatment should be targeted at the underlying cause of the immune response. For example, a case of nodular vasculitis associated with hepatitis C virus did not respond to antituberculosis multidrug therapy, but skin lesions did improve with pegylated interferon and ribavirin.4


Next Article:

Understanding of Mycoplasma-induced mucositis improving

Related Articles