Abstract

A 39-year-old woman was referred with a 1-year history of a 4-cm mass of the left axilla, compatible with a lymph node. Itchy red papules that evolved to crusty lesions and subsequently showed varioliform atrophic scarring appeared over the face, extensor surface of the arms, back, thighs, and scalp (1, 2). Her history included weight loss of 8 kg, but no other associated symptoms or contact with tuberculosis patients. The blood count showed a normochromic–normocytic anemia with an erythrocyte sedimentation rate (ESR) slightly elevated at 28 mm in the first hour (normal, < 20 mm). Tuberculin skin test was positive (13 mm with necrotic reaction) and anti-human immunodeficiency virus serology was negative. Four lesional skin biopsies and one lymph node biopsy were performed and sent for histopathology and culture. The skin biopsy showed small-vessel lumen occlusion by tiny thrombi, endothelial hyperplasia, and intense perivascular inflammatory reaction throughout the dermis, together with partial degeneration of collagen, compatible with tuberculid. Lymph node biopsy showed chronic, necrotizing, granulomatous lymphadenitis, consistent with a diagnosis of lymph node tuberculosis. Mycobacteria were absent on Ziehl–Neelsen staining and culture in all specimens. Figure 1Open in figure viewerPowerPoint Varioliform atrophic scarring over the extensor surface of the arms, typical of papulonecrotic tuberculid (PNT) Figure 2Open in figure viewerPowerPoint Varioliform atrophic scarring over the back, typical of papulonecrotic tuberculid (PNT) On the basis of the clinical features, positive tuberculin skin test, and histopathologic findings, a diagnosis of papulonecrotic tuberculid associated with tuberculous lymphadenitis was made. A triple therapeutic regimen with rifampicin, isoniazid, and pyrazinamide was started and the patient evolved with progressive clinical improvement. At the end of treatment at 6 months, there was clinical remission and improvement of anemia and ESR. Four months later, however, there was a clinical relapse of the lesions on the scalp, ultimately resulting in cicatricial alopecia with varioliform atrophic scarring (3, 4). A biopsy of these new lesions was performed and showed focal necrosis (V-shaped) in the epidermis and dermis with follicular involvement and thrombotic occlusion of vessels, confirming the diagnosis of tuberculid. The patient was retreated with rifampicin, isoniazid, pyrazinamide, and ethambutol for 9 months. A new investigation of another internal focus of tuberculosis was negative. Figure 3Open in figure viewerPowerPoint Cicatricial alopecia with varioliform atrophic scarring appearing after 6 months of treatment for tuberculosis Figure 4Open in figure viewerPowerPoint Cicatricial alopecia with varioliform atrophic scarring appearing after 6 months of treatment for tuberculosis In the last 2 years, the patient has had several recurring crops of lesions on the scalp. Further biopsies were taken, with histopathology showing nonspecific inflammatory changes. Cultures for Mycobacterium spp. were negative (five media: Lowenstein–Jensen, Lowenstein–Jensen supplemented with ferric ammonium citrate or pyruvate, Stonebrink and 7H9 supplemented with hemin) under different temperatures and light conditions. In addition, nucleic acid amplification for mycobacterial hsp65 using polymerase chain reaction restriction enzyme analysis methodology (Telenti A, Marchesi F, Balz M, et al. Rapid identification of mycobacteria to the species level by polymerase chain reaction and restriction enzyme analysis. J Clin Microbiol 1993; 31: 175–178; da Silva RA, Werneck Barreto AM, Dias Campos CE, et al. Novel allelic variants of mycobacteria isolated in Brazil as determined by PCR-restriction enzyme analysis of hsp65. J Clin Microbiol 2002; 40: 4191–4196) was negative. The patient is still being followed up in our clinic.

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