Erythema induratum with pulmonary tuberculosis: histopathologic features resembling true vasculitis
Authors: Lee Yong Suk , Lee Si Won , Lee Jong Rok , Lee Seung Chul 
Published: March 2003

A 22‐year‐old South Korean woman presented with a 4‐month history of several nodules on both legs. She looked healthy, but suffered from tenderness and swelling of the legs. Physical examination showed multiple, nonulcerating, erythematous nodules occurring on the calves, knee joints, and thighs (Fig. 1). A biopsy specimen of the skin revealed necrotizing vasculitis of medium‐sized arteries with fibrinoid necrosis at the border between the dermis and the subcutis. Dense cellular infiltrates, including numerous neutrophils and lymphocytes, presented within and around the vessel walls as in polyarteritis nodosa, with some eosinophils (Fig. 2A,B). There were no other generalized symptoms. She was diagnosed with cutaneous polyarteritis nodosa and was initially treated with systemic steroids. She was given an intravenous injection of Solu‐Cortef, 60 mg/6 h for 7 days. This was replaced with oral prednisolone for 2 weeks. The skin lesions and symptoms improved.

Small, nut‐sized, erythematous, brown‐colored nodules and patches on the lower extremities, even above the knee joints

image

(A) Dense infiltration within and around artery (× 40). (B) Slightly expanded lobular panniculitis with vasculitis (× 100)

image

Six months later, she complained of general weakness and recurrent skin lesions. Purified protein derivative (PPD) test gave a moderate positive reaction and chest X‐ray examination showed the features of pulmonary tuberculosis: radio‐opaque infiltrations in the right lower lung field. A repeated biopsy revealed mild vasculitis with more diffuse lobular infiltrations of the subcutaneous tissue compared with the former specimen.

Polymerase chain reaction (PCR) and tissue culture for Mycobacterium tuberculosis were performed from a biopsy specimen. DNA was extracted from skin tissue with an AplisystemTM DNA/RNA detection kit using the resin‐mediated boiling method (Stargene, Seoul, South Korea). The primers were designed on the basis of the M. tuberculosis gene IS6110 target (sense primer, 5′‐CCA GAT GCA CCG TCG AAC GGC TGA T‐3′ antisense primer, 5′‐CGC TCG CTG AAC CGG ATC GAT GTG T‐3′). The amplification was performed with uracil‐N‐glycosylase (UNG), to prevent carry‐over contamination, and internal control primers, to correct for false‐negative reaction (Kox LF, Rhienthong D, Miranda AM et al. A more reliable PCR for detection of Mycobacterium tuberculosis in clinical samples. J Clin Microbiol 1994; 32: 672–678; Longo MC, Berninger MS, Hartley JL. Use of uracil DNA glycosylase to control carry‐over contamination in polymerase chain reactions. Gene 1990; 93: 125–128). According to the manufacturer's instructions, amplification was carried out for 40 cycles with denaturation at 94 °C for 40 s, annealing at 70 °C for 1 min, and extension at 72 °C for 1 min in a thermal cycler (Perkin–Elmer Cetus, Norwalk, CT, USA). The results of PCR and tissue culture for M. tuberculosis using the biopsy specimen were all negative (Fig. 3).

Negative result in PCR for M. tuberculosis (negative control is not shown; M, marker; P, positive control; I, internal control; S, specimen)

image

The patient was finally diagnosed with erythema induratum with pulmonary tuberculosis and was started on antituberculosis medication (isoniazid 400 mg, rifampicin 600 mg, ethambutol 800 mg, and pyrazinamide 1500 mg daily). She showed prompt improvement after 2 weeks of medication. After 9 months of antituberculosis therapy, her skin lesions and chest X‐ray had cleared. She was followed up for 4 months with no recurrence of skin and pulmonary lesions.