Polymerase chain reaction in cutaneous tuberculosis
Özet
A 32-year-old man was first seen in 1989, when he had a 1-year history of a reddish-brown, nonscaling elevated, soft plaque with telangiectases on his nose (lesion A) (Fig. 1) and a 9-year history of slowly advancing, asymptomatic, multiple, hyperkeratotic, purple-brown, infiltrated nodular lesions on the left lateral aspect of the leg and the heel (lesions B) (Pig. 2). The patient was an official and did not describe any wound or abrasion. Multiple punch biopsy specimens had been taken from lesion B beginning in 1989 and on histologic Acid-fast stains failed to reveal organisms in any of the specimens taken from lesions A or B. Cultures, using the BACTEC radiometric system and Lowenstein-Jensen medium, and inoculations into animals were negative. Routine laboratory values were within normal limits. Chest roentgenograms were repeatedly negative and no acid-fast bacilli were detected in the sputum. The tuberculin test was positive. The patient had been treated with systemic antimicrobials and a variety of topical medications for lesion A, but with no response. Antituberculosis chemotherapy, consisting of isoniazid (300 mg daily), rifampicin (600 mg daily), ethambutol (1000 mg daily), and pyrazinamide (1500 mg daily), was initiated for lesion 8. After 2 months of treatment, pyrazinamide and ethambutol were discontinued because of toxic optic neuropathy. Isoniazid and rifampicin were continued for 4 more months. The lesion B did not regress and the therapy was stopped in 1990. The patient was treated conservatively from 1991 to 1994. Polymerase chain reaction (PCR) became available in our unit in 1993. Tissue biopsies were performed for histologic diagnosis again and PCR was carried out to investigate the presence of mycobacterial DNA in lesions of both locations in order to evaluate the diagnosis of lupus vulgaris.
