A 59-year-old male patient was admitted to our university hospital (Botucatu, SP, Brazil) complaining of a perianal suppurative ulcer developed two months before the first medical consultation. He was under therapy with prednisone 40 mg/day for six months due to a presumed diagnosis of a drug reaction. On physical examination, a clean 10-cm diameter phagedenic perianal ulcer (Figure ) and two longitudinal suppurative ulcers on the inguino-crural region were observed. During investigation, and soon after reducing the corticosteroid dose, disseminated erythematous papules and nodules were observed in the upper limbs (Figure ).Histopathology of the perianal ulcer revealed a dense histiocytic dermal infiltrate and a granulomatous inflammatory response with central caseous necrosis (Figure ). Fite-Faraco staining showed a few acid-fast bacilli and the hypothesis of cutaneous tuberculosis was raised. The histopathology of upper limbs papular and nodular lesions showed foamy macrophages with globi of bacilli, suggesting lepromatous leprosy (Figure ). The perianal and inguinal ulcers were considered uncommon manifestations of type 2 leprosy developed when corticosteroid was gradually diminished. The patient was treated as for multibacillary leprosy with multidrug therapy and thalidomide.\nFour weeks later, the patient had fever, weight loss, asthenia and worsening of the perianal ulcer (Figure ), but without erythema nodosum leprosum. With this clinical picture, new investigation was developed. The tuberculin skin test was positive (20 × 20 mm) and culture of M. tuberculosis – using a biopsy sample from the perianal ulcer – on Löwenstein-Jensen medium was positive (Figure ). Polymerase chain reaction (PCR) and DNA analysis from upper limb skin samples were positive for M. leprae (Figure ). With the new information the patient was finally diagnosed as presenting simultaneously lepromatous leprosy – type 2 reaction – and cutaneous tuberculosis expressed by the perianal ulcer. Screening for HIV, HBV or HCV infection as well as lung, renal or colon compromising were negative. Hence, the patient was treated with isoniazid, ethambutol and rifampin for nine months with complete healing of the perianal and inguinal lesions after two months (Figure ). After the tuberculosis treatment, the patient was submitted to additional multidrug therapy for 12 months with dapsone, rifampin and clofazimine with complete cure of leprosy.
A 47-year-old Tamil woman with poorly controlled long-standing diabetes mellitus presented with facial infiltration, multiple ichthyotic patches, and peripheral neuropathy associated with Charcot joints and trophic ulcers (Fig. ). She was a homemaker with poor social background and there was no contact history of TB or leprosy. She did not smoke tobacco or drink alcohol. She had received a BCG vaccination. She had a low BMI and a respiratory examination revealed B/L coarse crepitations. There was no peripheral neuropathy. A clinical diagnosis of lepromatous leprosy was made which was later confirmed with histology and slit-skin smears: bacteriological index (BI) of 5; morphological index (MI) of 2%. Initial investigations revealed persistently elevated ESR (100–122 mm/hour) and inflammatory shadows in a CXR. Two consecutive sputum smears were positive for AFB and the result of a Mantoux test was positive (18 mm). Her liver and renal functions were normal (Table ). She was negative for HIV screening. She was commenced on both TB (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) and multibacillary leprosy treatment (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) without a monthly loading dose of rifampicin. She had poor compliance and defaulted treatment several times and ultimately succumbed to the illness. An autopsy was not performed.