A 50-year-old non-diabetic, non-hypertensive man who had completed treatment for lepromatous leprosy two years back, was admitted at Green Pastures Hospital for type-2 lepra reaction (erythema nodosum leprosum). There was a past history of lepra reactions for which he underwent treatment. Currently the patient was again being treated for the same with prednisolone 30 mg once daily, thalidomide 100 mg twice daily and clofazimine 50 mg once daily. However, information about initial screening of tuberculosis was not available.\nThe patient was referred to our teaching hospital with complaints of fever, productive cough and dyspnoea of three months duration. The patient also complained of pain and distension of abdomen and decreased appetite for three months.\nClinical examination revealed tense abdomen with shifting dullness, respiratory system with bilateral crackles with bronchial breath sounds predominantly in the left infra clavicular area, and skin showed no active lesions of erythema nodosum leprosum. The laboratory investigations revealed hemoglobin: 11.8 mg/dl; total leukocyte count: 5900/mm3; erythrocyte sedimentation rate: 110 mm in first hour; random blood sugar: 109 mg/dl; serum electrolytes, sodium: 135 meq/L and potassium: 3.2 meq/L.\nTwo out of three sputum samples were positive for acid fast bacilli. Chest radiograph showed multiple heterogeneous opacities in bilateral lung fields and a cavitary lesion in left upper zone. A diagnosis of pulmonary tuberculosis and provisional diagnosis of peritoneal tuberculosis were made.\nDermatologist's opinion was sought for the lepra reaction. The patient was advised to stop prednisolone as no active lesions persisted. He was subsequently referred to DOTS clinic and was started on category-I treatment.
A 72-year-old Tamil man presented with a 2-year history of trophic ulcers, auto-amputated fingers, and facial infiltration (Fig. ). He was a retired mason from a poor social back ground with low income and did not have any other medical diseases. A general examination and neurological examination was normal. There was no significant contact history of leprosy or TB. He had received a BCG vaccination. He was an ex-smoker of tobacco and an ex-drinker of alcohol. His evaluation confirmed the clinical diagnosis of leprosy with highly positive slit-skin smears and histological evidence of lepromatous leprosy. He also gave a history of constitutional symptoms, evening pyrexia, and loss of weight and appetite. His ESR was 113 mm/hour and a sputum examination revealed AFB along with positive Mantoux test of 14 mm and CXR evidence of pulmonary TB. Basic investigations are given in Table . He was evaluated for both congenital and acquired immunodeficiency status, which did not reveal any abnormality. Although treatment for both conditions was commenced (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day and dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) in liaison with a respiratory team, he was lost to follow up.