A 59-year-old Sinhalese man presented with nonhealing ulcers and deformities of both upper and lower limbs and indurations of his face (Fig. ) for many years. He was clinically diagnosed to have borderline lepromatous leprosy, which was subsequently confirmed with slit-skin smears and histology. He was a laborer from poor social background and did not have a significant past medical history. He was emaciated with low BMI; a neurological examination did not reveal neuropathy. There was no contact history of leprosy or TB. He had received a BCG vaccination. He did not smoke tobacco and he drank alcohol occasionally. During his initial evaluation he was also found to have high ESR (> 100 mm/hour) with positive Mantoux test (21 mm) and sputum was positive for AFB. A CXR and contrast-enhanced computer tomography scan of his chest revealed the focus of pulmonary TB; bronchoalveolar lavage for TB culture revealed growth of AFB, but GeneXpert did not reveal rifampicin resistance. His HIV status was negative and repeated blood sugar levels remained within normal range. Other basic investigations are given in Table . He was commenced on multibacillary leprosy treatment (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) and subsequently added TB treatment (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) for 6 months. At 6 months, his ESR came down, sputum was negative for AFB, and skin lesions and ulcers improved.
A 57-year-old Sinhalese woman presented to the dermatology unit of the National Hospital of Sri Lanka with extensive seborrheic dermatitis and tender facial induration (Fig. ) of 1-year duration. She was a homemaker from an urban area with poor social background. She did not have diabetes or hypertension. She had received a Bacillus Calmette–Guérin (BCG) vaccination. She did not smoke tobacco or drink alcohol. A skin biopsy taken from indurated facial plaque revealed evidence of borderline tuberculoid leprosy with type 1 reaction. She did not have hypopigmented anesthetic patches or thickened peripheral nerves in the rest of her body. She was commenced on multibacillary treatment for leprosy. A year later, she developed fever, loss of appetite, loss of weight, and widespread skin abscesses all over her body. Her body mass index (BMI) was within normal range and the rest of the general examination was normal. A respiratory examination revealed bilateral (B/L) coarse crepitations; a neurological examination was normal. Her erythrocyte sedimentation rate (ESR) remained persistently elevated at more than 120 mm/hour. She had inflammatory shadows in a chest X-ray (CXR). A sputum examination for AFB was positive and GeneXpert confirmed rifampicin resistance. At that time, she revealed a diagnosis of human immunodeficiency virus (HIV) infection and tuberculous lymphadenitis, which was made 5 years back, where she had taken 6-month TB treatment but had defaulted on antiretroviral therapy. During this presentation, her CD4+ count was 57/μL. The rest of the investigations are summarized in Table . There was no contact history of leprosy or TB. She was started on a multidrug treatment regime, which included intravenously administered kanamycin (15 mg/kg per day), orally administered ethambutol (800 mg/day), orally administered levofloxacin (750 mg/day), isoniazid (300 mg/day), orally administered ethionamide (500 mg/day), orally administered cycloserine (750 mg/day), and orally administered pyridoxine (10 mg/day). A repeated split skin smear was negative and she continued with multidrug treatment-multibacillary therapy (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) for leprosy without rifampicin. Highly active antiretroviral treatment was restarted subsequently. At 6 months she had clinically, hematologically, and radiologically improved.