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 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.