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 49-year-old man, nonsmoker, was admitted to dermatology department and followed up for diffuse lepromatous leprosy. He was vaccinated with BCG and he had no past history of tuberculosis. Diagnosis of leprosy was documented based on histological and bacteriologic evidence: a slit skin smear from the ear lobe was positive for lepra bacilli (BI3+), histopathology from the lesion on the face showed granulomas consisting of epithelioid histiocytes and lymphocytes with central caseous surrounding vessels and nerves, and PCR of biopsy specimens were positive for Mycobacterium leprae. After successful treatment using dapsone (100 mg/day), rifampicin (600 mg/month), and clofazimine (300 mg/month and 50 mg/day) during twelve months, hypopigmented skin lesions on the trunk and congestive rhinitis disappeared and the slit skin smear was negative. One month after the end of the treatment, he presented with diffuse papulonodular lesions on the face and trunk, fever, and alteration of general status. On the basis of his symptoms, diagnosis of leprosy reaction (type II) was made and the patient was treated using prednisone at a dose of 40 mg/kg/day. Outcome was unfavorable after two months of corticotherapy, and we had to wait for two supplementary months before we could get clofazimine to add corticoid. After 1 month of this treatment, he presented with fever, weight loss, and asthenia. Clinical examination revealed fever of 39°C, nodular lesions over face, trunk, forearms, and dorsum of hands (Figures , , and ). He presented no neurologic impairment. Biological examination showed inflammatory syndrome: CRP 393 mg/L, total leukocyte count 16,2 × 109/L, neutrophilia 15,3 × 109/L, and lymphopenia 0,48 × 109/L. Serum creatinine and alanine aminotransferase were normal. HIV status was negative. Two out of three sputum samples were positive for acid fast bacilli. Chest tomography showed alveolar-interstitial opacities at the left lower lobe (). Bronchoscopy detected thickening of lower lobar bronchi, without malignancy in histopathology of biopsy specimens. The patient was treated by antitubercular treatment. One month after the onset of this treatment, there were only two nodular lesions on the trunk, fever disappeared, and general status improved.