Post-kala-azar Dermal Leishmaniasis Developing in Miltefosine-Treated Visceral Leishmaniasis
A 23-year-old lady was brought to our dermatology outdoor patient department by a health worker with hypopigmented macules on face, upper arms, and abdomen [Figures and ]. The lesions were nontender and sensation was intact. The peripheral nerves were not tender or thickened. On systemic examination, all findings were normal except mild anemia (9 mg/dl) and high erythrocyte sedimentation rate (ESR; 96 mm in the first hour). The recombinant K39 (rK39)-based immunochromatographic strip test was positive. Biopsy sample from hypopigmented macules did not reveal any acid fast bacilli but showed epidermal atrophy, follicular plugging with keratin, and presence of dense lymphocytic infiltrate in the dermis suggestive of PKDL. There was no demonstrable Leishman-donovan (LD) body []. There was no hepatosplenomegaly or lymphadenopathy. Enzyme-linked immunosorbent assay (ELISA) for HIV-1 and 2 was negative. She was treated for VL with miltefosine, 100 mg/day for 28 days about 6 years back under a phase IV WHO/TDR/ICMR-sponsored clinical trial. After treatment, she became clinically and parasitologically cured and had no complains in follow-up of 6 months. After 4 years of treatment with miltefosine, she developed skin lesions on the face, which spread to upper part of the body. As her daily activities were not hampered, she was reluctant to visit doctor for more than 2 years. A clinical diagnosis of PKDL was made and the patient was put on miltefosine, 50 mg twice daily with complete subsidence of the lesions in 3 weeks. She was advised to continue treatment for 3 months.\nA 27-year-old patient, farmer by occupation, presented with depigmented macules widely spread all over the body since last 4 years, which were more marked on the front and back of trunk. The lesions on the face were coalescent and they appeared more hypopigmented than depigmented [Figures and ]. On touch, sensation was normal and no peripheral nerve was thickened or tender. On systemic examination, all findings were normal except mild raised eosinophils, 85 (normal range, 1-6%) and high ESR (96 mm in the first hour). The rK39-based immunochromatographic strip test was positive. Biopsy tissue sample from hypopigmented lesion from upper back showed no acid fast bacilli, but epidermal atrophy, a minimal mixed chronic infiltrate consisting of plasma cells, lymphocytes, and histiocytes in periappendageal and perivascular areas of upper dermis, suggestive of PKDL. Pityriasis lichenoides chronica was ruled out as there was no basal cell vacuolation. Ultrasonography of the abdomen suggested no pathology. The history of the patient revealed that he was treated for VL with miltefosine, 100 mg/day for 28 days about 7 years back from a tertiary hospital. Then, he had fever and enlargement of liver and spleen (symptoms for VL) and after treatment he was cured. He had appearance of hypopigmented lesions since last 3 years which gradually deepened with time. As the lesions were not disturbing, he was reluctant to visit clinic. He was started with miltefosine, 100 mg/day with complete disappearance of the lesions in 5 weeks. He was advised to continue miltefosine for 3 months.