Cases reported "Leishmaniasis, Visceral"

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11/262. Visceral leishmaniasis masquerading as tuberculosis in a patient with AIDS.

    We report a case of visceral leishmaniasis presenting as significant lymphadenopathy in a patient with acquired immune deficiency syndrome. The lymphadenopathy was initially suspected to be tubercular in nature on pathological examination. This report highlights the increasing incidence of acquired immune deficiency syndrome and Leishmania co-infection in india, and the importance of demonstrating tubercle bacilli on culture before suggesting a diagnosis of tuberculosis.
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12/262. A clinical and histopathological study of macular type of post-kala-azar dermal leishmaniasis.

    Post-kala-azar dermal leishmaniasis (PKDL) is an uncommon sequel seen in patients with a previous attack of kala-azar (KA). It is characterized by hypopigmented macules and erythematous eruptions leading to the formation of papules, plaques and nodules. Little attention has been paid to the rare group of patients who present with only hypopigmented macules. The present study has described the distribution of lesions in macular PKDL and their histopathology.
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13/262. Dermatofibroma parasitized by Leishmania in HIV infection: a new morphologic expression of dermal Kala Azar in an immunodepressed patient.

    Visceral leishmaniasis is a protozoan infection that may complicate the course of patients with human immunodeficiency virus (HIV). Dermatofibroma is a cutaneous fibrohistiocytic lesion considered neoplastic by some authors and inflammatory by others. Eruptive dermatofibromas have been described in patients with HIV infection or with other altered immunity situations. We present the case of a 32-year-old, HIV-positive man with visceral leishmaniasis who complained of the appearance of a cutaneous lesion in the leg formed by the coexistence of dermatofibroma and Leishmania parasitic colonization. As far as we know, this type of association has not been reported previously. We consider that the dermatofibroma could have developed as an unusual form of fibrohistiocytic reaction to leishmania. From a practical approach, we recommend the search of leishmaniasis in dermatofibroma in immunosuppressed patients.
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14/262. Long-term remission of human immunodeficiency virus-associated visceral leishmaniasis after initiation of potent combination antiretroviral treatment: report of two cases.

    We describe two cases of human immunodeficiency virus-infected patients with visceral leishmaniasis in whom no clinical and parasitological disease relapses were observed after liposomal amphotericin b therapy combined with potent antiretroviral treatment.
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15/262. A new focus of visceral leishmaniasis in sub-Himalayan (Kumaon) region of northern india.

    A localised focus of visceral leishmaniasis is reported for the first time from Kumaon region of North india. During a period of 18 months from July 1997 to December 1998 several cases of pyrexia of unknown origin with unresponsiveness to antibiotics and anti-tubercular treatments were referred to the All india Institute of Medical Sciences, New Delhi. Five of these were diagnosed to have visceral leishmaniasis. One of these was also co-infected with hiv-1. All the five cases came from an adjoining area falling under Almora (4) and Nainital(1) districts. Of these four were males and one female. One patient died within 48 hours of hospitalization at AIIMS while rest of four responded completely to sodium stibogluconate therapy.
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16/262. Post-kala-azar dermal leishmaniasis during highly active antiretroviral therapy in an AIDS patient infected with leishmania infantum.

    We report a case of post-kala-azar dermal leishmaniasis (PKDL) in a woman with AIDS which occurred 13 months after a diagnosis of visceral leishmaniasis concomitantly with immunological recovery induced by highly active retroviral therapy. Cytokine pattern at the time of visceral leishmaniasis and PKDL diagnosis was studied and pathogenic implications were discussed.
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17/262. Visceral leishmaniasis and other severe infections in an adult patient with p47-phox-deficient chronic granulomatous disease.

    We report a rare case of a male patient without known immunodeficiency consecutively diagnosed with visceral leishmaniasis, brain abscess and cavitating pneumonia in the 3rd decade of life. Chronic granulomatous disease (CGD) was diagnosed by a nitroblue tetrazolium test. A p47-phox mutation of the nadph oxidase of the leukocytes was suspected by immunoblotting and confirmed by dna analysis. The patient was homozygous for this mutation while his mother and sister were heterozygous asymptomatic carriers. After the CGD diagnosis the patient started a chronic prophylactic regimen with subcutaneous interferon-gamma (0.05 mg/m2 of body surface/three times a week), and oral trimethoprim-sulfamethoxazole and itraconazole (both at 5 mg/kg/day) with no subsequent infections after 12 months of follow-up.
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18/262. Liposomal amphotericin b as first line and secondary prophylactic treatment for visceral leishmaniasis in a patient infected with HIV.

    Visceral leishmaniasis has emerged in both endemic and non-endemic areas as an opportunistic infection in HIV-positive subjects. At risk for infection are HIV-positive intravenous drug abusers with a low CD4 T cell count and a high HIV viral load. In these patients, who are not always symptomatic, leishmaniasis is probably due to endogenous reactivation and often presents in an atypical fashion. death results from uncontrolled bleeding or bacterial infections. The clinical and biological spectrum of this disease suggests that it should be included among the diagnostic criteria for AIDS. Visceral leishmaniasis responds poorly to therapy and, when responsive, the relapse rate is high. Treatment protocols and criteria to document cure after treatment have not been definitely established. Lastly, there is no effective immuno- or chemo-prophylaxis against this protozoan. We report the case of an HIV-infected patient affected by visceral leishmaniasis who was successfully treated with liposomal amphotericin b given both as first line and as secondary prophylactic therapy. The patient has remained disease-free for 26 months after his first remission whereas, to our knowledge, almost all immunocompromised patients relapse within 12 months.
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19/262. antimony excretion in a patient with renal impairment during meglumine antimoniate therapy.

    meglumine antimoniate was administered to a patient with visceral leishmaniasis with normal renal function. Soon after the first intramuscular administration of meglumine antimoniate 20 mg/kg, equivalent to 510 mg antimony (Sb), the patient developed septic shock with oliguria. creatinine clearance decreased to 23 ml/minute. Treatment was discontinued, and Sb urinary excretion was measured. After the initial dose, 500.25 mg Sb was recovered in urine over 8 days, corresponding to 98% of the amount of Sb given intramuscularly (66% eliminated within first 48 hrs). Nine days after the dose, meglumine antimoniate was reintroduced at a dosage of 11.7 mg/kg (equivalent to 300 mg Sb) every 48 hours with good tolerance. At that time creatinine clearance had returned to 87.8 ml/minute. By day 14 of therapy the interval was reduced to daily administration of the same dose; the dosage was increased to 16.6 mg/kg/day (equivalent to 425 mg Sb) from day 17 to day 31. The patient eventually completely recovered and was discharged with normal renal function. Although no specific guidelines exist for dosage adjustment in renal failure, monitoring of Sb urinary excretion indicates that the kidneys are the almost exclusive route of elimination.
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20/262. Therapy of visceral leishmaniasis in renal transplant recipients intolerant to pentavalent antimonials.

    Visceral leishmaniasis should be suspected in renal transplant recipients in whom a fever develops of unknown origin. A 53-year-old renal transplant recipient developed pyrexia, hepatosplenomegaly, and pancytopenia 4 years after transplantation. Antileishmaniasis serology was negative, and the diagnosis was confirmed through bone marrow examination. Treatment with glucantine (N-methylglucamine antimoniate) led to acute pancreatitis, and treatment with ketoconazole plus allopurinol for 21 days was effective to eradicate leishmania donovani.
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