Non-Fatal Leishmaniasis in a Renal Transplant Recipient

Lamas, Santiago; Orte, L; Parras, Fernando Alberca de Las; Laraña, J García; Matesanz, Rafael; Ortuño, J

doi:10.1159/000184076

Cited by 22 publications

(27 citation statements)

References 3 publications

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“…To our knowl edge, 10 cases of visceral leishmaniasis have been re ported in the literature so far. Five died due to superinfec tion or haemorrhage, and 5 survived after therapy with stibogluconate sodium [3,[5][6][7][8][9][10][11]. Our patient initially responded to the conventional doses of stibogluconate sodium (10 mg/kg/day for 3 weeks), but she relapsed after 3 months.…”

Section: Discussionmentioning

confidence: 96%

“…Kala-azar in renal transplant patients is infre quently reported [3,[5][6][7][8][9][10][11]. Renal transplant recipients are also predisposed to acquiring new leishmaniasis infec tion due to the immunosuppressed state [5], Visceral leishmaniasis is a serious disease in the immunocom promised host and high mortality rates have been re ported, as the diagnosis could be delayed, and treatment is not easy [3,6,8].…”

Section: Discussionmentioning

confidence: 99%

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Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems

Sharma¹,

Jha²,

Kumar³

et al. 1996

Am J Nephrol

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Visceral leishmaniasis is infrequently reported in renal transplant recipients. A 40-year-old renal transplant recipient developed hepatosplenomegaly and pyrexia of unknown origin 5 months after transplantation. Visceral leishmaniasis was confirmed on bone marrow examination. The usual dose of antiparasitic therapy with stibogluconate sodium failed to eradicate Leishmania donovani. High-dose conventional therapy with stibogluconate sodium for an extended period of time was successful in the treatment of a relapse of leishmaniasis.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems

Sharma¹,

Jha²,

Kumar³

et al. 1996

Am J Nephrol

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“…Recent reports have indicated that spontaneously controlled (subclinical) infections caused by the intracellular protozoan, Leishmania donovani, may reactivate in immunocompromised patients (1)(2)(3)(4)(5)(6)(7). In addition, primary treatment Receivedfor publication 27 May 1988 and in revisedform 18 November 1988. failures using ordinarily effective pentavalent antimony (e.g., sodium stibogluconate, or Pentostam [proprietary name of Burroughs Wellcome]) as well as prompt relapses have also been described in Leishmania donovani-infected patients who have AIDS or are receiving immunosuppressive agents (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Requirement for T cells and effect of lymphokines in successful chemotherapy for an intracellular infection. Experimental visceral leishmaniasis.

Murray

J²,

Granger³

et al. 1989

J. Clin. Invest.

117

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Although directly microbicidal, pentavalent antimony has failed as treatment for visceral leishmaniasis in patients who also have AIDS or are receiving immunosuppressive therapy. To define the role of T cells in the successful host response to chemotherapy, we examined the efficacy of pentavalent antimony (sodium stibogluconate, Pentostam) in normal and T cell-deficient BALB/c mice infected with Leishmania donovani. In euthymic (nu/+) mice, single injections of 250 and 500 mg/kg of Pentostam induced the killing of 67% and 89% of intracellular liver amastigotes, respectively. In contrast, in athymic nude (nu/nu) mice, up to three injections of 500 mg/kg achieved no L. donovani killing and did not retard visceral parasite replication. Once nude mice were reconstituted with nu/+ spleen cells, however, Pentostam exerted strong leishmanicidal activity, an effect that appeared to be transferred by either L3T4+ or Lyt-2+ cells. Responsiveness to chemotherapy could also be induced by providing nude mice with either interferon-'y or interleukin 2 alone. The absence of this T cell-and probably lymphokine-dependent mechanism is a likely explanation for treatment failures in immunocompromised patients infected with L. donovani and perhaps other systemic intracellular pathogens as well.

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“…All of the cases of posttransplant leish maniasis reported in the literature were diag nosed while investigating etiology of the fe ver [1][2][3][4][5][6][7], In our case, however, despite the presence of bicytopenia and splenomegaly, fever was absent. Our patient's liver biopsy findings were consistent with minimal hepa titis and signs of portal hypertension were apparent.…”

mentioning

confidence: 82%

“…a sub acute infectious disease caused by the proto zoan Leishmania donovani and endemic in Mediterranean countries, has been reported previously in small numbers of transplant recipients [1][2][3][4][5][6][7],…”

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confidence: 99%