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Leishmaniasis, Leishmania braziliensis, renal transplant, uveitis.

UNUSUAL MANIFESTATIONS OF LEISHMANIASIS IN RENAL TRANSPLANT

EDUARDO R.F. TÁVORA , EULER P. LASMAR1, JULIANA OREFICE2, CÉLIA M.F. GONTIJO3, JOSÉ S. ANDRADE FILHO1

INTRODUCTION

Leishmaniasis is a spectrum of diseases caused by protozoa of the Leishmania gennus, transmitted to humans by the bites of sandflies generally called phlebotomus. The parasites are seen in two forms: promastigotes in the midgut of the mosquito and amastigotes, in the host macrophages.
Clinically, it is useful to group the different species of Leishmania in four complexes: 1) L. donovani (L. donovani, L. infectum, L. chagasi); 2) L. tropica (L. tropica, L. major, L aethiopica); 3) L. mexicana (L. mexicana, L. amazonensis, L. venezuelensis); and 4) L. braziliensis, sub gennus viannia (L. braziliensis, L. panamensis, L. guyanensis). Only the leishmanias of donovani’s complex (the tropica complex) are able to produce the visceral form of the disease, whereas other species cause cutaneous or mucocutaneous presentations. Another important determinant of clinical disease is the degree of host immune response to the parasites. For example, the visceral form is followed by suppression of the celular response, specially by Th1 lymphocites. It is also important to note that usually the mucocutaneous forms are not seen when there is the presence of visceral leishmaniasis. Some patients showing visceral involvement present skin hyperpigmentation which gave the disease the name “kala-azar” (black fever in Hindi).(1,2)

CASE PRESENTATION

A 32 year old man, born in the countryside of Minas Gerais State, located in Brazil’s southeast region, was the recipient in 1990 of a renal transplant from a living related donor. His immunossupression regimen included Cyclosporin A (CyA), Azathioprine (Aza) and Prednisone (P). He exeprienced an uneventful course until December 1995, when Aza was discontinued due to a severe infection with Epstein Barr virus (EBV). Six months later (June 1996) the patient was admitted to the hospital with a high remittent fever, muscle pains and pruriginous cutaneous lesions in the lower extremities. Physical examination showed a pale, pourly nourished man, with hepatosplenic enlargement and erithematous papules with elevated margins on the legs. The laboratory tests showed anemia (Hb: 6.2 g%), leucopenia (WBC: 2.200/mm(3)) and reduced graft function (serum creatinine: 2.6 mg%). The serological tests for Leishmania, HIV, HBV, EBV (IgM) and Chagas’ disease were negative. Platelet count and liver function tests were normal. However, bone marrow smears from the sternum, iliac crest, and skin biopsies were all positive for Leishmania.

The patient was treated with meglumine antimoniate for twenty days. Thereafter the drug had to be discontinued, owing to severe neurological complications attributed to hypomagnesemia, thought to be due to toxic tubular side effects of the drug.

Although the treatment was interrupted, the patient displayed clinical improvement of the leishmaniasis picture and was discharged. In December 1996 he was readmitted with fever, showing a red right eye, diagnosed by the ophthalmologists as uveitis. The aetiological agent was L. braziliensis which was demonstrated in the aqueous humour, the vitreous body and in another bone marrow smear as well as by parasite culture, electrophoresis for isoenzimes, RFLP and polymerase chain reaction (PCR)(3). The patient was successfully treated by intravenous and local administration (intravitreous) of amphotericin B. The patient was lost to follow-up for the next months and returned at the beginning of 1998 in a poor clinical condition, expiring thereafter in November 1998.

DISCUSSION

Leishmaniasis is a common disease throughout the world, including all continents except Oceania (Australia) and Antarctica. It is estimated that 400,000 new cases are added annually to the population of approximate 12 million infected people. A Medline search revealed only 22 reported cases of leishmaniasis in immunossupressed transplant patients until 2001. This paucity of cases seems paradoxal because transplant patients are typically susceptible to any infection. Despite being a rare disease, leishmaniasis is considered rather serious; the mortality rate is approximately 30%(4). In our experience of 700 consecutive renal transplant, the two patients who contracted the disease both died of complications.

This case presentation was unique for the following reasons: it combines a cutaneous and visceral form of the disease; the Leishmaniasis braziliensis is not generally recognized as a cause of visceral lesions (liver, spleen, bone marrow, eyes); an ocular manifestation is not previously mentioned in the literature let alone the presence of leishmanias in the aqueous humour and the vitreous body; Furthermore, the “in situ” treatment with amphotericin B, is to our knowledge a unique therapy.

It is known that the optimal action of the antimonials depends upon an intact immune system, as these compounds do not work well in immunossupressed patients, owing to their low efficacy and the high frequency of recurrences in leishmaniasis. Among the various alternatives to the use of antimonials, liposomial amphotericin has shown to yeld promising results, due to better long-term results, and low toxicity(5). This is particularly important when amphotericin B must be used with CyA, one of the immunossupressive mainstays of organ transplantation.

In conclusion, leishmaniasis is a rare but serious infectious complication in renal transplant patients L.braziliensis can also cause the visceral form of the disease, which can be treated by amphotericin B, either by sistemic (IV) or by local administration.

REFERENCES
(1) White Jr., A.C. In: Textbook of Internal Medicine. 3rd ed., Kelly W.N. (ed.).
Lippincott, Raven, 1997, ch. 324.

(2) Pearson, R.D.; Souza A.Q. In: Cecil Textbook of Medicine, 20th ed., Benne
Plum (ed.). Saunders, 1996, ch. 377.

(3) Orefice J.L.; Orefice, F.; Lasmar, E.P.; Gontijo, C.M.F. Rev. Bras.Oftalmol.
58(1): 65, 1999.

(4) Berenguer, J.; Gomez-Compdera, F.; Padilha, B. et al. Transplantation. 65 (10):
1401, 1998.

(5) Bobetis, J.N.; Petanis, A.; Stathakis,C.; Helioti, H.; Koskakis, A.; Giamarellom, H.
Clinical Infectious Diseases. 28: 1308,1999.

Em Formato Antigo