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Am. J. Trop. Med. Hyg., 81(2), 2009, pp. 209-212
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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CASE REPORT


AA-Amyloidosis Caused by Visceral Leishmaniasis in a Human Immunodeficiency Virus-Infected Patient

Serge de Vallière, Charles Mary, Jeanna E. Joneberg, Samuel Rotman, Roberto Bullani, Gilbert Greub, Julian D. Gillmore, Pierre A. Buffet, AND Philip E. Tarr*
Infectious Diseases Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland; Laboratoire de Parasitologie, Hôpital de la Timone, Marseille, France; Department of Pathology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland; Nephrology Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland; Parasitology Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland; National Amyloidosis Center, Royal Free and University College Medical School, London; Service des Maladies Infectieuses, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France; Infectious Diseases Service, Kantonsspital Bruderholz, University of Basel, Switzerland

 

ABSTRACT

AA-amyloidosis in the setting of chronic visceral leishmaniasis (VL) has been reported in animal models but documentation in humans is unavailable. Here, we report on a Portuguese man who in 1996 was diagnosed with both human immunodeficiency virus (HIV)-infection and VL. Antiretroviral treatment led to sustained suppression of HIV viremia but CD4+ lymphocytes rose from 8 to only 160 cells/mL. Several courses of antimony treatment did not prevent VL relapses. Renal failure developed in 2006 and renal biopsy revealed AA-amyloidosis. The patient had cryoglobulinemia and serum immune complexes containing antibodies directed against seven leishmanial antigens. Antimony plus amphotericin B, followed by oral miltefosine resulted in a sustained VL treatment response with elimination of circulating Leishmania infantum DNA and CD4+ recovery. The concomitant reduction of serum AA levels and disappearance of circulating leishmanial immune complexes suggests that prolonged VL may lead to AA-amyloidosis in immunocompromised humans.

Received December 1, 2008. Accepted for publication April 22, 2009.

Acknowledgment: The authors are grateful to Dr. Thomas C. Jones for critical review of the manuscript.

* Address correspondence to Philip E. Tarr, Infectious Diseases Service, Kantonsspital Bruderholz, University of Basel, 4101 Bruderholz, Switzerland. E-mail: philip.tarr{at}unibas.ch

Authors’ addresses: Serge De Vallière and Jeanna Joneberg, Infectious Diseases Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, 1011 Lausanne, Switzerland, Tel: 41-21-314-4852. Charles Mary, Laboratoire de Parasitologie, Hôpital de la Timone, 13385 Marseille Cedex 5, France, Tel: 33-4-91-38-60-90. Samuel Rotman, Department of Pathology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, 1011 Lausanne, Switzerland, Tel: 41-21-314-7148. Roberto Bullani, Nephrology Service, BU 17, Centre Hospitalier Universitaire Vaudois and University of Lausanne, 1011 Lausanne, Switzerland, Tel: 41-21-314-4850. Gilbert Greub, Parasitology Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland, Tel: 41-21-314-4979. Julian D. Gillmore, National Amyloidosis Center, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, Tel: 44-20-74-33-27-26. Pierre A. Buffet, Service des Maladies Infectieuses, Hôpital Pitié-Salpêtrière, 47 Boulevard de l’Hôpital, 75651 Paris Cedex 13, France, Tel: 33-1-42-16-01-31. Philip E. Tarr, Infectious Diseases Service, Kantonsspital Bruderholz 1-07, 4101 Bruderholz, Switzerland, Tel: 41-61-436 2212, Fax: 41-61-436 3670, E-mail: philip.tarr{at}unibas.ch.

Reprint requests: Philip E. Tarr, Infectious Diseases Service, Kantonsspital Bruderholz, University of Basel, 4101 Bruderholz, Switzerland, Tel: 41-61-436 2212, Fax: 41-61-436 3670, E-mail: philip. tarr{at}unibas.ch.






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