Produção Nacional
Revisado por pares
Dengue Shock Syndrome in a Liver Transplant Recipient
2006; Wolters Kluwer; Volume: 82; Issue: 6 Linguagem: Inglês
10.1097/01.tp.0000235151.60237.fe
ISSN1534-6080
AutoresJosé Huygens Parente Garcia, Tarciso Daniel Santos Rocha, Cyntia Ferreira Gomes Viana, Bronner P. Gonçalves, Evelyne Santana Girão, J.B.M. Vasconcelos, Gustavo Coelho, Dirk Schreen, Paulo Everton Garcia Costa, Ivelise Regina Canito Brasil,
Tópico(s)Malaria Research and Control
ResumoDengue fever is the world's most important viral hemorrhagic fever disease. It is a major cause of mortality and morbidity in tropical areas (1). Its clinical outcome ranges from asymptomatic cases through dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). We report the first case of DSS in a liver transplant recipient. A 66-year-old man had been the recipient of a cadaveric ABO compatible donor liver allograft. He was diagnosed with hepatitis C cirrhosis and classified Child Pugh B9. The postoperative immunosuppressive treatment consisted of prednisone and tacrolimus. Three weeks after transplant, he developed diarrhea associated with fever and abdominal pain. On the physical examination, he had jaundice. On the admission day, investigations revealed a platelet count of 103,000/mm3, a creatinine of 1.5 mg/dL, a hemoglobin of 13 g/dL (packed cell volume, 38.6), a serum aspartate aminotransferase of 931 U/L, and a serum alanine aminotransferase of 427 U/L. At admission, an abdominal ultrasonography (US) revealed ascites and hepatomegaly. Doppler US was normal. The patient's blood and urine culture were sterile. Antibiotic therapy with vancomycin, ganciclovir and cefepime was initiated. Twelve hours after admission, the patient became anuric. He deteriorated into a stage of profound shock. Dopamine was initiated. On the day after admission, the patient's platelet count, hemoglobin, serum aspartate aminotransferase, alanine aminotransferase, and prothrombin time (International Normalized Ratio) were 30,000/mm3, 14.2 g/dL (cell packed volume, 42.3), 14,096 U/L, 2,717 U/L and 2.4, respectively. The patient's general condition became worse. The patient died within two days of admission. Serology and polymerase chain reaction (PCR) for cytomegalovirus were negative. Serum quantitative PCR and liver tissue immunohistochemistry and PCR confirmed the dengue diagnosis of type 3 dengue virus. The patient had no documented previous history of dengue infection. He fulfilled the World Heath Organization criteria for grade IV DSS. Immune response plays an important role in the pathophysiology of DHF-DSS. Sequential infection with different dengue virus genotypes is related to the development of DHF-DSS. After the first infection, antidengue antibodies against the specific genotype responsible for this infection will be present in the patient's blood. These antibodies are not effective against others genotypes, but they are responsible for a robust immunologic responsiveness in a second infection. Activated T-cell and cytokine mediators initiate hemorrhagic manifestations and capillary leakage of plasma in DSS (2). Cytokines, mainly IL-6, IL-10, and macrophage migration factor (MIF) are believed to be involved in the pathogenesis of dengue infection and serve as a predictor of its outcome (3). Liver transplant recipients are immunosuppressed in order to avoid rejection. Their T-cell responsiveness is diminished, which may explain the lack of cases of DSS in transplanted patients. The case that we reported in an area that is endemic for dengue hemorrhagic fever is extremely important to alert physicians for its diagnosis. José H.P. Garcia Tarciso D.S. Rocha Cyntia F.G. Viana Bronner P.A. Gonçalves Evelyne S. Girão João B.M. Vasconcelos Gustavo R. Coelho Dirk Schreen Paulo E.G. Costa Ivelise R.C. Brasil Department of Surgery Federal University of Ceará Ceará, Brazil
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