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Thrombocytopenia as the presenting manifestation of human T-lymphotropic virus type III infection in infants
Authors:F T Saulsbury  R J Boyle  R F Wykoff  T H Howard
Institution:1. Department of Neurology, Emory University School of Medicine, 6300 Woodruff Memorial Research Building, 101 Woodruff Circle, Emory University, Atlanta, GA 30322, USA;2. Department of Human Genetics, Emory University School of Medicine, 6300 Woodruff Memorial Research Building, 101 Woodruff Circle, Emory University, Atlanta, GA 30322, USA;3. Department of Pediatrics, Emory University School of Medicine, 6300 Woodruff Memorial Research Building, 101 Woodruff Circle, Emory University, Atlanta, GA 30322, USA;1. Trauma Unit, Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands;2. Department of Surgery, Maasstad Hospital, Rotterdam, The Netherlands;3. Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands;4. Consumer and Safety, Amsterdam, The Netherlands;1. Amsterdam School of Communication Research (ASCoR), University of Amsterdam, Postbus 15791, 1001 NG, Amsterdam, The Netherlands;2. Research Foundation Flanders (FWO-Vlaanderen) Associated with School for Mass Communication Research, KU Leuven, Parkstraat 42, 3000, Leuven, Belgium;3. MIOS (Media, ICT, and Interpersonal Relations in Organizations and Society), University of Antwerp, Sint-Jacobsstraat 2, 2000, Antwerp, Belgium;1. Institute of Clinical Medicine, University of Oslo, Norway;2. Health Services Research Unit, Akershus University Hospital, Norway;3. Department of Pulmonary Medicine, Medical Division, Akershus University Hospital, Norway;4. Section for Orthopaedic Emergency, Orthopaedic Department, Oslo University Hospital, Norway;5. Department of Vascular Surgery, Oslo University Hospital, Aker, Norway;6. Department of Orthopaedics, Østfold Hospital, Norway;7. Department of Orthopaedics, Akershus University Hospital, Norway;8. Department of Medicine, Østfold Hospital, Norway
Abstract:Three infants between 8 and 9 months of age developed thrombocytopenia resulting from immune-mediated platelet destruction, as evidenced by the presence of serum antibody to platelets and elevated platelet-associated immunoglobulin G in two patients, and abundant bone marrow megakaryocytes in all patients. The patients had a satisfactory response to corticosteroid therapy, and platelet counts have remained normal during observation after therapy. All patients had serum antibody to human T-lymphotropic virus type III, and HTLV-III was isolated from the peripheral blood lymphocytes in two patients. The HTLV-III infections were presumably acquired via blood transfusions in the neonatal period; none of the patients' mothers belonged to a risk group for HTLV-III infection, and all were HTLV-III seronegative. Although thrombocytopenia was the major clinical manifestation, the patients had a number of immunologic abnormalities characteristic of HTLV-III infection; these included hyperimmunoglobulinemia, a decreased proportion of peripheral blood T cells, and a marked reduction in the proportion of peripheral blood T helper-inducer lymphocytes. We conclude that the patients had immune-mediated thrombocytopenia caused by HTLV-III infection.
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