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Treatment of Severe Thrombocytopenia with Intravenous Immunoglobulins and Corticosteroids in a Patient Receiving Continuous Ambulatory Peritoneal Dialysis
Author(s) -
Hitoshi Sugiyama,
Minoru Satoh,
Masahiro Odawara,
Haruo Ichikawa,
Keisuke Maruyama,
Masami Hashimoto,
Mitsuhiro Matsuda,
Yoshio Nagake,
Naoki Kashihara,
Hirofumi Makino
Publication year - 1997
Publication title -
nephron
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 1423-0186
pISSN - 0028-2766
DOI - 10.1159/000190310
Subject(s) - medicine , continuous ambulatory peritoneal dialysis , intravenous immunoglobulins , ambulatory , peritoneal dialysis , dialysis , hemodialysis , antibody , intensive care medicine , surgery , immunology
Hitoshi Sugiyama, MD, Department of Medicine III, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700 (Japan), Tel. +81 86 223 7151 (ext 7235), fax +81 86 222 5214, E-Mail sugiym-h@po.harenet.or.jp Dear Sir, While bleeding tendency and platelet dysfunction are known in uremic patients, severe thrombocytopenia is rarely encountered. We describe a uremic patient with acute severe thrombocytopenia who was undergoing continuous ambulatory peritoneal dialysis (CAPD). The patient was successfully treated with intravenous immunoglobulins and corticosteroids. Peritoneal dialysis was maintained during treatment for thrombocytopenia. A 57-year-old Japanese man, who was receiving CAPD, was referred to our department because of acute severe thrombocytopenia. CAPD was initiated 5 years earlier after uremia due to chronic glomerulone-phritis had been diagnosed. His platelet count ranged from 150 to 280 × 109/1 during this 5-year period, but fell to 100 × 109/1 six days before admission and continued to decrease (to 3 × 109/1 on admission) (fig. 1). He had hemorrhagic vesicles in the oral mu-cosa, gingival bleeding, and ecchymoses on both legs. He was also hoarse due to bleeding of the vocal cords. Megakaryocytes in bone marrow were plentiful and increased in size. The level of platelet-associated IgG (PAIgG) was increased (68.2 ng/l07 cells). There were no symptoms or laboratory findings to suggest the presence of autoimmune disease. We made a presumptive diagnosis of thrombocytopenia caused by immunologic platelet destruction. High-dose steroid therapy was considered inappropriate because of the risk of significant side effects, especially since the patient had developed bacterial

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