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題名 | Effect of Intravenous Immunoglobulin on Cyclosporine-Associated Hemolytic-Uremic Syndrome in a Renal Transplant Recipient=靜脈注射免疫球蛋白用於治療腎臟移植病人發生Cyclosporine相關的溶血尿毒症候群的效果 |
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作者 | 文耀閣; 顏旭亨; 楊郁; 張家築; 陳美玲; | 書刊名 | 臺灣腎臟醫學會雜誌 |
卷期 | 18:2 2004.05[民93.05] |
頁次 | 頁75-79+94 |
分類號 | 415.816 |
關鍵詞 | 溶血尿毒症候群; 腎毒性; 靜脈注射免疫球蛋白; Cyclosporine; Hemolytic uremic syndrome; Nephrotoxicity; Intravenous immunoglobulin; |
語文 | 英文(English) |
中文摘要 | 溶血尿毒症候群是一個眾所皆知發生在器官移植後接受calcineurin inhibitors cyclosporine或tacrolimus治療患者的併發症。溶血尿毒症候群是一種嚴重的情況,具有破壞性的病程,其臨床表徵包含三個主要特色:微小血管病變性溶血,血小板減少症,以及急性腎衰竭。我們在此報告一位接受屍腎移植的三十歲女性病人於移植後早期階段發生cyclosporine相關的溶血尿毒症候群。此病人於移植手術後第八天,尿量減少,血清creatinine值由1.2mg/dL上升至2.2mg/dL,血紅素和血小板數分別由8.1g/dL和149,000/mm^3,下降至6.1g/dL和23,000/mm^3,reticulocyte數為10%,血清haptoglobin值明顯下降以及lactate dehydrogenase值上升至2,326U/L;此外,血液抹片可發現schistocytes。腎臟切片呈現典型的栓塞性微小血管病變以及急性cyclosporine腎毒性。我們立即停止Cyclosporine,而轉換成tacrolimus使用,並且實施每日血漿置換治療。不幸地,第三次的血漿置換術因雙腔導管發生嚴重出血的併發症而無法繼續進行,主要歸因於溶血尿毒症候群併發的嚴重血小板減少症。因此,我們改採用靜脈注射免疫球蛋白作為替代性治療,其血液學的病變快速緩解,腎功能隨後也順利地恢復。我們結論tacrolimus轉換合併給予靜脈注射免疫球蛋白似乎是一種安全而且有效的治療選擇用於處理cyclosporine引起之溶血尿毒症候群。 |
英文摘要 | Hemolytic-uremic syndrome (HUS) is a well-documented complication of solid organ and bone marrow transplant recipients treated with calcineurin inhibitors cyclosporine or tacrolimus. The syndrome is a serious condition with a devastating process characterized clinically by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. We report herein on a 30-year-old female cadaveric renal transplant recipient who developed cyclosporine-induced hemolytic-uremic syndrome (HUS) in the early post-transplant period. On post-operative day 8, urine output decreased and serum creatinine increased from 1.2mg/dL to 2.2mg/dL. Hemoglobin and platelet count fell from 8.1g/dL and 149,000/mm3 to 6.1g/dL and 23,000/mm3 respectively. Reticulocyte count was 10%. The patient's serum haptoglobin level fell to an undetectable range and her lactate dehydrogenase level rose to 2,326U/L. Furthermore, schistocytes were detected in the peripheral smear. Renal allograft biopsy specimens showed the characteristic features of thrombotic microangiopathy and acute cyclosporine nephrotoxicity. Cyclosporine was discontinued and the patient was switched to tacrolimus in conjunction with daily plasma exchange. Unfortunately, the third session of plasma exchange could not be performed because of double-lumen catheter-associated bleeding complication, which was mainly attributed to severe thrombocytopenia. Therefore, intravenous immunoglobulin (IVIG) was administrated as an alternative therapy. Hematological resolution occurred promptly and renal function recovered uneventfully. We conclude that tacrolimus conversion with concomitant administration of IVIG seems to be a safe and effective therapeutic option in the management of cyclosporine-associated HUS in renal transplantation. |
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