中文摘要 |
目的:出血時間延長發生於全身性紅斑性狼瘡的原因很多,包括血小板數目降低、存在自體抗體、肝腎功能不全、或使用特殊藥物等,本實驗研究及分析全身性紅斑性狼瘡病人出血時間延長的相關影響因子。方法:我們回溯性地查閱在2004年1月至2007年9月當中於台北榮總253位曾接受出血時間測試的全身性紅斑性狼瘡的病例,我們進一步分析相關臨床資料,包括年齡、性別、用藥、實驗室檢查等。結果:共37位全身性紅斑性狼瘡病人有出血時間延長,216位出血時間正常。有顯著差異的因子包含血色素值(10.9 ± 2.2 vs. 12.2 ± 1.7 g/dL, p<0.005);血小板數目(178,200 ± 14,200 vs. 238,900 ± 5,200/cumm, p<0.005);INR及APTT時間延長的頻率;抗凝脂抗體的存在(43.2% vs.18.1%, p<0.005);血中肌酸酐上升(29.7% vs. 11.6%, p<0.001);及是否有尿蛋白(56.8% vs. 32.9%,p=0.005)。共有51位病人接受腎臟切片檢查,除了一位病人的腎切片為糖尿病腎病變及2位局部性腎絲球硬化症外,全都顯示有狼瘡性腎炎。出血時間延長的紅斑性狼瘡病人所使用的藥物,除了較高比例的脈衝類固醇使用(8% vs. 2%, p=0.032)及抗結核藥物(2% vs. 0%)外,其餘藥物於兩組並無顯著差異。結論:全身性紅斑性狼瘡患者合併出血時間延長是一複雜的情況,應注意病人是否有貧血、血小板數目低下、腎功能不全、抗磷脂抗體的存在。而進一步的檢查包括血小板功能測定及各式自體抗體也是未來研究的重點。 |
英文摘要 |
Objective: The prolongation of bleeding time (BT) in systemic lupus erythematosus (SLE) may be due to a variety of factors, including thrombocytopenia, the existence of autoantibodies, renal or hepatic dysfunction, or usage of special medications. In this study, we investigated and analyzed the possible causes of prolonged BT in SLE patients. Methods: We retrospectively reviewed medical records of 253 SLE patients who had received BT tests from January 2004 to September 2007. We collected data on the clinical characteristics, current medications, and laboratory data. Results: Thirty-seven SLE patients had prolonged BT and 216 patients were normal. There were significant differences in both groups in terms of serum level of hemoglobin (10.9 ± 2.2 vs. 12.2 ± 1.7 g/dL, p<0.005); platelet count (178,200 ± 14,200 vs. 238,900 ± 5,200/cumm, p<0.005); the frequency of INR prolongation (10.8% vs. 1%, p<0.001); APTT prolongation (16.2% vs. 4.6%, p<0.012); frequencies of serum antiphospholipid antibodies (43.2% vs. 18.1%, p<0.005); increasing serum level of Cr (29.7% vs. 11.6%, p<0.001); and overt proteinuria (56.8% vs. 32.9%, p=0.005). Fifty-one patients underwent renal biopsy with predominant lupus nephritis, especially ISN/RPS class IV and V. Significance in the usage of medications in the prolonged BT and normal groups was noted, with methylprednisolone pulse therapy and anti-TB agents: 8% vs. 2%, and 2% vs. 0 (p=0.032 for pulse therapy, and p=0.001 for anti-TB agents). The usage of other medications was not significant. Conclusion: BT prolongation in SLE is a complex clinical problem. In this study, we found that many factors are associated with BT abnormality, including anemia, thrombocytopenia, renal dysfunction and the presentation of antiphospholipid autoantibody. A further cohort study of platelet function and the existence of other autoantibodies should be performed in SLE patients with prolonged BT. |