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.
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.