Zeigler Z R, Megaludis A, Fraley D S
Department of Medicine, Montefiore University Hospital, University of Pittsburgh School of Medicine, Pennsylvania.
Am J Hematol. 1992 Feb;39(2):90-5. doi: 10.1002/ajh.2830390204.
Bleeding times, von Willebrand activities, and platelet retentions were examined before and following d-DAVP in 13 uremic patients. Shortening of the bleeding time from 16.6 +/- 2.2 (SEM) to 6.8 +/- 0.7 min was seen in six patients. However, bleeding times remained greater than or equal to 20 min in the remaining seven individuals. The only baseline parameter that correlated with response to d-DAVP was the amount of blood loss (mg/min) during the bleeding time test. Responders had normal blood loss values averaging 6.2 +/- 1.5 mg/min. By contrast, these values were elevated in 6/7 of the non-responders and averaged 28.4 +/- 5.9 mg/min (P = 0.01). Von Willebrand activities increased following d-DAVP in the responders but not in the non-responders. Platelet retention was uniformly low in all patients and improved from 21.0 +/- 7.0% to 75.0 +/- 7.9% (P = less than 0.001) following d-DAVP in responders but not non-responders. To further define the retention abnormality in uremia, the two-stage platelet retention assay was performed prior to d-DAVP. Most of the patients (9/12) had both first- and second-phase abnormalities. Therefore, the retention defect in uremia appears to be more complex than that seen in von Willebrand's disease (2nd phase abnormality only). Nevertheless, d-DAVP seems to improve platelet rheology in uremic individuals whose von Willebrand activities increase with d-DAVP.
对13例尿毒症患者在使用去氨加压素(d-DAVP)前后进行了出血时间、血管性血友病因子活性及血小板滞留率的检测。6例患者的出血时间从16.6±2.2(标准误)分钟缩短至6.8±0.7分钟。然而,其余7例患者的出血时间仍大于或等于20分钟。唯一与对d-DAVP反应相关的基线参数是出血时间测试期间的失血量(毫克/分钟)。有反应者的失血量正常,平均为6.2±1.5毫克/分钟。相比之下,6/7的无反应者的这些值升高,平均为28.4±5.9毫克/分钟(P = 0.01)。有反应者在使用d-DAVP后血管性血友病因子活性增加,而无反应者则未增加。所有患者的血小板滞留率均一直较低,有反应者在使用d-DAVP后从21.0±7.0%提高到75.0±7.9%(P<0.001),无反应者则未改善。为进一步明确尿毒症患者的滞留异常情况,在使用d-DAVP前进行了两阶段血小板滞留试验。大多数患者(9/12)第一阶段和第二阶段均有异常。因此,尿毒症患者的滞留缺陷似乎比血管性血友病(仅第二阶段异常)更为复杂。尽管如此,d-DAVP似乎能改善那些血管性血友病因子活性随d-DAVP增加的尿毒症患者的血小板流变学。