The Incidence Of Prescribing Errors In An Eye Hospital

Background  

Relatively little is known about the incidence of prescribing errors and there has been no work on this in a single specialty ophthalmic hospital. Knowing where and when errors are most likely to occur is generally felt to be the first step in trying to prevent these errors. This study is an attempt in, the setting of an eye hospital, to try to identify and attribute these medication errors.     

抗高血压药物与罹患癌症的风险:324168例参与随机临床试验病人的荟萃分析和试验序贯分析

长期以来,一直存在抗高血压药物是否有致癌作用的争议.自从在年龄>50岁的妇女中使用萝芙碱提取物造成乳腺癌发病率增加的报道后[1],这一争议已持续了30年.Sipahi和同事们最近的研究显示:血管紧张素受体拮抗剂(angiotensin receptor-blockers,ARB)有较高的致癌风险.这一发现再次引发了抗...     

Red cell alloimmunization in multitransfused HLA-typed patients

The authors studied retrospectively the formation of clinically significant red cell (RBC) alloantibodies in 958 HLA-typed, multiply transfused patients receiving kidney (603 patients) or liver (263 patients) transplants or plateletpheresis transfusions (92 patients). RBC alloantibodies were found in 91 (9.5%) of these patients and multiple antibodies in 35 (3.7%). Rh (D, C, c, and E) antibodies accounted for 49 percent of the total and Kell antibodies for 31 percent. Antibodies were found in 15 percent of apheresis recipients and in 8.6 percent of renal and 9.5 percent of liver transplantation patients. No association was found between any HLA-A, HLA-B, or HLA-DR phenotype and the presence of RBC alloantibodies, either in general or when analyzed according to the specific antibody. Renal transplant patients with RBC alloantibodies were somewhat more broadly HLA-alloimmunized than were those without RBC alloantibodies. Patient gender did not affect these results. The authors concluded that the immune response to RBC alloantigens is independent of HLA type but is associated with an increased level of HLA antibody formation.     

Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function

Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report). A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC- gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC- delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function.     

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