A total of 777 patients with thrombocytosis, defined as a platelet count of greater than 500 x 10(9)l-1, seen in a University hospital over a 1-year period, were studied prospectively for aetiology. The most frequent causes of thrombocytosis were infection (21.9%), rebound thrombocytosis (19.4%), tissue damage (17.9%), chronic inflammatory disorders (13.1%) and malignancy (5.9%). Thrombocytosis associated with multiple causative factors, occurring simultaneously, was seen in 6.1% of cases. Thrombocytosis of greater than or equal to 1 million x 10(9)l-1 was found most frequently in patients with multiple aetiological factors occurring at the same time, in myeloproliferative disorders, or in postsplenectomy patients.

No abstract

No abstract

Background and Aims:Blood donation from glucose-6-phosphate dehydrogenase (G6PD)-deficient and sickle cell trait (SCT) donors might alter the quality of the donated blood during processing, storage or in the recipient's circulatory system. The aim of this study was to determine the prevalence of G6PD deficiency and SCT among blood donors coming to King Khalid University Hospital (KKUH) in Riyadh. It was also reviewed the benefits and risks of transfusing blood from these blood donors.Materials and Methods:This cross-sectional study was conducted on 1150 blood samples obtained from blood donors that presented to KKUH blood bank during the period April 2006 to May 2006. All samples were tested for Hb-S by solubility test, alkaline gel electrophoresis; and for G6PD deficiency, by fluorescent spot test.Results:Out of the 1150 donors, 23 (2%) were diagnosed for SCT, 9 (0.78%) for G6PD deficiency and 4 (0.35%) for both conditions. Our prevalence of SCT and G6PD deficiency is higher than that of the general population of Riyadh.Conclusion:We recommend to screen all units for G6PD deficiency and sickle cell trait and to defer donations from donors with either of these conditions, unless if needed for special blood group compatibility, platelet apheresis or if these are likely to affect the blood bank inventory. If such blood is to be used, special precautions need to be undertaken to avoid complications in high-risk recipients.

The trigger of the coagulopathy that complicates heat stroke is obscure, but direct platelet activation by heat is a possibility we set out to study. Platelet rich plasma (PRP), prepared from blood donors, was incubated at increasing temperatures (38-45 degrees C) and then platelet aggregation was undertaken in response to decreasing low doses of ADP (less than 2.0 mumol/l). Hyperaggregability was manifested when the incubation temperature reached 43 degrees C and was maximum at 44 degrees C before complete inhibition of responses at 45 degrees C. The platelet hyperactivity induced by heating at 44 degrees C persisted after reincubating PRP samples at 37 degrees C. These platelet responses could not be triggered in PRP samples prepared from subjects after the overnight ingestion of aspirin or after the addition of aspirin to PRP before starting the heating procedure. However, aspirin was less effective when added to PRP after the appearance of the heat-induced hyperaggregability. In conclusion, these results indicate that platelets can be activated directly by heat. This mechanism which may be operational in heat stroke, is unaffected by cooling (body cooling being basic in the management of heat stroke) but can be prevented by the early administration of aspirin.