A 71-yr-old male was seen because of the development of severe bleeding diathesis secondary to an acquired factor V inhibitor. The lack of clinical and laboratory response to fresh frozen plasma prompted us to treat him with platelet transfusions during 4 separate bleeding episodes; on each occasion he received 1 0-1 5 U of homologous platelet concentrates. There was a remarkable clinical response associated with a marked correction of the prolonged prothrombin time. prolonged partial thromboplastin time. and prolonged Russell viper venom time; this correlated with higher factor V levels and complete neutralization of the inhibitor. The beneficial effect of platelet transfusion lasted 5-6 days. The inhibitor was of low titer. and it was precipitated by staphylococcal protein A. The in vivo response to platelet transfusion correlated with subsequently performed in vitro experiments. Nonwashed control platelet pellets mixed with inhibitor plasma partially corrected the prolonged PTT. whereas washed platelets or albumin density gradient separated
A family with a high incidence of spontaneous thromboembolism over four generations has been investigated. The propositus is a 21-yr-old male with a history of thrombophlebitis. Medical histories of 46 family members were obtained. Twelve of these individuals have experienced deep venous thromboses and/or pulmonary emboli. Seven members of the kindred, with a prior history of thrombotic phenomena, were investigated in detail. These subjects were found to have normal plasma concentrations of immunoreactive antithrombin (mean 96%), decreased plasma levels of progressive antithrombin activity (mean 50%), and greatly reduced amounts of plasma heparin cofactor activity (mean 42%). The abnormal antithrombin (“Chicago”) was found to elute from heparin- Sepharose at a higher ionic strength than normal inhibitor. The functionally defective antithrombin molecules exhibit a reduced ability to neutralize thrombin in the presence or absence of heparin (approximately 10%-20% of normal). The molecular defect of this protease inhibitor thus appears to be distinct from those of previously described abnormal antithrombins.
There has been significant decrease in maternal morbidity and mortality of sickle cell disease patients during pregnancy due to better understanding of the pathophysiology of the disease and physiologic changes during pregnancy.Prophylactic blood transfusion does not appear to reduce complications in patients with sickle cell anemia. Patients with sickle hemoglobin C disease and with Sp thalassemia' have fewer complications but still need close monitoring.Blood transfusion therapy should be made available for medical and obstetrical complications to include increasing hypoxemia, progressive anemia, acut chest syndrome, twin pregnancy, splenic sequestration syndrome, preeclampsia, septicemia, or prior to general anesthesia and surgery. Blood transfusion therapy is associated with hepatitis, allergic reaction, alloimmunization, AIDS, and iron overload states. These aspects should be considered prior to using blood transfusion therapy.Excellent prenatal monitoring and aggressive intervention should be instituted when problems arise for the successful management of the pregnant patient with sickle cell disease. Prenatal diagnosis and cord blood screening should be made available for the infant. Appropriate pediatric referral and prophylactic penicillin is recommended for the infant with sickle cell disease.
1. Mating greatly increases the oviposition rate of female Cecropia silkmoths. 2. Implantation of the spermatheca from a mated female (either with or without sperm) into a virgin female did not alter the typical virgin oviposition pattern. 3. After implantation of the bursa copulatrix (minus the spermatophore) from a mated female, the virgin female oviposited eggs in the typical mated pattern. 4. Similar implantations of bursae from virgin females or from females which had mated with castrate males did not alter the virgin oviposition pattern. 5. Injections of hemolymph from mated females into virgin females caused an increase in oviposition rate. Blood from virgin females had no effect on oviposition. 6. Thus, the change in oviposition upon mating is due to a blood-borne factor which is secreted by the bursa copulatrix after contact with sperm or other substance from the testis. This bursa factor most probably acts to trigger the release of the oviposition-stimulating hormone from the intrinsic cells of the corpora cardiaca.
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