Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three kinds of anticoagulant therapy for obstetrical DIC were studied. 1. Antithrombin-III (AT) or gabexate mesilate for acute DIC, mainly for abruptio placentae. 2. Heparin or heparin-AT combination therapy for toxemia pregnancy. 3. Low molecular weight heparin (LMWH) for fetus of intrauterine growth retardation (IUGR). The results obtained were as follows, 1. a) Platelet count, and fibrinogen were significantly increased in AT therapy group compared with gabexate mesilate group. b) In clinical manifestation, renal failure and hemorrhagic diathesis were improved especially in AT group. 2. In heparin-AT group, high systolic blood pressure was improved during administration of AT, the high level of thrombin antithrombin complex was also found in these period. 3. a) The improvement of the gain of estimated fetal body weight was found after administration of LMWH. b) Redistribution of blood flow in one case of severe IUGR was observed during administration of LMWH.
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PMID:[Anticoagulant therapy in obstetrical disorders]. 217 Jul 3

A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.
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PMID:[Antiplasmin drugs and factor XIII concentrates in the treatment of a patient with acute promyelocytic leukemia (M3)]. 281 Jul 83

Disseminated intravascular coagulation (DIC) has been described as an occasional complication of abdominal aortic aneurysm. This is usually a perioperative coagulopathy, which may progress into a hemorrhagic diathesis. Rarely, DIC is present preoperatively as a result of the aneurysm itself. In the presence of additional pathophysiologic factors, a "compensated state" of secondary fibrinolysis may deteriorate into a clinically manifest coagulopathy. Heparin can be a useful adjunct in preoperative management of DIC, but definitive treatment requires surgical repair of the aneurysm. Long-term follow-up is essential to ensure that DIC is due to the aneurysm and that other disease processes are not overlooked. We report a case of DIC caused by an abdominal aortic aneurysm, with resolution after surgical treatment.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 373 72

Heparin-dependent intravascular coagulation is a widely recognized syndrome in which heparin acts as a hapten for an antiplatelet antibody and causes accelerated intravascular thrombosis and thrombocytopenia that may culminate in organ loss, hemorrhagic diathesis, and even death. Diagnosis is made in vitro by observing heparin-stimulated aggregation of normal platelets suspended in the patient's platelet-poor plasma. Treatment consists of cessation of heparin and use of antiaggregating agents with or without warfarin sodium. Management of patients with prior heparin-dependent intravascular coagulation who require cardiopulmonary bypass has not been reported. We now have successfully managed three such patients and herein present guidelines for management. Each patient was undergoing heparin therapy and manifested hallmark heparin tachyphylaxis, thrombocytopenia, and increased thrombotic symptoms (further venous thrombosis after cardiac catheterization in two cases and exacerbation of unstable angina in the other). In vitro aggregation studies were abnormal. Heparin was stopped, and antiaggregative therapy was begun with good response in each instance. In vitro studies were done serially until the antiplatelet antibody reaction had vanished (usually 4 to 8 weeks), and coronary revascularization was then conducted with full heparinization. Further heparin exposure postoperatively was avoided. There was no perioperative evidence of intravascular thrombosis or bleeding diathesis, and in vitro heparin-dependent aggregation did not recur. We conclude that patients with previously documented heparin-dependent intravascular coagulation can safely sustain the massive heparin rechallenge of cardiopulmonary bypass, provided that in vitro aggregation has ceased and rechallenge therapy is not prolonged.
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PMID:Cardiopulmonary bypass for patients with previously documented heparin-induced platelet aggregation. 671 46

Post-operative venous thrombosis, blood loss and pre- and post-operative plasma heparin concentrations were studied in a prospective double blind trial with low-dose heparin therapy in 59 patients undergoing transvesical prostatectomy. Thrombosis rate, diagnosed with the 125I-fibrinogen method, was significantly reduced in the first 5 post-operative days, i.e. during but not after the period of heparin therapy. One patient who developed major thrombosis in spite of heparin prophylaxis is presented. Heparin therapy did not increase average blood loss, but was suspected to be the cause of severe bleeding in 1 patient, who may have had a latent hemorrhagic diathesis. Plasma heparin levels were significantly raised during heparin therapy, and were significantly lower in both heparin and placebo treated patients on days when thromboses started.
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PMID:The effects of low-dose heparin treatment on patients undergoing transvesical prostatectomy. 725 29

The history of the antithrombotic agents--aspirin, heparin, warfarin, and the thrombolytics--is a rich and lively odyssey of serendipity, perseverance, vision, and conflict involving a number of striking personalities. The history of aspirin spans ages and continents from Hippocrates' analgesic for women in labor to the rediscovery of the white willow bark by English country scholar Reverend Edward Stone. Bayer chemist Felix Hoffmann reinvented aspirin for his ailing father; suburban physician L.L. Craven pioneered the prophylactic antithrombotic uses of aspirin; and Sir John Vane elucidated aspirin's mechanism of action as the inhibition of prostaglandin synthetase. Heparin was discovered by McLean, working as a medical student in 1915 in search of a pure procoagulant in dog liver. His original impure material differed somewhat from today's heparin, but purified heparin was rapidly accepted for a myriad of clinical uses; to this day, diverse new properties of this complex glycosaminoglycan continue to be elucidated. The oral anticoagulants emerged from veterinary research in the 1920s on a hemorrhagic disorder afflicting cattle that consumed spoiled sweet clover hay. Several chance encounters led Karl Link and his University of Wisconsin team to the identification of dicumarol as the offending agent in 1939 and its widespread therapeutic use by Wright and others in the 1940s. Link later developed warfarin as a rodenticide, but its use in humans soon followed in the 1950s. Vitamin K was discovered in the 1930s; its involvement in the mechanism of the anticoagulant agents was not delineated until the 1970s. The intrinsic ability of clotted blood to liquify and the fibrinolytic properties of normal urine were noted in the 1800s. Tillett and Sherry's group stumbled on the fibrinolytic properties of streptokinase in the 1930s and pioneered the therapeutic use of streptokinase in the 1940s and of urokinase in the 1960s. Several teams found tissue-type plasminogen activator in various body sites beginning in the 1940s, leading to its cloning and widespread use in the 1980s; anisoylated plasminogen-streptokinase activator complex is an example of rational drug design. The discoverers of these diverse agents have not only provided physicians with a potent armamentarium of antithrombotic drugs but also helped elucidate much basic science and vividly demonstrated the merits of perseverance, independent thought, and adherance to the scientific method.
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PMID:History of drugs for thrombotic disease. Discovery, development, and directions for the future. 828 78

Three-hundred fifty-one women were referred for thrombosis and hemostasis evaluation after suffering recurrent miscarriages. All patients were referred by a high-risk obstetrician or reproductive medicine specialist after anatomic, hormonal or chromosomal defects had been ruled out. These patients were assessed over a three year period. The mean patient age at referral was 34 years and the mean number of miscarriages was 2.9 (2-9). All patients underwent a thorough evaluation for thrombophilia and, when indicated, a hemorrhagic disorder. Of the 351 patients, 29 (8%) had no defect. Of the remaining 322 patients, 7 (2%) had a bleeding disorder: 3 with platelet dysfunction, 1 with Factor XIII deficiency, 3 with von Willebrand's and 3 with Osler-Weber-Rendu. The remainder of the patients had a thrombophilia as follows: 195 (60%) had antiphospholipid syndrome, 64 (20%) had Sticky Platelet Syndrome, 38 (12%) had MTHFR mutation, 23 (7.1%) had PAI-1 polymorphism, 12 (3.7%) had Protein S deficiency, 12 (3.7%) had Factor V Leiden, 3 (1%), had AT deficiency, 3 (1%) had Heparin-Cofactor II deficiency, 3 (1%) had TPA deficiency, and 6 (2%) had Protein C deficiency. There were a total of 364 defects found in the 312 patients harboring thrombophilia; thus, several harbored two and a few harbored three separate defects. All patients with thrombophilia were treated with preconception ASA at 81 mg/day with the immediate post-conception addition of heparin or LMW heparin (Dalteparin). Both ASA and heparin/LMW heparin were used to term. The first 120 patients were treated with unfractionated heparin at 5,000 U every 24 hours, subcutaneously and the last 192 have been treated with Dalteparin at 5,000 U/day subcutaneously. The patients with MTHFR were also treated with folate at 5 mg/day + pyridoxine at 50 mg/day. All patients were carefully monitored with CBC and platelet counts, anti-Xa levels, frequent ultrasounds and physical exams. Only 2 of the thrombophilia patients suffered another miscarriage; all others had a normal term delivery. There were no pregnancy-related thromboses, no delivery complications and no episodes of post-partum thrombosis. The only bleeding consisted of 1-4 cm bruises at injection sites. No episodes of thrombocytopenia (HIT) were noted. In our experience, thrombophilia is a common cause of recurrent miscarriage and all patients with no anatomical, hormonal or chromosomal defect should be evaluated for thrombophilia or a bleeding disorder. The success rate of normal term delivery in these 312 patients was 94% using ASA + heparin or Dalteparin. In addition, side effects of therapy were minimal.
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PMID:Recurrent miscarriage syndrome and infertility due to blood coagulation protein/platelet defects: a review and update. 1567 68