Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the risk of intracranial hemorrhage in patients with malignant gliomas who are treated with anticoagulant drugs for late postoperative venous thromboembolism, the authors retrospectively reviewed the computerized data base of all patients with primary brain tumors seen at the University of California, San Francisco, over a 9-year period. Of 915 patients 18 years of age or older who had a pathological diagnosis of malignant glioma and an initial Karnofsky performance scale score of 60% or higher, 36 (4%) developed venous thromboembolism 6 to 246 weeks postoperatively and 22 were treated with anticoagulant drugs. Anticoagulant therapy usually consisted of intravenous heparin for 7 to 10 days, followed for at least 3 to 6 months by either subcutaneous heparin (5000 to 8000 U twice daily) or oral warfarin. All patients were closely monitored to ensure control of hypertension, compliance with therapy, maintenance of prothrombin time within the therapeutic range, and early recognition of adverse side effects. No patient had an intracranial hemorrhage. Thus, anticoagulant agents can be safely administered after intracranial operations for malignant gliomas without increased risk of morbidity or mortality if the patients are carefully monitored according to established guidelines.
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PMID:Risk of intracranial hemorrhage in glioma patients receiving anticoagulant therapy for venous thromboembolism. 381 30

This literature review was conducted to determine: (a) the rate of bleeding (major, minor and fatal) during long term oral anticoagulant therapy (greater than 4 weeks) in various disorders (ischaemic cerebrovascular disease, prosthetic cardiac valves, chronic atrial fibrillation, ischaemic heart disease and venous thrombosis); and (b) the clinical and laboratory risk factors which predispose such patients to bleeding. Using strictly defined methodological criteria, 167 studies were evaluated and classified into 1 of 5 categories based on the strength of the study design, with level I (randomised trials) representing studies which provided the most reliable information and level V (cases series) the least reliable. The risk of bleeding was substantial, and was most marked in patients with ischaemic cerebrovascular disease (29%), ischaemic heart disease (19%) and venous thromboembolism (23%). Major bleeding in venous thrombosis and cerebrovascular disease was frequently associated with an underlying risk factor. In venous thromboembolism these coexisting conditions (cancer, recent surgery and paraplegia) were also predisposing factors for thrombosis. In cerebrovascular disease major bleeding was almost always intracerebral, possibly because of associated hypertension or the cerebrovascular disease per se. We were unable to determine whether bleeding events were concentrated soon after commencing anticoagulant therapy. Haemorrhagic episodes frequently occurred when the prothrombin time (or thrombotest) was within the targeted therapeutic range, but the relationship between bleeding and the level of anticoagulant therapy was properly evaluated in only 1 study (in venous thrombosis) which demonstrated that the risk of bleeding was reduced by using a less intense anticoagulant regimen. In conclusion, the risk of bleeding during oral anticoagulant therapy is substantial. Our analysis was limited by the lack of concise reporting of clinical and laboratory information and we would suggest that future clinical studies report these in greater detail.
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PMID:Risk of haemorrhage associated with long term anticoagulant therapy. 390 38

Twenty-four patients had intracerebral hemorrhage while they were being treated with anticoagulants. Hypertension was present in 67% of the cases, head trauma was an uncommon preceding event, and simultaneous bleeding in other organs occurred in only one instance. Neurologic abnormalities progressed for several hours in 58%. Seizures occurred at onset in 12.5%. The location of the hemorrhage was as follows: cerebellum (nine cases), lobar white matter (six), basal ganglia (five), thalamus (two), and hemisphere, unspecified (two). In 61%, the hemorrhages occurred within 6 months of therapy. In 75%, the prothrombin time was beyond 1 1/2 times the control value. Mortality was 62.5%. Survivors had smaller hematomas than did patients with fatal hemorrhage.
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PMID:Anticoagulant-related intracerebral hemorrhage. 401 Sep 61

On 169 occasions anticoagulant therapy for thromboembolic disease was stopped electively and patients were followed for 16 subsequent weeks. The records of those who remained well and those who suffered a relapse were compared in an attempt to identify factors that might affect liability to thromboembolic relapse. During the follow-up period there were 37 thromboembolic recurrences, an incidence of 22 per cent. None occurred among the patients in whom the original diagnosis of thromboembolic disease was discarded or when a predisposing cause had ceased to be present. There was an inverse relation between liability to relapse and degree of prothrombin time prolongation.NO SIGNIFICANT RELATION COULD BE SHOWN BETWEEN LIABILITY TO RELAPSE AND ANY OF THE FOLLOWING: sex and age; type and severity of the initiating thromboembolic episode; history of earlier thromboembolic disease or relapse after stopping earlier anticoagulant courses; presence of hypertension, hypercholesterolaemia, or diabetes mellitus; type of anticoagulant drug used, duration of therapy, and method of stopping treatment. Patients with overt occlusive arterial disease at more than one site had a significantly increased liability to relapse when compared with patients with symptomatic disease at a single site. In the group of 134 subjects receiving anticoagulant therapy for coronary arterial disease, occurrence of a thromboembolic episode during the course of treatment and the presence of angina of effort in the months before it was discontinued were both associated with a significant increase in liability to relapse. It is suggested that, ideally, anticoagulant therapy should be continued indefinitely in any patient whose pattern of disease thus increases the likelihood of a thromboembolic recurrence.
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PMID:Recurrence of thromboembolic disease after discontinuing anticoagulant therapy. A study of factors affecting incidence. 542 82

Intracranial hemorrhage was the most serious hemorrhage as measured by death and disability, occurring during long-term anticoagulant drug therapy of 1,626 patients. Among 95 hemorrhagic episodes considered life-threatening or potentially crippling, 30 were intracranial and 56 were gastrointestinal. Over two-thirds of the patients with intracranial hemorrhage died, as against one-tenth of those with gastrointestinal hemorrhage. The incidence of intracranial hemorrhage is increased among hypertensive patients, but the results of a controlled study indicate that the incidence of intracranial hemorrhage is not affected by whether or not the hypertensive patient is receiving anticoagulant therapy. Hypertension is the important precipitating factor, not the prothrombin level. Even at excessively low prothrombin levels only one intracranial hemorrhage occurred in 337 instances. In this series, reducing coagulability to a desirable range did not increase the probability of intracranial hemorrhage. Once bleeding occurred, however, it increased the risk of death and disability.
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PMID:Hemorrhage during long-term anticoagulant drug therapy. 1. Intracranial hemmorrhage. 592 38

Sixty-four patients (43 men and 21 women) with acute viral hepatitis were subjected to clinical, clinical chemical and electroencephalographic examinations. A pathological EEG was found in 19 patients. The average age was the same in the entire group, in the group with normal EEGs and in the group with pathological EEGs (35.4, 35.8 and 35.2 years respectively). The proportion of HBsAg-positive to HBsAg-negative hepatitis in the groups with pathological and normal EEGs did not show any appreciable difference. Of the patients with pathological EEGs, 36.8% were drug addicts, and only 8.9% of these these with normal EEGs. A dependence of the EEG on the laboratory values SGOT, SGPT, prothrombin time or bilirubin was not found. In 14 of the 19 patients, there was a slight general alteration with irregular alpha rhythm and markedly increased 5--7 c/sec theta activity. In 5 patients, there was a moderately severe general alteration with predominant theta rhythm and interspersed delta waves. In 5 patients, the EEG normalized; it remained pathological in 14 patients. Even after exclusion of all other factors, such as drugs or hypertension, which might have led to a pathological EEG, we found pathological EEG findings in 15.6% of the 64 patients with acute viral hepatitis and no clinical encephalopathjy.
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PMID:EEG changes in acute viral hepatitis. 615 95

We confirmed our previously reported findings that subcutaneous administration of heparin (200 U q 12 hr) in rats with experimental partial renal infarction prevents the development of progressive renal failure and hypertension, as well as the glomerular abnormalities which occur in the remaining viable renal tissue. In the present study, heparin, in the dosage used to prevent progressive renal failure, caused a marked and sustained prolongation of the activated partial thromboplastin time and prothrombin time, as well as a transient prolongation of the bleeding time. Administration of coumadin at doses which caused a significant prolongation of the prothrombin time and bleeding time also inhibited the development of progressive hypertension and uremia in rats with experimental partial renal infarction. These findings indicate that inhibition of blood coagulation effectively protects rats with experimentally decreased renal mass from the development of progressive renal failure and hypertension and support the concept that the glomerular thrombosis plays an important role in the pathogenesis of these complications.
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PMID:Inhibition by anticoagulant drugs of the progressive hypertension and uremia associated with renal infarction in rats. 621 41

Heymann nephritis was induced in rats with spontaneous hypertension (group HN), and renal lesions were investigated at the twentieth and thirty-sixth week. An identical group given antihypertensive drugs (group HN-AH), an identical group given anticoagulant drugs (group HN-AC), and a nonimmunized control group of spontaneously hypertensive rats (controls) were also examined. Massive proteinuria, hypoalbuminemia, and hyperlipidemia were present in groups with induced Heymann nephritis (HN, HN-AH, and HN-AC). Coagulation studies demonstrated a shortening of prothrombin time, an increase in serum fibrinogen and thrombocytes, and a reduction of antithrombin III in the groups HN and HN-AH. Necrotizing lesions were observed only in group HN and without further elevation in blood pressure. Intravascular thrombosis was prominent at the twentieth week, and marked fibrinoid necrosis appeared at the thirty-sixth week. These vascular lesions were not observed in the HN-AH, HN-AC, and control groups. Thus, a state of hypercoagulability in addition to high blood pressure probably contributes to the genesis of necrotizing vascular lesions in spontaneously hypertensive rats with nephritis.
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PMID:Necrotizing vascular lesions in spontaneously hypertensive rats with nephrotic syndrome: hypercoagulability as a contributory factor. 638 12

Three patients with severe hemophilia A with inhibitors to factor VIII were treated with activated factor IX complex. Bleeding was controlled adequately during surgical procedures involving each of the three. Partial thromboplastin times showed a variable shortening and prothrombin times were significantly shortened to values less than normal. Hemostasis was substantiated by the use of epsilon aminocaproic acid. Neither anamnestic responses nor thrombotic complications were observed. A transient hypertension developed in two patients shortly after infusion with the activated factor IX complex.
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PMID:Activated factor IX complex in treatment of surgical cases of hemophilia A with inhibitors. 697 16

Three patients developed hepatic injury two months, ten months and two years, respectively, after hydralazine therapy for hypertension. Clinical and biochemical recovery followed discontinuation of drug therapy. Liver biopsies of the three patients revealed varying degrees of centrilobular necrosis. Complement 3 and Complement 4 levels were measured and found to be low in the patient with poor liver synthetic function, as was evident from the low serum albumin level and prolonged prothrombin time. Hydralazine-induced liver injury may be due to abnormality of drug metabolism in the liver.
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PMID:Hydralazine-induced hepatitis. 721 34


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