Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to predict cardiovascular complications in patients with prostatic cancer treated with oestrogen. A randomised prospective study of oestrogen therapy versus orchiectomy was performed. Patients with pre-existing cardiovascular morbidity were excluded (16%). Prior to the initiation of therapy, patients were subjected to exercise stress tests, physiological evaluation of peripheral circulation, blood volume estimation, chest X-ray, blood test, including hormones, lipoproteins, and antithrombin III, and a physical examination and history by a cardiologist. The oestrogen treatment and the orchiectomy group did not differ with regard to these pretreatment variables; 25% of the patients given oestrogen therapy had cardiovascular complications during the initial treatment year compared with none in the orchiectomy group. Three statistical discriminating techniques were employed and they allowed us to identify 2 strong discriminating variables for cardiovascular complications if oestrogen therapy is instituted in patients with prostatic cancer but without overt clinical cardiovascular disease. These 2 discriminators were luteinising hormone (LH) and ST-segment depression during exercise. This means that a patient with ST-segment depression during an exercise test and/or a high luteinising hormone concentration should not be treated with oestrogen.
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PMID:Patients at high risk of cardiovascular complications in oestrogen treatment of prostatic cancer. 264 97

Eicosapentaenoic acid (EPA), the precursor fatty acid of three series of prostaglandins, has been reported to have an antiatherothrombotic potential. We gave highly purified EPA in a soft capsule (90% ethylester form of EPA; EPA-E) to 6 healthy male volunteers for 4 weeks. After the administration of 900 mg/day of EPA-E for two weeks or longer, a significant reduction in plasma beta thromboglobulin level was observed, and after 4 weeks' administration, significantly blunted pressor responsiveness to infused angiotensin II was observed. These changes were not observed 4 weeks after EPA-E had been discontinued. After 4 weeks' ingestion of EPA-E, the platelet count, mean platelet volume, platelet aggregation with adenosine diphosphate or collagen, plasma recalcification time, prothrombin time, plasma antithrombin III, fibrinogen or plasmin concentrations, serum concentrations of total cholesterol, triglycerides, total phospholipid, nonesterified fatty acid or high-density lipoprotein cholesterol were unchanged. From the data presented it can be said that EPA-E causes a mild depression of vascular contractility and of platelet aggregability in vivo and exerts a beneficial influence on several cardiovascular factors.
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PMID:Effects of highly purified eicosapentaenoic acid on plasma beta thromboglobulin level and vascular reactivity to angiotensin II. 282 70

The successful evaluation of tamoxifen as an antiestrogenic therapy for advanced breast cancer in the early 1970's, has resulted in its availability in more than 70 countries around the world. Currently the drug development process is focusing attention upon long-term adjuvant therapy and the future prospect of chemosuppression. Progress at this stage, however, must be cautious. Trials conducted using women with stage I disease have a high proportion of women who may never have a recurrence. At this point, the risk is justified because the toxicity of tamoxifen is low and disease recurrence is invariably very difficult or impossible to control. Future studies in the general population must be carefully weighed to ensure that the hazards do not exceed the benefits. The pharmacology of tamoxifen seems to be a balance of estrogenic and antiestrogenic effects. Longer treatments with the drug must be carefully monitored. Uterine tissue should be examined to ensure that excessive stimulation does not occur. This is particularly true in the light of the recent report that a human uterine carcinoma, transplanted into athymic mice, can grow more rapidly during tamoxifen therapy (Satyaswaroop et al., 1984; Clark and Satyaswaroop, 1985). In fact, we have recently confirmed this observation in a collaborative study with Dr. Satyaswaroop. We have demonstrated that when athymic mice are transplanted in one axilla with an MCF-7 breast tumor and the human endometrial tumor in the other, tamoxifen causes the endometrial tumor to grow, but not the breast tumor. This again illustrates the target site specific effects of tamoxifen. If, in the long run, the estrogenic side effects of tamoxifen are too severe then there is a case for the development of a non-estrogenic antiestrogen. Clearly this may provide benefit for short term (1-2 years) therapy and avoid any estrogen-like stimulation of tumor growth. Similarly, the concern about antithrombin III depression will be avoided. On the negative side, however, the concerns about atherosclerosis and osteoporosis will again have to be addressed with a new generation of agents.
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PMID:Long-term tamoxifen therapy to control or to prevent breast cancer: laboratory concept to clinical trials. 328 87

Complexes antithrombin III-heparin-thrombin exhibiting the anticoagulation and nonenzymatic fibrinolytic activities were isolated from human blood children of 4-II years old with burns or with traumatic shock and from rat blood. The complexes antithrombin III-heparin-thrombin with high nonenzymatic fibrinolytic activity were shown to develop during activation of the anticoagulation system. In depression of the anticoagulation system these complexes, isolated from blood, demonstrated the lower nonenzymatic fibrinolytic activity, thus indicating that complex-formation is restricted.
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PMID:[The role of the antithrombin III-heparin-thrombin complex in the defense reaction of the anticoagulation system]. 340 Jan 89

The authors made a randomized prospective study of estrogen therapy versus orchidectomy in patients with prostatic cancer (n = 100, Huddinge Hospital, Sweden) to investigate the possibility of predicting cardiovascular events during hormonal treatment. Patients with preexisting cardiovascular morbidity were excluded (16%). Prior to the allocation of therapy, the following were performed: exercise stress test; physiologic evaluation of the peripheral circulation; blood volume estimation; chest x-ray; blood tests, including hormones, lipoproteins, and antithrombin III; and a physical examination and history by a cardiologist. Thirteen (25%) of the patients given estrogen therapy (n = 53) had cardiovascular complications during the first year of treatment compared with none in the orchidectomy group. The authors made a multivariate discriminant analysis of the pretreatment examinations of the estrogen-treated patients; this resulted in a discriminant function including S-T segment depression in lead CH2 during the exercise stress test and blood tests for cholesterol, follicle-stimulating hormone, and luteinizing hormone. This function correctly classified 84% of the estrogen-treated patients as patients with or without risk of a cardiovascular complication. Briefly stated, if patients with prostatic cancer are examined by means of exercise stress tests and blood tests for luteinizing hormone, cholesterol, and follicle-stimulating hormone prior to treatment, the discriminant function enables the authors to identify an extremely high-risk group for cardiovascular complications if estrogen therapy is commenced. The strong association of an increased luteinizing hormone with cardiovascular complications during estrogen treatment makes it mandatory to investigate its role in the pathogenesis of atherosclerosis and cardiovascular events.
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PMID:Prediction of cardiovascular complications in patients with prostatic cancer treated with estrogen. 357 55

It has been reported that patients with preeclampsia have decreased levels of antithrombin III heparin cofactor and that the degree of depression parallels the severity of disease. To determine the time course of development and resolution of this deficiency, and to gain insight into the cause of this deficiency, plasma antithrombin III antigen and heparin cofactor activity levels were measured serially in 11 women with mild preeclampsia. Although the ATIII antigen level remained stable during the antepartum period, the level of heparin cofactor was noted to fall progressively during the antepartum period. Both ATIII antigen and heparin cofactor increased promptly postpartum. The discrepancy between the levels of ATIII antigen and heparin cofactor activity suggests that in both mild and severe preeclampsia there is utilization of antithrombin III to form inactive protease inhibitor complexes.
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PMID:Heparin cofactor activity and antithrombin III antigen levels in preeclampsia. 376 1

The rabbits with CCl4-induced hepatic failure have revealed changes in hemostasis responses to streptokinase administration. The main distinction of hepatic dystrophy was the depression of plasma fibrinolytic activity accompanying the decrease in fibrinogen and antiplasmin concentrations. Streptokinase administration to rabbits with productive inflammatory liver disorders produced changes in hemostasis identical to those observed in intact rabbits, fibrinogen levels, however, remained unchanged. The common feature of all the toxic liver disorders is the increase of antithrombin III levels after streptokinase administration, whereas the antithrombin levels in the control animals were decreased.
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PMID:[Action of streptokinase on the hemostatic indices of rabbits with a toxic lesion of the liver due to carbon tetrachloride]. 381 94

The blood clotting systems of 21 women, aged 18 to 38 years, who had begun using oral contraceptives, were studied. 2 brands of oral contraceptives were used, both containing 1 mg progestogen and .08 mg estrogen. Tests were performed before oral contraceptive usage was begun, and again after the tenth and twentieth days. The antithrombin III and thrombin generation results were compared with the records of patients with chronic thromboembolic disease. Oral contraceptives with a quick, dramatic depression of antithrombin activity and an acceleration of thrombin generation within the first cycle. The depression of antithrompin III activity occurred within 7 days, while thrombin generation occurred within 10 days, but was further accelerated by 20 days (p .001). Levels of both returned to normal after discontinuation of oral conceptive use. Results obtained from using oral contraceptives were similar to those of the patients with thromboembolic disease. It was suggested that the change in antithrombin III activity was the most clinically significant of the 2 changes involved.
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PMID:Antithrombin 3 depression and thrombin generation acceleration in women taking oral contraceptives. 555 23

Total hemolytic activity of serum (CH50), complement components C3 and C4, alpha 1antitrypsin (alpha 1AT), alpha 1antichymotrypsin (alpha 1X), antithrombin III (AT III), alpha 2 macroglobulin (alpha 2M), and inter-alpha-inhibitor (I-alpha-I) were measured in 23 Japanese and 19 European children with the Mucocutaneous Lymph node Syndrome (MCLS) during the acute phase of disease. Second sera, obtained after day 20 were available from 18 Japanese and 10 European children. In 28 out of 31 children with mild disease, as assessed by the coronary risk score of Asai and Kusakawa, complement was normal or elevated during the acute phase. In 10 out of 11 children with high risk scores, CH50 was below the normal range. One child in this group had ECG changes during the acute phase, one patient died and two others developed coronary aneurysms. C1I was elevated in all 42 cases, alpha 1AT in 40, and alpha 1X in 38 patients. alpha 1AT was depressed in two children, one of whom developed an aneurysm. One of the four children with depression of alpha 1X died of myocardial infarction. Decreased concentrations of AT III, alpha 2M and I-alpha-I were frequent and tended to mark the more severe courses of the disease. A third group of 20 children was evaluated 5 weeks to 6 months after the acute illness. Mean concentrations of all five protease inhibitors were completely normalized in this group. The results of this study indicate that consumption of complement and of protease inhibitors occurs in many cases of MCLS during the acute phase. Determination of CH50 appears to be useful to identify high risk patients early in the course of their illness. Transient deficiency of substances for control of inflammation may in part be responsible for the severe vascular lesions seen in some patients.
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PMID:Complement and protease inhibitors in the mucocutaneous lymph node syndrome. 619 94

The use of continuous, low-dose heparin in total parenteral nutrition (TPN) formulas to limit central venous thrombosis was retrospectively evaluated. Seven of 129 patients (5.4%) developed central vein thrombosis when TPN solutions provided less than 6,000 units (usually 1,000 units/liter) heparin per day. In the subsequent period when heparin was increased to 6,000 units per day, 10 of 858 (less than 1.2%) patients developed a TPN-related thrombosis (P less than 0.0005). The incidence of antithrombin III (AT III) deficiency in a subset of high-risk patients scheduled to receive TPN was 51% (23 of 55). Twelve of the 23 had clinical evidence of thrombosis, whereas only 3 of 22 patients with normal AT III levels did (P less than 0.01) A major contributing factor to the development of thrombosis in TPN appears to be depression in antithrombin III levels, which is commonly found in patients who require this therapy. Low-dose heparin appears to reduce the incidence of thrombosis with TPN when provided continuously in sufficient amounts.
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PMID:Limitation of central vein thrombosis in total parenteral nutrition by continuous infusion of low-dose heparin. 641 93


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