Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen replacement in menopause should be used for specific symptoms such as ovarian failure, hot flushes, vaginal atrophy, atrophy of the vulva, and atrophic urethritis. The dose should be as low as possible to be effective and perscribed for as short as time as possible, since there are possible risks of uterine cancer, breast cancer, increased blood pressure, gallstones, deep vein thrombosis, and thromboembolism. Estrogens should be administered to provide the maximum benefit with the minimum risk involved. Estrogens should not be given to patients with known contraindications such as: suspected breast or uterine cancer; undiagnosed genital bleeding; Dubin-Johnson syndrome; acute hepatic disease; previous or present thromboembolism; or severe thrombophlebitis. Careful evaluation should be made before administering estrogen to women with uterine myomata, hyperlipidemia, hypercholesterolemia, sevare varicose veins, chronic hepatic dysfunction, diabetes mellitus, porphyria, or severe hypertension.
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PMID:Estrogen replacement in the menopause. 39 Apr 56

A perspective study by the Royal College of General Practitioners reported that the risk of developing deep venous thrombosis of the legs in women taking oral contraceptives was 5.66 times higher than women not on medication. Estrogen-progestogen compounds are highly potent hormones that produce alterations in metabolic and endocrine functions. Clinical examination of the leg is the most reliable method of determining the earliest indication of thrombophlebitis even with the latest diagnostic tools of venography. The key to diagnosis and treatment of pulmonary embolism, which often occurs with patients with thrombophlebitis, is a patient's complaint of leg pains. Those who have undergone surgery, especially abdominal and pelvic, are bedridden, and those who are taking oral contraceptives are at risk of thrombophlebitis. Deep thrombophlebitis of the leg is not recognized clinically in 50-80% of those with venographically documented thrombophlebitis because the signs and symptoms are so protean. Treatment with heparin and leg bandages is most common. Heparin is often followed with coumarin therapy. Some methods of diagnosis are calf tenderness, edema, skin temperature, Homan's Sign, Lowenberg's Sign, Pratt's Sign, cyanosis, systemic signs, and contrast venogram.
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PMID:A review of the birth control pill and its relationship to thrombophlebitis. 44 35

6 patients with deep vein thrombosis triggered by drug therapy, that is oral contraceptives in 5 and the anticonvulsant tranexamic acid in 1, are described. These cases were among 40 symptomatic patients out of a total group of 81 with congenital coagulation inhibitor defects studied over 10 years at the Institute of Medical Semiotics, Padua, Italy. The 5 women with deep vein thrombosis ranged in age from 20-34, and had typically taken oral contraceptives containing 35 mcg ethinyl estradiol in combined or phasic preparations, for 1 to 8 cycles. One women, however, had been prescribed sequential pills containing 50 mcg mestranol. Another had taken oral contraceptives with impunity for 3 years, but developed deep vein thrombosis after taking tranexamic acid for 10 days. All recovered after heparin or oral anticoagulant therapy, except a 21 year old whose condition evolved into complete ileo-caval obstruction up to the renal veins, and was treated with urokinase. the congenital defects involved were 3 probable heterozygous true deficiencies of antithrombin III (low ATIII antigen and activity); a decreased protein C antigen to factor X antigen ratio; a heparin cofactor II deficiency; and a type I protein S deficiency (low free protein S, with normal total protein S and normal levels of C4B-bp.) While 5 of these 6 women had family histories of thromboembolic disease, the drug was prescribed without knowing that they were heterozygous for a coagulation inhibitor deficiency. The incidence of drug-induced thromboembolism was low in this series overall, where most of the events were triggered by surgery or trauma.
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PMID:The role of drugs, particularly oral contraceptives, in triggering thrombosis in congenital defects of coagulation inhibitors: a study of six patients. 178 39

5 cases of vascular complications--hemorrhagic stroke, myocardial infarction, retinal vein thrombosis, thrombotic stroke and deep vein thrombosis--in young women taking low dose oral contraceptives are described from the Department of Obstetrics and Gynecology, University of the Witwatersrand, Johannesburg, South Africa. The hemorrhagic stroke occurred in 1987 in a 24-year old heavy smoker taking Triphasil (Wyeth) for 12 months. She recovered fully. A 34-year old woman had an anteroseptal infarction while on Minovlar ED (Schering, 50 mcg ethinyl estradiol and 1 mg norethisterone acetate) for 2 years. She had no risk factors other than smoking 5 cigarettes daily. The woman with retinal vein thrombosis had 2 episodes, the 1st while taking Restovar 28 (Organon, 37.5 mcg ethinyl estradiol and 0.75 mg lynestrenol) for 7 years. 19 months later she began Diane (Schering AG, 50 mcg ethinyl estradiol and 2 mg cyproterone acetate) and had a bilateral retinal vein thrombosis leaving her partially blind. The woman with thrombotic stroke was 24 when she was struck in 1986, after 1 year of taking Logynon ED (Schering AG, 6/5/7 days, 30,40/40 mcg ethinyl estradiol and o.5/0.75/0.125 mg levonorgestrel). The patient with deep vein thrombosis was 19, smoked, and had used Triphasil for 2.5 years.
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PMID:Vascular complications in women using the low steroid content combined oral contraceptive pills: case reports and review of the literature. 220 50

Vascular risk, mainly thromboembolitic risk, attributed to oral contraceptives (OCs) since 1962, has been primarily linked to ethinyl estradiol (EE). OCs which combine estrogen and have been associated with cerebral vascular accidents. A 1977 study showed a 40% increase of mortality due to cardiovascular complications in women taking OCs. There were of both an arterial and a venous character. The risk of myocardial infarction was 3 times more frequent among OC users. Deep venous thrombosis and pulmonary embolism were more numerous. Some other risk factors include smoking, hypertension, diabetes, and age 35. The risk of heart attack vanishes a few years after stopping OC use. The reduction of EE (and similarly progesterone) dosage from 100-50 mcg also lower the risk of hypertension, cerebral vascular accidents, and venous thrombosis. Prolonged use of OCs causes disorders of hemostasis affecting the walls of blood vessels, modifying the viscosity of blood flow (increase of hematocrits, reduction of venous tonus), modifying plasmatic coagulation (increase of platelets, increase of factors VII and X and plasma fibrinogen, and decrease of antithrombin III activity), and increased fibrinolysis. These anomalies are exclusively associated with high doses of estrogens. 5% of women using OCs develop moderate hypertension of 5-10 mm Hg of systolic pressure 5 years later, but after cessation it is reversed. OCs stimulate the renin-angiotensin-aldosterone system causing accelerated production of angiotensin II with the resultant forceful vasotension. 3 months after quitting OC use, high blood pressure returns to normal. EE can provoke diabetes; it increases very low density lipoprotein (VLDL) and high density lipoprotein (HDL) production, but total cholesterol is hardly affected. The androgenic property of progestogens reduces HDL. Combined OCs are contraindicated for women with hypertension, hyperlipidemia, diabetes, and a family history of vascular accidents.
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PMID:[Oral contraception and the vascular risk]. 251 20

In a prospective multicenter study, 244 men with highly or moderately differentiated prostatic cancer in stage I, II or III (VACURG) were consecutively randomized to three groups of treatment: Group A (77 patients) received polyestradiol phosphate (Estradurin, Leo) 80 mg i.m. every fourth week + ethinyl estradiol (Etivex, Leo) 150 micrograms daily, group B (72 patients) estramustine phosphate (Estracyt, Leo) 280 mg twice daily, and group C (76 patients) no therapy. Only men without current or previous other malignancy and without cardiovascular disease were admitted to the study. After 4 1/2 years 125 of the 244 patients had left the study, 9 because of cancer progression (stage IV, VACURG). The most serious complications were cardiovascular, including ischemic heart disease, cardiac decompensation, cerebral ischemia and venous thromboembolism, which occurred in 24 patients from group A and 9 from group B as compared to only one patient in group C. The subgroup superficial or deep venous thrombosis comprised 11 group A and 2 group B patients. Estrogens (E + e) offered as palliative treatment to patients with non-generalized prostatic carcinoma is burdened with a high incidence of serious cardiovascular complications.
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PMID:Cardiovascular complications of estrogen therapy for nondisseminated prostatic carcinoma. A preliminary report from a randomized multicenter study. 352 68

Focus in this discussion of pulmonary embolism is on the following: risk factors (age, heredity and blood type, obesity, estrogen and oral contraceptive use/pregnancy, cardiovascular disease, cancer, and other risk factors); pathophysiology and presenting symptoms; laboratory procedures and findings (radiography, electrocardiography, lung scanning, and evaluation of lower extremity veins); treatment modalities (heparin therapy, thrombolysis, and surgery); and prevention. Pulmonary embolism may be the primary cause or a major contributory cause in as many as 200,000 deaths per year in the US. Most of these deaths occur in patients in whom the diagnosis is not suspected and, thus, not treated. The mortality rate for untreated pulmonary embolism is approximately 30%. 90% of patients survive the initial embolic event, but the correct diagnosis is made in no more than 2/3 of cases. Risk factors for the development of deep venous thrombosis are based upon the Virchow-Aschoff postulates, which include: trauma or disruption of the vein wall; stasis of blood flow in the veins; and increased coagulability of the blood. More than 85-90% of all pulmonary emboli originate from deep venous thromboses in the popliteal and femoral deep veins. Other important, although less frequent, sites of origin of venous thromboembolism include the pelvic veins, the renal and hepatic veins, the axillary veins in the upper extremities, and the right atrium. Accurate diagnosis and effective prevention and treatment depend on the clinician's awareness of risk factors for development of deep vein thrombosis. Estrogen may accelerate intimal proliferation in arteries and veins, and it may also increase permeability of venous vascular endothelium. The risk of thromboembolism increases as the dose of estrogen increases. Both pregnancy and oral contraceptive use significantly decrease venous tone and the velocity of blood flow in the calf of the leg. Appropriate treatment includes thrombolytic therapy for patients with massive pulmonary embolism, which results in hypotension or shock. Anticoagulant therapy with herapin followed by an oral anticoagulant is the primary treatment for most patients with submassive emboli in which there is less cardiovascular compromise. When thrombolytic therapy is used, it should always be followed by anticoagulant therapy. Prevention of primary or recurrent deep vein thrombosis is directed toward improving venous blood flow and reducing hypercoagulability.
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PMID:Pulmonary embolism: incidence, diagnosis, prevention, and treatment. 398 Feb 63

Drug companies have been at work throughout the 1960s, 1970s, and 1980s trying to reduce the steroid content of their oral contraceptives (OCs). Researchers have been successful in reducing steroid content while maintaining effectiveness, thereby making OCs safer. In the 1st half of the natural menstrual cycle, a woman secretes estrogen as the dominant steroid product. In the 2nd half, estrogen is the principal reproductive hormone. Estrogens inhibit ovulation, possibly by inhibiting implantation, altering ovum transplant, or in some way preventing corpus luteum function, which is necessary to maintain early pregnancies and the endometrium. There are still only 2 estrogens and 6 progestins on the market today. They are probably the most thoroughly studied chemical ever seen in the history of pharmacy or medicine. 1 of the estrogens, mestranol, is really a drug of the past. In the body, mestranol is converted to ethinyl estradiol, the other estrogen on the market. Consequently, there is no reason to use mestranol itself. Within the dose range of 50-100 mcg, there's little difference in contraceptive effect. Progestins are the other active ingredient in the combination OC. Their principal action is the thickening of the cervical mucus, which prevents sperm penetration. Also, with sufficient progesterone, ovulation is inhibited, but this happens in only 40% of those patients taking, for instance, the "mini-pill" (which consists of progesterone only). The progestins and the estrogens work in concert to make OCs a highly effective contraceptive method. Recent surveys conducted by the Centers for Disease Control and National Cancer Institute looked into the relative effectiveness of OCs. Nordette had a use effectiveness failure rate of 3.5; Ovral, 3.6. Loestrin 1/20 -- norethindrone acetate, 1 mg, and estinyl estradiol, 20 mcg -- shows a failure rate of 4.5. This indicates that the threshold for an effective dose of estinyl estradiol in OCs is 30 mcg. For 1 mini-pill, Ovrette, the failure rate is 9.5 -- much higher. Depo-Provera has a failure rate of 0.7. The primary complaint from women taking OCs is spotting and breakthrough bleeding during the cycle. 30-50% of women given OCs stop taking them within a year. OC side effects include nausea, fluid retention, breast tenderness, leukorrhea, hypomenorrhea, headaches, spotting around the face, hypertension, and visual changes. 1 of the risks of birth control pills may be cervical dysplasia -- changes in the cells of the cervix. The relative risk of cervical cancer with OCs after 5-9 years is approximately 1.8. Clinical cases of deep vein thrombosis number 1/1000 per year among nonusers of OCs. Among users, the rate is 3 times as high: 3/1000. The most serious potential adverse effect is myocardial infarction. Of the excess deaths attributed to OCs (23.3 total per 100,000 users), 22.7 are due to myocardial infarctions and hemorrhage. The discussion also briefly reviews other methods of contraception -- Depo-Provera, male contraceptives, implants, the diapragm, and IUDs.
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PMID:Prescription contraceptives: countering the risks. 405 Jun 70

4 kinds of progestin only oral contraceptives (OCs) and numerous combined OCs containing ethinyl estradiol (EE) or occasionally mestranol and either norgestrel or norethindrone are currently available in Australia. All progestins except norgestrel are effective in vivo after metabolism to norethindrone. Mestranol is effective in the human after demethylation to EE. The main side effects of OCs, including menstrual disturbances and changes in weight and mood, are primarily of nuisance value. Menstrual blood loss with OCs is almost invariably less than during spontaneous menses, but breakthrough bleeding and midcycle spotting may cause concern in patients. Amenorrhea and weight gain are rare with low dose pills. Approximately 6 in 1000 women remain anovulatory for 12 months or more after discontinuing OCs, but it is not yet know whether the amenorrhea is related to pill use and it is usually corrected by induction of ovulation. Cardiovascular side effects including venous thrombosis and pulmonary embolism are seen less frequently with new lower dose pills. The effects of OCs on the cardiovascular system are complex and depend on the interaction of estrogen and progestin. Amounts of estrogen and progestin should be the lowest possible to prevent ovulation, and routine monitoring should be provided for all women using pills. Older high dose formulations altered lipid metabolism in the direction of greater risk of coronary heart disease. Although research suggests the lowest dose triphasic pills have no significant effect, not enough large studies have been done with matched controls. Any effects on carbohydrate metabolism of the low dose pills are apparently minor and of little clinical significance. Insulin dependent diabetics with adequate supervision may safely use low dose pills. Combined OCs reduce the incidence of endometrial and ovarian malignancy. No relationship between OCs and the risk of breast cancer has been demonstrated except possibly in women under 35 when the cancer developed. The risk of intraepithelial neoplasia may be increased in women taking OCs for more than 8 years. Data on drug interactions are inconclusive, but women on rifampicin should use some other method. Absolute contraindications to OCs include breast cancer, history of deep venous thrombosis or pulmonary embolism, active liver disease, use of rifampicin, familial hyperlipidemia, previous arterial thrombosis, and pregnancy, while relative contraindications include smoking, age over 35, hypertension, breastfeeding, and irregular spontaneous menstruation. Progestin only OCs have a higher rate of failure and irregular bleeding than combined pills and their main use is for breastfeeding women and those with contraindications to estrogen. The pill of 1st choice should be a triphasic low-dose formulation.
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PMID:Oral contraceptives. 650 52

In a randomized study, 63 postmenopausal patients with advanced breast cancer were treated with ethinyl estradiol (EE2) or the antiestrogen tamoxifen to compare the efficacy and side effects of both drugs. EE2 was always given in combination with chlorothiazide to prevent fluid retention. Pretreatment characteristics of the patients of both groups did not differ significantly. Objective remissions were achieved in 31% of the EE2-treated patients and in 33% of the tamoxifen-treated patients. The median duration of remission was 12 months (range, 5-32) for the EE2 group and 11 months (range, 5-26) for the tamoxifen group (P greater than 0.1), and the estimated median survival times from the start of treatment were 31 and 25 months, respectively (P greater than 0.1). The best treatment results in both groups were obtained in patients with estradiol receptor-positive tumors and less advanced disease. After therapy was stopped, objective withdrawal responses were observed in EE2- but not in tamoxifen-treated patients. Two patients receiving EE2 had to discontinue treatment because of drug-related liver function impairment. Both patients had cholelithiasis. Two patients in the tamoxifen-treated group discontinued therapy because of nausea. Deep venous thrombosis occurred in one patient receiving EE2, whereas two patients receiving tamoxifen developed superficial thrombophlebitis. Other side effects in both groups of patients, including initial hypercalcemia, were mild. It is concluded that both treatment regimens, EE2 or tamoxifen, are equally effective with respect to induction and duration of remission in postmenopausal patients with advanced breast cancer. Side effects of EE2 therapy appeared to be more serious than those of tamoxifen treatment.
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PMID:Tamoxifen versus ethinyl estradiol in the treatment of postmenopausal women with advanced breast cancer. 723 48


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