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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies on the use of oral contraceptives in the West have shown that they induce changes in total serum cholesterol, triglycerides, high density lipoproteins, low density lipoproteins, and very low density lipoproteins -- changes which are implicated in the development of atherosclerosis. In India, however, women consume low fats, low cholesterol and fewer calories; they drink less alcohol and rarely smoke; and they engage in more physical activities. 2 groups of Indian women were tested for lipid metabolism alterations during and after use of oral contraceptives supplied by the Indian government. 1 group of 23 women, aged 20-30, received low dose oral contraceptives containing 30 ug ethinyl estradiol and 1 mg of norethisterone acetate, and their serum lipid levels were tested after 3 and 6 months of use. A 2nd group of 12 multiparas, aged 25-35, who had been taking oral contraceptives for 1 1/2 to 2 years (either 50 um ethinyl estradiol and .5 mg norgestrel, called Ovular or Primovlar-50, or 30 ug ethinyl estradiol and .5 mg ethynodiol diacetate, called Ovular-50) were examined for serum lipid levels 3 and 6 months after withdrawal from the pills. In the 1st group no significant change was observed in any lipid fraction after 3 or 6 months of oral contraceptive use. In the 2nd group low density lipoprotein levels were significantly lower 3 and 6 months after withdrawal, in comparison with the basal values of the 1st group. It is concluded that low dose oral contraceptives supplied by the Indian government have no significant effect on serum lipids after 6 months of use.
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PMID:Effect of administration and withdrawal of oral contraceptive pills on serum lipids and lipoproteins. 316 63

To further understand the pathophysiology of arterial diseases induced by oral contraceptives (OCs), a case report is presented of a young woman who died of extensive visceral artery thrombosis. The possible role of estrogens and progestogens and of cigarette smoking as the predisposing factors in this patient are discussed. A 26-year-old woman, who complained of progressive abdominal pain and whose past medical and surgical history was negative, was admitted to the general surgery service. She was the mother of 1 child and had had 2 previous spontaneous abortions. She had received ethinyl estradiol 35 mcg with norethindrone 500 mcg and 1000 mcg for 3 months, but because of a problem with breakthrough bleeding the medication was changed to mestranol 50 mcg with norethindrone 1000 mcg. She had been taking Ortho-Novum 1/50 for 2 1/2 years. She had smoked 25-35 cigarettes daily for about 10 years but denied use of alcohol or other drugs. She was not known to be diabetic, hypertensive, or dyslipidemic, and had no history of atherosclerosis in her family. For 7 months prior to her admission, the patient complained of abdominal pain, which progressively increased in intensity and duration, interrupted by periods of well-being. The patient reported 2 recent, isolated episodes of mild proctalgia but no tenesmus or melena. There had been no fever, but the patient had been anorexic for the past 2 weeks and reported losing 10 kg in the past month. She had no complaints apart from those related to the gastrointestinal system. At an emergency laparotomy, gangrenous acalculous cholecystitis and infarction of the terminal ileum were discovered. A cholecystectomy with resection of the terminal ileum and the right colon was performed. An end-to-end primary anastomosis was performed. On exploration of the superior mesenteric artery, a thrombus was discovered at its origin. As a transverse arteriotomy showed a good retrograde flow, a thrombectomy was performed. There appeared to be an unsatisfactory antegrade flow. The superior mesenteric artery then was transposed in an end-to-end fashion on the abdominal aorta. An immediate postoperative arteriogram showed thrombosis of the celiac axis at its origin. Revascularization failed to improve the condition of the intestine. The patient died. The intent of this case report is to emphasize that the association between smoking and oral contraceptives can cause cardiovascular disease in young women, and a failure to recognize this association can result in delayed diagnosis and worsen the prognosis.
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PMID:Intimal hyperplasia and thrombosis of the visceral arteries in a young woman: possible relation with oral contraceptives and smoking. 337 98

The endogenous lipoprotein system (very low-density lipoprotein [VLDL], intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL] cascade) holds the key to understanding the mechanisms by which hormones, diet, and drugs interact to regulate the plasma cholesterol level. Crucial components of this system are hepatic LDL receptors that mediate the uptake and degradation of plasma LDL. With experimental animals, it has been possible to demonstrate that hepatic LDL receptors are sensitive to hormonal, dietary, and pharmacologic manipulation. The decrease in number of hepatic LDL receptors in hypothyroidism or after cholesterol feeding leads to elevation of plasma LDL cholesterol levels. Conversely, the increase in number of hepatic LDL receptors results in lowering of plasma LDL cholesterol levels. This can be observed in hyperthyroidism, during administration of pharmacologic doses of 17 alpha-ethinyl estradiol, or during treatment with cholesterol-lowering drugs such as the bile acid-binding resins and cholesterol-synthesis inhibitors. Since cholesterol excretion from the body occurs via the liver, the increased efficiency of disposal of plasma cholesterol by increasing hepatic LDL receptors will ultimately lead to depletion of excessive body cholesterol. Pharmacologic regulation of hepatic LDL receptors should be a valuable tool in the prevention and therapy of atherosclerosis.
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PMID:Regulation of plasma cholesterol by hepatic low-density lipoprotein receptors. 354 61

The effect of a combined treatment with ethinyl estradiol and norethisteron for height reduction on serum lipids and lipoproteins was investigated in 23 excessively tall girls (greater than 97th percentile). Serum cholesterol, triglycerides, HDL-C and LDL-C were determined before and 3, 6, 9 and 12 months after the onset and 3 to 12 months after cessation of therapy. Treatment with ethinyl estradiol and norethisteron resulted in significant (p less than 0.01) mean increases in serum cholesterol, triglycerides, HDL-C, and LDL-C of 20.6%, 95.5%, 23.6%, and 22.2% above pretreatment values, respectively. This increase occurred during the first 3 months of therapy and thereafter no further significant change was observed. After cessation of therapy elevated levels returned to pretreatment levels within 3 to 12 months in all but two patients. The results obtained suggest an influence of ethinyl estradiol and norethisteron on serum lipids and lipoproteins. Whether these reversible changes of serum lipids and lipoproteins are associated with an increased risk for developing atherosclerosis has to be evaluated in long term investigations.
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PMID:Increase of serum lipids and serum lipoproteins in girls under therapy with estrogen and norethisteron for height reduction. 360 68

Concern about a possible association between oral contraceptives (OCs) and cardiovascular problems has led to investigation of the effects of OC use on plasma lipids and lipoproteins. The lipoprotein metabolic system involves chylomicrons derived from dietary fat, very-low-density lipoproteins (VLDL) derived primarily from the liver, and high-density lipoproteins (HDL). VLDLs form remnantlike particles termed intermediatedensity lipoproteins (IDLs), which ultimately are converted to low-density lipoproteins (LDLs). Understanding of how these particles relate to the atherogenic process is incomplete, although the spectrum of VLDL-LDL particles is involved in atherosclerosis. Whereas the LDLs and IDLs can deliver cholesterol to the artery wall, the HDLs seem to be involved in bidirectional cholesterol transport and are capable of accepting cholesterol from tissues and other lipoprotein classes. This property has caused HDL to become known as an antiatherogenic lipoprotein. Estrogen appears to increase VLDL production rates as well as the clearance of remants and LDL, although genetic factors may be involved. Estrogen's effect on HDL seems to be a more uniform increase in production. In contrast, synthetic progestational steroids appear to reduce HDL, in part due to the increased metabolism of HDL lipids mediated by hepatic lipase activity. They appear to interact with estrogen to raise LDL and VLDL levels. Epidemiologic studies suggest that low- and high-density cholesterol provide the best clinical indices of cardiovascular risk. When the HDL level is low, coronary risk amplifies; when the HDL level is high, the LDL effect on coronary risk compresses. There is as yet no precise information on the extent to which changes in lipoproteins, especially HDL, affect the development or progression of coronary artery disease.
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PMID:Effects of oral contraceptives on lipid metabolism. 372 87

Estrogen replacement therapy (ERT) is the most effective treatment for vasomotor hot flushes and urethrovaginal atrophy in postmenopausal women. Evidence also suggests that ERT delays osteoporosis and may even reduce the risk of atherosclerosis. Despite continuing controversy, the risks of ERT are now considered minimal. With individualized therapy and appropriate monitoring, ERT with progestin supplements appears to be safe and effective for the great majority of postmenopausal women.
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PMID:Is estrogen replacement therapy necessary? 407 11

Endogenous sex hormone activity results in higher levels of VLDL, LDL, and apo B in males than in females, while HDL and particularly HDL2, and apo A1 levels are lower, apo A2 being reduced to a lesser degree. This sex-related difference appears progressively during puberty. There is increasing elevation of LDL cholesterol, apo B, and VLDL TG in women at the menopause, HDL cholesterol levels either diminishing or remaining constant. These differences in lipoprotein and apoprotein concentrations probably play a major role in protecting women against atherosclerosis development during the period of gonadal activity. Similar differences are provoked by exogenous hormone activity: the androgens increase LDL cholesterol and reduce HDL cholesterol, and total cholesterol is therefore only slightly altered. Estrogens provoke elevation of VLDL TG only at supraphysiological doses of the order of 30-50 mcg ethinyl estradiol. In contrast, reductions in LDL cholesterol and increases in HDL cholesterol occur even after low physiological doses of estrogens. This latter increase is dose-related and can be as high as 20%. The action of progestogens is less clearly defined and depends on the molecule administered, the dosage, and its possible androgenic action. When the latter activity is marked, lipoprotein and apoprotein variations are similar to those resulting from testosterone effects. The influence of sex hormones on the course of idiopathic hyperlipidemias varies. They may have a beneficial effect, but this is a fairly rare event and occurs only in very precise situations: improvement of type 3 hyperlipidemia by low dose estrogen therapy; improvement of moderate isolated hypercholesterolemia in menopausal women with low doses of estrogens, and improvement of type 5 mixed hypertriglyceridemia by certain progestogens such as oxandrolone. They usually produce the opposite effect, however, with marked increases of type 1, 4, and 5 hyperlipidemia under estrogens, sometimes leading to attacks of pancreatitis and elevation of preexisting hypercholesterolemias or mixed hyperlipidemias resulting in vascular accidents due to thrombosis. (author's modified)
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PMID:[Sex hormones and metabolism of lipoproteins]. 634 27

Oral contraceptives containing DL-norgestrel or norethindrone with ethinyl estradiol were administered by random assignment to 21 menstruating women, matched for anthropometric measurements, age, diet, alcohol consumption, smoking, and exercise habits. Pretreatment and 7-week treatment blood samples were obtained and assayed for serum cholesterol, triglyceride high-density lipoprotein cholesterol (HDL-C), and total high-density lipoprotein (HDL), HDL2a, HDL2b, and HDL3 subclasses by analytic ultracentrifugation. Subjects using the norethindrone oral contraceptive had a significant increase in HDL-C: baseline, 46 mg/dl; 7 weeks, 51 mg/dl. Values for the subjects using the norgestrel oral contraceptive were not significantly changed: 46 and 44 mg/dl, respectively. Users of the norethindrone oral contraceptive had significant elevations of total HDL and HDL3, while norgestrel oral contraceptive users demonstrated no significant changes. HDL2b increased with the norethindrone oral contraceptive and declined with the norgestrel oral contraceptive. The changes in HDL2b from baseline to treatment were not significant (p greater than 0.05), but the change with the norethindrone oral contraceptive did differ significantly from that with the norgestrel oral contraceptive (p less than 0.02). These changes may indicate oral contraceptive-induced alterations in HDL structure and metabolism that could be related to the risk of development of atherosclerosis.
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PMID:Effects of two low-dose oral contraceptives on serum lipids and lipoproteins: differential changes in high-density lipoprotein subclasses. 640 27

The incidence of cardiovascular disease is lower in women than in men, but is raised in men with prostatic cancer treated with estrogens. Changes of the plasma lipoproteins are related to the development of ischaemic cardiovascular disease and can be brought about by hormonal treatment. We have therefore studied plasma lipoproteins during estrogen treatment and after orchidectomy. 16 patients with prostatic carcinoma were treated with ethinyl estradiol daily by mouth and polyestradiol phosphate intramuscularly once a month. 15 other patients were treated by bilateral orchidectomy. Cholesterol (C), triglyceride (TG), and phospholipid (PL) concentrations in plasma and in the very low density (VLDL), low density (LDL) and high density lipoprotein (HDL) fractions were determined before starting treatment and 2 weeks and 8 weeks later. In the estrogen treated group the mean plasma C concentration decreased by 14 and 10%, while the mean HLD-C increased by 23 and 53%, and the mean LDL-C decreased by 24 and 25% at 2 and 8 weeks respectively. The mean PL concentration in HDL increased by 36 and 79% while that in LDL decreased by 12 and 18%. The mean plasma TG concentration was increased by 36 and 46%, mainly reflecting a rise of TG in the HDL-LDL fraction. Orchidectomy created only slight changes of plasma lipids. After 8 weeks the mean C concentration in plasma was raised by 10% and the mean PL concentration by 11%, owing to a 13% rise in the mean HDL-PL level. The changes in plasma lipoprotein pattern created by high doses of estrogens are mainly thought to protect against the development of atherosclerosis. The slight changes that take place after orchidectomy can hardly affect the incidence of cardiovascular disease.
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PMID:Plasma lipoproteins during anti-androgen treatment by estrogens or orchidectomy in men with prostatic carcinoma. 726 28

On the basis of clinical observations suggesting interactive effects of biliary obstruction and estrogen therapy on plasma cholesterol levels, a prospective study of the effect of ethinyl estradiol on plasma lipid levels was carried out in a patient with total biliary obstruction. A daily dose of 50 micrograms of ethinyl estradiol raised the plasma free cholesterol concentration from 265 mg/dl to 550 mg/dl over a period o 3 weeks; there was no change in plasma ester cholesterol concentration. Withdrawal of the estrogen was followed by a fall to baseline of the free cholesterol concentration over a 45-day period; once again there was no change in ester cholesterol. Plasma phospholipid concentration rose and fell in direct proportion to the changes in free cholesterol; plasma triglyceride concentration was unaffected by the estrogen. To account for the results of this study, it is suggested that the already elevated plasma levels of lipoprotein-X in biliary obstruction are further elevated by estrogen administration.
Atherosclerosis 1981 Oct
PMID:Selective elevation of plasma free cholesterol concentration by administration of estrogen in the presence of total biliary obstruction. 730 54


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