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

Several recent studies have confirmed the pathogenic effect of endogenous hypertriglyceridaemia (type IV) on atherosclerosis and thrombosis. Our understanding of the pathophysiological mechanism involved in these hypertriglyceridaemias is constantly improving. Iatrogenic hypertriglyceridaemia can be caused by several classes of drugs including synthetic oestrogens, especially the oestrogen-progesterone contraceptives, and to a lesser extent natural oestrogens taken orally as replacement treatment during menopause, certain hypotensive drugs (non-cardioselective beta-blockers and thiazidic diuretics), corticosteroids, retinoids, cyclosporine, enzyme inductors and iodine produces (by iodine-induced hypothyroidism). All these situations should be recognized and when high lipid levels are observed treatment protocols should be modified or interrupted. Whether associated with a rise or a fall in cholesterol-LDL, such conditions should always taken into consideration due to the increased risk of atherosclerosis, thrombosis or even acute or subacute pancreatitis.
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PMID:[Iatrogenic hypertriglyceridemia]. 876 85

Hypothyroidism promotes both significant diastolic hypertension and hypercholesterolemia and, as a consequence, their combination has been suggested to accelerate atherosclerosis. Prevalence of elevated LDL-cholesterol is significantly increased not only in overt hypothyroidism, but also in subclinical hypothyroidism. Serum TSH will be determined in all the patients, as a first line test and only the patients with TSH values over 5 microU/ml will be further investigated: serum T4, FT4 and antimicrosomal and antithyroglobulin antibodies. In the study group were not included severe nonthyroid illness, major depression, untreated Addison's disease and the patients using some drugs that interfere with serum TSH level.
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PMID:Overt and subclinical hypothyroidism and atherosclerotic arteriopathy of the lower limbs (clinical and subclinical). 817 76

Large-scale and systemic epidemiological, pathological and experimental studies emphasized and documented the childhood origin of atherosclerosis. There is increasing consensus that lipid levels in children to a large extent determine the rate of coronary artery disease (CAD) in the adult population. Minimal sudanophilic intimal deposits, and the presence of intracellular and extracellular lipid, and a slight increase in interstitial ground substance in 3 years of age or older patients are found. In the Bogalusa Hearth Study aortic fatty streaks were strongly related the antemortem levels of both total cholesterol and low-density lipoprotein cholesterol (LDL-C) independent of race, sex, and age, and were negatively correlated with the ratio of high-density lipoprotein (HDL-C) to low-density plus very-low-density lipoprotein cholesterol (LDL-C+VLDL-C). The potential for primary prevention is real and the strongest piece of evidence for its is the remarkable trend in CHD mortality rates in recent times, rapidly downward in many western countries. A number of factors influence plasma levels of lipid and lipoproteins in newborn, in infants, in children and adolescents and their relevance as possible predictors of adult coronary artery disease. They are certain inherited disorders of dyslipoproteinemia (familial hypercholesterolemia, familial combined hyperlipidemia, hyperapobetalipoproteinemia, and hypoalphalipoproteinemia) and secondary causes of hyperlipidemia (congenital biliary atresia, glycogen storage diseases, hypothyroidism, diabetes mellitus and nephrotic syndrome, etc).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atherosclerosis and juvenile dyslipidemias]. 818 5

The hormonal system is a communication system between cells and organs. Hence it is not surprising that it influences almost all physiological functions and, at least partially, our behaviour and fate. The sexual phenotype is determined by the sex hormones. Normally, the phenotype is in accordance with gonadal and genetic sex, but occasionally, as a consequence of enzymatic defects in the biosynthesis of sex hormones or of androgen resistance, gonadal and genetic sex are in discordance with the phenotype, the latter determining generally the civil sex and the sex of rearing. Whereas the gender role is generally determined by the sex of rearing and the phenotype, itself under hormonal influence, homo- and transsexuality constitute notorious exceptions to this rule. Although several authors consider homo- and transsexuality to be the consequence of an impairment in androgenic impregnation in the perinatal period, there are at present no convincing arguments for an hormonal origin for either homo- or transsexuality, although such a possibility can't be excluded either. Besides their role in psychosexual behaviour, sex hormones play also a role in our life expectancy. Indeed, although maximal life expectancy of man is genetically determined, a major determinant of individual life expectancy is cardiovascular pathology. The latter is partly responsible for the difference in life expectancy between men and women, cardiovascular mortality increasing rapidly at menopause and being halved by oestrogen replacement therapy. Also atherogenesis as such is, to a large extend, under hormonal control. Indeed insulin resistance and hyperinsulinism, which develop as a corollary of the aging process, is an important cause of atherosclerosis as well as of hypertension. Other hormones also play an important role in our behaviour. We can mention here the role of the thyroid hormones in the physical and mental development of children as well as in the regression of the intellectual functions in hypothyroidism; the role of growth (and sex) hormones in the clinical symptomatology of aging; the memory enhancing effects of the antidiuretic hormone; the role of growth factors (as well as of sex hormones) in tumorigenesis; the role of corticoids (and sex hormones) in the modulation of immunological processes etc. In brief, hormones influence all aspects of our life.
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PMID:[Do hormones determine our fate?]. 820 84

Secondary causes of hyperlipidemia are important to recognize. In fact, hyperlipidemia may be a clue to the presence of an underlying systemic disorder. It may greatly heighten the risk of atherosclerosis with a raised LDL-c, triglyceride-rich lipoprotein excess, and increased lipoprotein(a) as well as lowered HDL-c. The search for secondary causes may provide a clue as to why patients with primary lipid disorders suddenly develop worsening lipid profiles. The point is a crucial one because some acquired causes of hyperlipidemia, such as alcohol, estrogens, steroids, or pregnancy, when superimposed on a primary familial form of hypertriglyceridemia can result in a saturated removal system and a buildup of chylomicrons, which can lead to life-threatening pancreatitis. A convenient way to remember secondary causes is to think of the four D's of diet, drugs, disorders of metabolism, and diseases. Although diets rich in saturated fats and cholesterol are a common cause of the mild hypercholesterolemia seen in our society, alcohol excess and weight gain can explain much of the tendency toward hypertriglyceridemia. Interestingly anorexia nervosa has long been associated with severe but reversible hypercholesterolemia. Several classes of drugs need to be considered as common causes of altered lipid profiles. Glucocorticoids and estrogens elevate triglycerides and raise levels of HDL-c. Anabolic steroids taken orally markedly reduce levels of HDL-c in contrast to injectable testosterone, which does not adversely affect the LDL-to-HDL ratio. Oral contraceptives affect atherosclerotic risk depending on the kind and doses of progestin/estrogen. In those with an underlying primary hypertriglyceridemia and associated obesity, estrogenic medications can depress triglyceride removal mechanisms, leading to the chylomicronemia syndrome and pancreatitis. Antihypertensives have variable effects on lipids and lipoproteins. Although short-term thiazide usage raises cholesterol, triglycerides, and LDL-c, long-term usage is not necessarily associated with significant alterations in lipid levels. Alpha blockers may cause an increase in HDL-c, whereas beta blockers raise triglycerides and lower HDL-c. Sympatholytics, angiotensin converting enzyme inhibitors, and calcium channel blockers are essentially lipid neutral. Retinoids can be associated with increased LDL-to-HDL ratios and occasionally striking elevations in triglycerides. Cyclosporine raises LDL-c and lipoprotein(a). Classes of drugs that may raise HDL-c include cimetidine, antiepileptic drugs, and tamoxifen, but the effect may be seen primarily in women. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered. A thyroxine and TSH level should be obtained on all new cases of clinically important hyperlipidemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Secondary causes of hyperlipidemia. 828 27

Hyperlipidemia is first detected by an increase in the plasma concentrations of cholesterol and/or triglycerides, and implies an abnormality of plasma lipoprotein metabolism. Disorders of lipoprotein metabolism are often classified specifically according to the lipoprotein affected. The WHO classification of lipoprotein phenotypes is a useful means of showing which lipoproteins are present in excess in individual hyperlipidemic patients. Hyperlipoproteinemia can be secondary to other well-known diseases that affect plasma lipoprotein metabolism, for example, diabetes mellitus, hypothyroidism or nephrotic syndrome. When such diseases are excluded, the hyperlipoproteinemia is defined as primary hyperlipoproteinemia. Many primary hyperlipoproteinemias have a genetic basis and the underlying molecular defect has been clarified in some genetic disorders. Hyperlipoproteinemia is considered to be one of the major risk factors for atherosclerosis and the development of atherosclerosis depends on the type of hyperlipoproteinemia. In this sense, familial hypercholesterolemia is a clinically important primary hyperlipoproteinemia because of its high risk of ischemic heart disease and its high prevalence in a normal population (1/500). It is necessary to make an exact diagnosis of specific genetic disorder, if possible, to provide prognostic and therapeutic information.
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PMID:[Primary hyperlipoproteinemia]. 841 90

It has been demonstrated that high cholesterol levels are correlated with development of atherosclerosis, while high levels of high density lipoprotein (HDL) are associated with reduced cardiovascular mortality. Some endocrine disorders accelerate atherosclerosis in association with hypercholesterolemia, hypertension, low level of HDL and hypertriglyceridemia. In patients with acromegaly, hypertriglyceridemia is sometimes accompanied with and aggravated by the presence of impaired glucose tolerance. In patients with hypothyroidism, coronary atherosclerosis may develop in association with hypertension, hypercholesterolemia and moderate elevation of triglyceride which is often accumulation of intermediate lipoprotein. Cushing syndrome may accelerate atherosclerosis by the fact that corticosteroid may induce or exacerbate several known coronary risk factors including hypertension, hypercholesterolemia and impaired glucose tolerance. Estrogen has beneficial effects on the cardiovascular system for postmenopausal women by affecting lipid metabolism, decrease of LDL and increase of HDL.
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PMID:[Atherosclerosis and endocrine disorders]. 841 91

Thyroid hormones may exert cardiovascular actions by direct effects on the myocardium, by interacting with the sympathetic nervous system and through alterations of the peripheral circulation. Then, thyroid hormones increase myocardial contractility and relaxation, sensitise the myocardium to sympathetic nervous system and decrease arterial resistance. Hyperthyroidism results in an enhanced myocardial contractility, an increased cardiac output and a fall in systemic vascular resistance. Nevertheless "high output" cardiac decompensation may occur. Thyrotoxicosis may trigger arrythmia and disease seems to be associated with an increase in the frequency of mitral valve prolapse. Even in mild or subclinical hyperthyroidism complication may occur. Sympathetic blocking agents are the treatment of choice in addition to aetiologic treatment. Hypothyroidism is associated with bradycardia, a decreased cardiac output, increased vascular resistance and perhaps a decreased sensitivity of the sympathoadrenal system. An increase in cholesterolemia leads to an additional risk for the development of atherosclerosis. Main cardiovascular complications of hypothyroidism are angina pectoris, diastolic hypertension, atrio-ventricular blocks or pericarditis. Mild hypothyroidism might also be correlated with an increase in adverse effects.
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PMID:[Heart and thyroid]. 859 89

Genetic hepatic lipase (HL) deficiency is associated with low density lipoprotein (LDL) rich in triglycerides (TG), whose affinity for B:E receptors is decreased. In rats, experimental hypoinsulinemia produces HL deficiency. However, the relation between human insulin-dependent Diabetes Mellitus (IDDM), HL activity and the characteristics of LDL have not been studied. The objective of our study is to evaluate the relation between HL activity and the chemical composition of LDL in treated IDDM patients. Subjects were 15 IDDM patients and 15 controls (C), matched for sex and body mass index (BMI). The IDDM patients were classified by the WHO criteria, were free of nephropathy and hypothyroidism, and received no medication except insulin. Controls were clinically healthy and normolipidemic with no family history of diabetes. The IDDM group was divided into two subgroups: subgroup IDDM-A (n = 9) with HL values > or = 4.3 and IDDM-B (n = 6) with HL < or = than 4.2 mumoles glycerol/ml h. the HL in IDDM was lower than in C (p < 0.001). Table 1 shows clinical data. Blood samples were drawn after 12 h fasting. Percentage of HbA1c and plasma concentrations of glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol and TG were assayed. LDL was separated by sequential ultracentrifugation at densities of 1.019-1.063 g/ml and its chemical composition was analyzed. The most relevant results were: plasma TG concentration was higher in IDDM than in C (p < 0.05) (Table 2), although average values DMID not exceed the reference values of 200 mg/dl. The TG-LDL were higher in IDDM than in C: 24.8 +/- 2.7 vs 17.5 +/- 1.1 mg/dl plasma, media +/- SE, (p < 0.02). This difference reflected the values of IDDM-B, whose plasma concentrations of TG-LDL were higher than in C: 32.3 +/- 3.6 vs 17.5 +/- 1.1 mg/dl (p < 0.001), and also higher than in IDDM-A (p < 0.02). (Table 3). The chemical composition of LDL in IDDM-B contained a higher percentage of TG than C: 8.5 +/- 0.7 vs 6.8 +/- 0.3% (p < 0.05), a lower percentage of cholesterol than IDDM-A: 39.0 +/- 1.7 vs 45.2 +/- 2.2% (p < 0.05) and also a larger percentage of proteins than IDDM-A: 28.9 +/- 1.9 vs 20.8 +/- 1.0% (p < 0.01). The correlations between TG/cholesterol and HL activity in IDDM were r = -0.53 (p < 0.05) and in IDDM-B, r = -0.81 (p = 0.05). The noteworthy result of this study is the modification of the LDL particle in IDDM, rich in TG in patients with low HL activity. Anomalies in the chemical composition of LDL like those described decrease the uptake of this particle by its physiological B:E receptors. It has recently been demonstrated that LDL is an indisoluble association of lipids and apoproteins, and that both act simultaneously to hold the apoB in a spatial position that expresses normal epitopes. It has been described that particles of LDL rich in TG and poor in cholesterol, shows low affinity for LDL receptors in human fibroblasts. Also in IDDM the interaction of LDL rich in TG with B:E receptors is decreased. This might be one more mechanism contributing to the accelerated atherosclerosis of these patients. Our results suggest that there may be a threshold of HL activity for the complete hydrolysis of the TG of LDL, for the normalization of the TG/cholesterol relation and for the conformation of typical LDL particles.
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PMID:[Low density lipoprotein rich in triglycerides and hepatic lipase activity in insulin-dependent diabetic patients]. 872 71

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.
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PMID:Secondary hypertension: evaluation and treatment. 894 19


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