Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease remains the major cause of death in the industrialized world with dyslipidemia, hypertension and cigarette smoking leading a long list of risk factors. Recently, controversy arose from some critical articles expressing concern about the evaluation and interpretation of statistical data of epidemiologic studies. One study using covariance analysis reported an absence of the widely accepted negative association between coronary heart disease (CHD) and high density lipoprotein (HDL) cholesterol. Also criticism was expressed regarding the cost-effectiveness of preventive measures such as the use of lipid lowering drugs on life expectancy. Because of such recent scientific controversy and discussions already taking place in the media, we have summarized in this article recent epidemiologic evidence including a meta-analysis of the major epidemiologic studies on HDL. We have directed particular attention to 3 large epidemiological studies, i.e., the Familial Atherosclerosis Treatment Study (FATS), the Program on the Surgical Control of the Hyperlipidemias (POSCH), and the Cholesterol Lowering Atherosclerosis Study (CLAS), all of which have clearly demonstrated a desirable effect of intensive lipid lowering therapy on coronary lesions.
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PMID:[Risk factors for coronary heart disease]. 194 9

The aim of this paper was search for possible relationship between cholesterol and phospholipids in erythrocyte++ membrane and pathological entities i.e. hypertension and dyslipidemia. Both are the main risk factors of atherosclerosis and in both condition disturbances at the cell membrane level were detected. 124 persons (both men and women in a age group 20-59), employees of industrial enterprise were included into study. Standard questionnaire was performed as well as body weight and height, blood pressure, biochemical tests-lipids, cell membrane lipids serum and intracellular electrocytes as well as 24 h electrolyte urine excretion. The following findings were reported: cell membrane cholesterol concentration correlates with sex, age, body weight, systolic and diastolic blood pressure and triglycerydes HDL-cholesterol and serum phospholipids. The biggest influence on cholesterol concentration in cell membrane have the following factors: sex, age and serum triglycerides. The most important finding was that the lipid metabolism disturbances has impact on triglyceride elevation in serum and that arterial hypertension is connected with decreased cholesterol concentration in erytrocyte membrane.
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PMID:[Cholesterol and phospholipid levels in erythrocyte membrane of patients with blood lipid disorders and hypertension]. 209 42

The serum lipoprotein Lp(a) concentration was measured in 1065 individuals in order to assess whether there was a relation between the type of dyslipidemia and the level of Lp(a). Males and females, aged between 2 and 83 years old, were included in the study. Quantification was performed by an immunonephelometric technique. The whole population was divided into normolipidemic (NL), type IIa without xanthoma (type IIa), type IIa with xanthoma (FH), type IIb and type IV phenotypes. Lp(a) level was arbitrarily divided into 5 subclasses in each group of dyslipidemia and in the normolipidemic group. In addition each group was divided according to sex and whether or not they were under treatment. We observed a significant difference between the median Lp(a) level of the normolipidemic group (NL) and of the dyslipidemic group as a whole. Median Lp(a) levels in the 4 dyslipidemic groups did not differ significantly. Sex, age and treatment did not influence the distribution of Lp(a) values distribution. Only weak correlations (Spearman's rank test) were observed between Lp(a) and other lipid parameters (total cholesterol, LDL, apo B, HDL, triglycerides): the highest correlation (r' = 0.15) was between Lp(a) and apo B. We conclude that Lp(a) level is not influenced by the type of dyslipidemia, sex or hypolipidemic drugs.
Atherosclerosis 1990 Nov
PMID:Lp(a) levels in different types of dyslipidemia in the French population. 214 72

Atherosclerosis and its various clinical manifestations are now highly predictable and preventable diseases. Dyslipidemia appears to be a necessary cause, and hypertension and cigarette smoking are both powerful and modifiable contributing causes. Health professionals should incorporate cardiovascular risk assessment and risk factor modification within the context of their delivery of personal health services. Such services probably already have contributed to the decline of cardiovascular mortality, and the current levels of risk factors in the United States population indicate that substantial further reduction should be possibly by creating a smoke-free environment by the year 2000 and by implementing the recommendations of the National Cholesterol and High Blood Pressure Education Programs.
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PMID:Cardiovascular risk factors. 218 65

Coronary heart disease is the leading cause of death among patients with non-insulin-dependent diabetes mellitus (NIDDM). NIDDM patients have a high frequency of dyslipidemia, which along with obesity, hypertension, and hyperglycemia may contribute significantly to accelerated coronary atherosclerosis. Because risk factors for coronary heart disease are additive and perhaps multiplicative, even mild degrees of dyslipidemia may enhance coronary heart disease risk. Therefore, therapeutic strategies for management of NIDDM should give equal emphasis to controlling hyperglycemia and dyslipidemia. The National Cholesterol Education Program recently issued guidelines for treatment of hyperlipidemia in adults including diabetic patients. Because of the unique features of diabetic dyslipidemia, however, we suggest that certain modifications in these guidelines be made to meet specific needs of diabetic patients. For example, therapeutic goals for serum cholesterol reduction should be lower in diabetic patients than in nondiabetic subjects. Particular emphasis should be given to weight reduction in NIDDM patients. In some diabetic patients, monounsaturated fatty acids may be a better replacement for saturated fatty acids than carbohydrates. The target for cholesterol lowering should include both very-low-density lipoprotein and low-density lipoprotein (LDL) (non-high-density lipoprotein) rather than LDL alone. To obtain a substantial reduction of cholesterol levels, drug therapy may be required in many patients. However, first-line drugs for nondiabetic patients (nicotinic acid and bile acid sequestrants) may be less desirable in NIDDM patients than hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors and even fibric acids. In fact, HMG CoA reductase inhibitors may be the drugs of choice for NIDDM patients with elevated LDL cholesterol and borderline hypertriglyceridemia, whereas gemfibrozil appears preferable for NIDDM patients with severe hypertriglyceridemia.
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PMID:Management of dyslipidemia in NIDDM. 219 Jul 70

Dyslipidemias are frequent in diabetic subjects: they increase the risk for atherosclerosis, in addition to the risk of diabetes mellitus per se. The pathogenesis of dyslipidemias differs between type I and type II diabetes: untreated type I diabetic subjects demonstrate frequently increased triglyceride concentrations due to diminished removal of triglyceride-containing particles, as a result of diminished activity of lipoprotein lipase. In addition, more triglycerides are produced due to increased lipolysis and increased free fatty acid supply to the liver. Type II diabetic subjects demonstrate very low density lipoprotein (VLDL) over-production due to obesity, insulin resistance and caloric overconsumption. In addition, triglyceride removal may be diminished due to diminished lipoprotein lipase activity when diabetes mellitus is poorly controlled. In addition, high density lipoprotein (HDL) is frequently lowered. During decompensation low density lipoprotein (LDL) concentrations may also increase. LDL particle composition is frequently abnormal. A severe dyslipidemia in diabetes mellitus is frequently a combined effect of diabetes mellitus and a congenital lipoprotein abnormality. The evaluation and treatment of dyslipidemias in diabetic subjects should be performed similarly to non-diabetics according to the guidelines published recently by the Working Group 'Lipids' of the Swiss Foundation of Cardiology. Additional accents in diabetic subjects are necessary. It is recommended that serum cholesterol, triglycerides and HDL are determined in every patient when diabetes mellitus is diagnosed. If serum cholesterol is greater than 6.5 mmol/l and the cholesterol/HDL-ratio is greater 6.5, dietary treatment should be reinforced; if its effect is insufficient, drug therapy should be considered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dyslipidemia in diabetes mellitus: significance, diagnosis and treatment]. 223 46

Hypercholesterolemia and increased concentrations of an apolipoprotein E (apoE)-containing HDL subclass, high density lipoprotein1 (HDL1) have been observed in streptozocin-alloxan diabetic dogs consuming normal amounts of dietary cholesterol. The aim of this study was to characterize the response of HDL1 and its targeting ligand, apoE, to insulin and HMG-CoA reductase inhibitor treatment in pancreatectomized diabetic dogs. Following induction of diabetes, plasma total cholesterol, HDL1, and apoE concentrations were all increased. Urinary mevalonate excretion, an index of cholesterol synthesis in humans, was 6-fold that of nondiabetic controls. Lipoprotein fractionation by Pevikon block electrophoresis and gel filtration chromatography showed that the increased cholesterol and apoE were associated with alpha 2-migrating particles corresponding to HDL1. Insulin treatment, resulting in near normal fasting blood glucose concentrations in the group as a whole (average 5.1 mM, 92 mg/dl), led to variable reductions in apoE, total plasma cholesterol, and HDL1. Uncorrected dyslipidemia during intensified insulin treatment appeared to be related to failure to achieve euglycemia. Despite unremitting hyperglycemia, treatment with lovastatin resulted in pronounced decreases in plasma cholesterol, HDL1 and apoE to concentrations below those observed in nondiabetic animals. Mevalonate excretion also fell, but remained twice normal. Thus neither modality corrected all of the abnormalities in canine diabetic dyslipidemia. Since apoE-containing HDL1 may mediate cholesterol traffic between the periphery and the liver (reverse cholesterol transport), the present observations suggest that increased cholesterol synthesis is accompanied by parallel abnormalities in cholesterol flux through the reverse transport pathway in the canine model.
Atherosclerosis 1990 Sep
PMID:Plasma apolipoprotein E, high density lipoprotein1 (HDL1) and urinary mevalonate excretion in pancreatectomized diabetic dogs: effects of insulin and lovastatin. 224 16

Genetic factors play an important role in the development of many common diseases of adulthood that result in early morbidity and mortality. Prevention of these disorders and their sequelae is best established through early detection and early intervention. Although it may be feasible to screen the entire population for some disorders (e.g., hypertension), this approach would be expensive and impractical for others (e.g., colon cancer). The family history provides an inexpensive and convenient method of identifying families at risk for premature diseases of adulthood. Family screening for a disorder should be recommended if there is increased risk for the disorder among family members, if screening methods are available to detect the condition at an early age or preclinical stage, and if early intervention will alter the course of the disease. For many disorders screening and intervention can prevent the occurrence of clinical disease. The prenatal counseling session affords an ideal setting for identifying families at risk for diseases of adulthood with major genetic components. By reviewing the family history, key family members can be identified and investigated, in order to establish a specific genetic diagnosis. At-risk relatives can then be counseled and screened for the disorder preclinically and premorbidly. The screening and intervention available for a disease depends on the nature of the disorder, our understanding of its physiology and etiology, and our current technology. The disorders discussed earlier are typical of conditions of adulthood that are influenced strongly by genetic factors, especially when they appear in younger adults. Atherosclerosis, colon cancer, and diabetes are complex phenotypes. Each can be caused by single-gene defects, but commonly the genetics are more complex. Empiric data help to establish the risk to an individual in the latter cases. In all three examples, early detection should lead to treatment, which can prevent more serious sequelae: by treating the dyslipidemia, coronary artery disease can be prevented; by removing the benign polyp, malignant cancer can be avoided; and when impaired glucose tolerance is detected, diet and exercise can prevent or delay frank diabetes and its complications. The complete evaluation of individuals at risk for disorders such as those in Table 1 and their families can be a complicated task. Referral to a center experienced in the genetics of common diseases often may be necessary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetics of common diseases of adulthood. Implications for prenatal counseling and diagnosis. 228 33

The diagnosis of intestinal ischaemia still presents numerous problems in terms of nosography, epidemiology, diagnosis and treatment with the result that it is more often excluded than diagnosed. The aim of the present study was to discover whether intestinal ischaemia was clinically identifiable by any specific early signs and symptoms and whether there were any concomitant risk factors. The medical reports on 44 patients consecutively admitted to the San Giovanni Battista Hospital, Turin in 1985-86 with suspected intestinal ischaemia were therefore examined. It was found that intestinal ischaemia was only occasionally (30% of cases) diagnosed at the onset of clinical symptoms. In the 10 patients with ischaemic colitis, the risk factor linked to the causes of the disease was systemic hypovolaemia arising in diffuse atherosclerosis. In the 8 cases of chronic ischaemia and the 26 of intestinal infarction the remote anamnesis revealed symptoms that should have aroused suspicion of intestinal ischaemia partly because the patients were suffering from widespread atherosclerosis. In fact a review of the risk factors for the onset of atherosclerosis (i.e. high blood pressure, smoking, dyslipidemia, obesity and age over 65) revealed that about 60% of the patients under study presented 3 or 4 them simultaneously. To conclude, the data emerging from the study indicate the existence of symptoms and risk factors to diffuse atherosclerosis that should permit the early diagnosis of intestinal ischaemia.
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PMID:[Intestinal ischemia: nosographic framework and risk factors]. 231 16

Auto-immune immunoglobulin-lipoprotein complexes (Ig-Lp), as well as other modified lipoproteins, are activators of the transformation of macrophages into foam cells which may be the first step in atherogenesis. In humans circulating Ig-Lp have been demonstrated in autoimmune hyper- or dyslipidemia (AIH, DIH) and found to be associated with conditions related to atherosclerosis. Thus Ig-Lps may be significant and potentially primary atherogenic factors. In order to test this hypothesis we compared the distribution of Ig-Lps in 14 WHHL homozygote rabbits and in 15 normal fed and 8 cholesterol-fed NZW rabbits, all males aged 4-6 months. The Ig-Lps were detected by ELISA using 2 different capture anti-Lp and 4 indicator antibodies specific for either total Igs or the IgA, IgM or IgG classes. Some Ig-Lp of all classes were found in normal fed NZW. As compared with these normal levels, IgA-Lp are increased 2.5-fold in both the WHHL and the cholesterol-fed NZW rabbits (P = 0.0002). During cholesterol feeding the increase of IgA-Lp and total cholesterol and their decrease after returning to a normal diet were parallel in NZW rabbits, but their variation was mainly independent. IgM-Lp was also increased, but to a much lesser extent, in WHHL and in cholesterol-fed NZW. IgG-Lp was not increased in WHHL and only moderately increased in some of the cholesterol-fed NZW. The WHHL and the cholesterol-fed NZW rabbits did not differ by the IgA-Lp content of the serum, but the level of IgM-Lp was higher in the former.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1990 Jun
PMID:Circulating IgA-Lp complexes in Watanabe heritable hyperlipidemic and cholesterol fed NZW rabbits. 237 87


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