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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data from several different studies are reviewed suggesting that a subset of hypertension is associated with metabolic abnormalities involving lipids, insulin, and often obesity, all aggregating strongly in families. Persons with 'familial dyslipidaemic hypertension (FDH)' have an especially high risk of early coronary disease. The clinical and biochemical features of FDH are compared with Reaven's Syndrome X, familial combined hyperlipidaemia, dense LDL subfractions, diabetes, impaired glucose tolerance, central and general obesity, pre-diabetes, pre-hypertension, and heterozygous lipoprotein lipase deficiency. Some contribution from major gene effects is suggested in specific subsets reported in several different genetic studies reviewed in this report. It seems likely that multiple metabolic abnormalities are genetically heterogeneous. The data also suggest significant contributions from environmental factors such as diet and physical activity.
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PMID:Familial dyslipidaemic hypertension and other multiple metabolic syndromes. 148 41

The primary and secondary prevention of cardiovascular diseases and, therefore, the therapy of hyperlipidemia is essential in strategies to lower morbidity and mortality from coronary heart disease (CHD), the most relevant atherosclerosis-associated disease. These programs imply not only a medical but also an economic challenge to our health system. That is why all therapeutic measures have to be evaluated regarding their cost-effectiveness. A cost-effectiveness profile was calculated for all the therapies of hyperlipidemia (nutritional therapy, dietetic nutritionals, drugs and LDL-apheresis) with respect to the following parameters: total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides. The daily costs of all interventional measures are compared to the success rate, whereby an index of daily therapy costs and 1% change per lipid parameter was calculated. Nutritional therapy is by far the cheapest, and LDL-apheresis the most expensive but also the most effective and reliable therapeutic measure. It has to be considered, however, that dietary intervention can be very successful in overnutrition while in rare cases of severe homozygous familial hypercholesterolemia there is no therapeutic alternative to LDL-apheresis. Life-style modifications, such as changing nutritional habits, may contribute towards reducing or removing one or more risk factor(s) (e.g. malnutrition is associated with overweight, hyperlipoproteinemia (HLP), hyperinsulinemia (syndrome X), hyperfibrinogenemia and hypertension). But neither health politicians nor the population seem to be conscious of the fact that life-style changes help to reduce medical expenditure. Considering the fact that nearly every medical service is getting more and more expensive, the need to introduce financial regulations is evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Economic aspects of therapy for lipid metabolism disorders]. 150 39

The aim of this study was to compare the causes of death and parameters related to alcohol consumption, between subjects diagnosed as diabetic, clinically by their general practitioner, or glucose intolerant and in particular as diabetic, using the epidemiological criteria of an abnormal glucose level following an oral glucose tolerance test. The subjects in this study were 7035 working men, aged between 44 and 55 years, who attended the first follow-up examination of the Paris Prospective Study, between 1968 and 1973. They were classified as 'clinically diagnosed diabetic' or, following an oral glucose tolerance test and the World Health Organisation criteria, as having 'oral glucose tolerance test diagnosed diabetes', impaired glucose tolerance or normoglycaemia. The relative risk of death by cirrhosis, in comparison with the normoglycaemic group, was 21 (95% confidence interval: 9.1-49) in the group diagnosed diabetic by the oral glucose tolerance test, significantly different (p less than 0.02) from the group diagnosed diabetic clinically 3.1 (0.41-24); factors indicative of excessive alcohol consumption at baseline differed accordingly. In contrast, the relative risks for death by coronary heart disease were similar, 2.1 (1.0-4.1) and 2.7 (1.4-5.4) respectively; all of the factors defining the insulin resistance 'Syndrome X' (hyperglycaemia, hyperinsulinaemia, hypertension, hyperlipidaemia and also central obesity) and predictive of coronary heart disease were elevated in both groups of diabetic subjects. 'Diabetes', as diagnosed by the oral glucose tolerance test, might be the consequence of excessive alcohol consumption which could lead to insulin resistance, then to coronary heart disease, as well as to alcohol-related diseases.
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PMID:Cardiovascular and alcohol-related deaths in abnormal glucose tolerant and diabetic subjects. 154 80

Each hyperlipidemia patient requires individual management. Treatment choices are thus made for each patient on the basis of evaluation of their overall cardiovascular risk. This evaluation involves four types of characteristics: those which cannot be changed (age, gender), classical lipid and non-lipid risk factors, and finally cardiovascular status with two types of evaluation (clinical status and sub-clinical, atherosclerosis). Three examples are presented here, enabling more precise assessment of lipid risk: syndrome X which shows to what extent risk factors are often associated, combined familial hyperlipidemia which emphasises the importance of family history, and lipoprotein (a). The latter is a risk factor relatively inaccessible to treatment but which enables better evaluation of the risk of the patient and choice of a stricter treatment goal when it is very high.
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PMID:[New lipid factors of cardiovascular risk]. 782 48

A 60-year-old man was admitted to the Kyushu University Hospital because of poor glycemic control of diabetes mellitus. Although he had been treated with glicrazide and nifedipine for his diabetes and hypertension, the controls of the diseases were unsatisfactory. Plasma triglyceride level was 186 mg/dl. Furthermore, extreme insulin resistance was found by measuring glucose infusion rate with an euglycemic hyperinsulinemic clamp method. These findings were compatible to those seen in syndrome X. After admission, diet therapy of 1,800 Cal was started and his metabolic disorders such as hyperglycemia, hyperlipidemia, and hypertension were all improved. Moreover, euglycemic hyperinsulinemic clamp study also revealed a decreased insulin resistance after diet therapy. Our experience from the case suggested that insulin resistance may closely related with the metabolic disorders of the disease "syndrome X".
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PMID:[A case of syndrome X whose hyperglycemia, hyperlipidemia and hypertension were improved as accompanying with decreased insulin resistance]. 785 34

Recent epidemiologic studies in the United Kingdom have led to the hypothesis that adverse nutritional experiences in utero have a powerful influence on the development of degenerative diseases in adulthood. Poor fetal growth as measured by weight, length, head, chest, and abdominal circumferences is a strong predictor of hypertension, diabetes, hyperlipidemia, alteration in clotting factors, Syndrome X,* and mortality from cardiovascular and chronic obstructive airways disease. The theory of fetal origins of adult disease proposes that early defects in the development, structure, and function of organs lead to a programmed susceptibility, which interacts with later diet and environmental stresses to cause overt disease many decades after the original insult.
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PMID:Maternal and fetal determinants of adult diseases. 789 83

Obesity frequently clusters with hypertension, hyperlipidemia, non-insulin-dependent diabetes mellitus, and ischemic heart disease with hyperinsulinemia as syndrome X. Although central obesity has been recognized to have a strong genetic component, few candidate genes have been studied in this disorder. After a recently described association between the apolipoprotein-D (Apo-D) gene polymorphism and non-insulin-dependent diabetes mellitus by our group, we have now looked at a TaqI polymorphism of the Apo-D gene in two other components of syndrome X, namely obesity and hyperinsulinemia. Apo-D genotype differences were found between obese subjects (n = 57) and slim controls (n = 57; P = 0.006). Furthermore, in the obese group an association was found between the Apo-D genotype and fasting insulin (P < 0.001). Preliminary evidence, therefore, suggests that the TaqI Apo-D polymorphism can be used as a genetic marker for obesity and several components of syndrome X.
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PMID:Apolipoprotein-D polymorphism: a genetic marker for obesity and hyperinsulinemia. 791 35

Two follow-up studies were carried out to determine whether lower birthweight is related to the occurrence of syndrome X-Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia. The first study included 407 men born in Hertfordshire, England between 1920 and 1930 whose weights at birth and at 1 year of age had been recorded by health visitors. The second study included 266 men and women born in Preston, UK, between 1935 and 1943 whose size at birth had been measured in detail. The prevalence of syndrome X fell progressively in both men and women, from those who had the lowest to those who had the highest birthweights. Of 64-year-old men whose birthweights were 2.95 kg (6.5 pounds) or less, 22% had syndrome X. Their risk of developing syndrome X was more than 10 times greater than that of men whose birthweights were more than 4.31 kg (9.5 pounds). The association between syndrome X and low birthweight was independent of duration of gestation and of possible confounding variables including cigarette smoking, alcohol consumption and social class currently or at birth. In addition to low birthweight, subjects with syndrome X had small head circumference and low ponderal index at birth, and low weight and below-average dental eruption at 1 year of age. It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named "the small-baby syndrome".
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PMID:Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. 843 55

Coronary heart disease (CHD) is the most important cause of death and disability among older women. A 50-year-old woman has a 46% risk of having CHD and a 31% risk of dying from it. Female CHD patients have a distinct clinical presentation, which includes more severe thromboembolic disease without coronary arteriosclerosis. Syndrome X also appears to be more prevalent in women. Oestrogen deficiency may be a trigger for this syndrome. The magnitude of the effect of various risk factors may also differ between women and men. In addition, there are risk factors unique to women. Lipid profiles differ between men and women. After menopause, the lipid profile changes unfavourably, with increasing levels of LDL cholesterol and decreasing levels of HDL cholesterol. Cigarette smoking, hypertension, diabetes mellitus, and obesity are all recognised risk factors for CHD in women. It is important to recognise that risk factors for CHD differ between men and women. Advising women to quit cigarette smoking, avoid obesity, increase physical activity, and prevent and treat hypertension and hyperlipidaemia will result in a reduction in CHD risk. Additional studies are needed to further contribute to our understanding of the complex risk factors underlying the development of CHD in women.
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PMID:Risk factors for cardiovascular disease in women: assessment and management. 886 75

Obesity is commonly associated with insulin resistance. The etiology of insulin resistance syndrome such as syndrome X or deadly quartet is not clear. We have proposed visceral fat syndrome, in which fat accumulation is predominant in the intra-abdominal cavity, frequently accompanied by disorders of glucose and lipid metabolism, and also hypertension. Excess free fatty acid of the portal circulation may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. Enhanced production of PAI-1 by increased visceral fat may be partly responsible for the development of cardiovascular disease in patient with visceral fat assmulation.
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PMID:[Obesity and insulin resistance syndrome]. 891 27


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