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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Overnutrition manifested by obesity has emerged as a major health problem in affluent countries. In spite of increased interest in fitness, obesity is on the increase in the United States. This is particularly so among children and adolescents. Although obesity is associated with many risk factors for diseases, the mechanisms whereby it enhances disease risk are not fully understood. Such an understanding is needed to develop strategies for management of these conditions. In this report we suggest that overnutrition produces clinical diseases only in individuals who already possess a metabolic weakness or "defect" in a given system. In the absence of such underlying defects, overnutrition, or obesity, is well tolerated. One of the most common consequences of obesity is dyslipidemia, that is, elevations of very low-density lipoprotein (VLDL) triglycerides and low-density lipoprotein (LDL) cholesterol and low concentrations of high-density lipoprotein (HDL) cholesterol. The major effect of overnutrition on lipoprotein metabolism is to stimulate the production of VLDL. For patients who have an underlying defect in lypolysis of VLDL triglycerides, hypertriglyceridemia will develop in the obese state. For those who have defective clearance of LDL, obesity will accentuate hypercholesterolemia. Both of these effects can be explained by overproduction of VLDL, due to obesity, combined with a genetic defect in clearance of VLDL or LDL. The mechanism whereby obesity causes a lowering of HDL cholesterol is uncertain, although it could enhance removal of HDL by an excess of adipose tissue. Another disease associated with obesity is cholesterol gallstones. The presence of obesity more than doubles the risk for gallstones. Two underlying factors increase the danger for gallstones: a deficiency of hepatic secretion of bile acids and a tendency for formation of cholesterol crystals in bile. Overnutrition promotes the synthesis of whole-body cholesterol, and the only route for excretion of this excess cholesterol is through the biliary tree.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Metabolic and health complications of obesity. 226 44

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

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

The metabolic and cardiovascular complications of obesity are dependent upon the distribution of body fat excess: predominantly abdominal or "android" obesity is more pathogenic than "gynoid" obesity which predominates in the lower part of the body. Adipose tissue overloads localized to the abdomen are associated with hypermortality from vascular diseases, even in patients who are not overweight. The metabolic characteristics of abdominal adipocytes, which have increased lipolytic capacity, might account for this situation, as they would facilitate hyperinsulinism, insulin resistance and such-metabolic disturbances as arterial hypertension, diabetes mellitus and dyslipidemia. Androgens seem to play a key role in the development of obesity morphotypes. These notions have important practical applications: an excess of body fat is not necessarily pathogenic; as regards vascular and metabolic risks, body fat distribution seems to be more important than overweight.
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PMID:[Influence of the distribution of body fat on vascular risk]. 295 Apr 48

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors--dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia--likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin. 305 23

Primary and secondary risk factors and prevention strategies for coronary artery disease are reviewed. Cigarette smoking, hypertension, dyslipidemia, heredity, diabetes mellitus, obesity, beta blockades, and coronary artery bypass surgery are some of the topics discussed.
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PMID:Preventive cardiology for coronary artery disease. 384 6

Risk factors for the development and progression of coronary atherosclerosis, hypertension, and cerebrovascular diseases are found in more than 10 per cent of children and adolescents in the United States. This article presents the criteria for the diagnosis of three of these risk conditions--dyslipidemia, hypertension, and obesity--and it reviews principles and specifics of their management in young people.
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PMID:Familial cardiovascular risk factors: diagnosis and management in the young. 384 7

We studied outcome of management of metabolic cardiovascular risk factors in 155 randomly chosen Hispanic hypertensive patients (mean age, 63 +/- 1 years; 79% female) screened for dyslipidemia. Hypertriglyceridemia (n = 12) or high risk-adjusted low-density lipoprotein cholesterol (LDL-C) (n = 89) was found in 65%. Triglycerides did not change (6.16 +/- 0.58 to 7.44 +/- 2.34 mmol/L; P = NS) over 2.2 +/- 0.5 years. Only 58 patients with high LDL-C were treated, and 8 had no follow-up lipid tests. In the other 50, LDL-C decreased by 10 +/- 3% (P < .001) over 2.8 +/- 0.2 years but attained goal in only 12. In a subset of 24 patients with extended follow-up (3.8 +/- 0.2 years), there was an initial marked decline in LDL-C, followed by a rebound to baseline levels. In 29 of 54 patients with normal LDL-C, lipid testing was markedly overused compared with recommendations. Obesity (n = 94, 61%) did not improve in those with repeated data (+0.6 +/- 0.8 kg; P = NS; n = 40) over 2.7 +/- 0.3 years. Forty-four of 63 patients with type II diabetes had repeated measurement of glycosylated hemoglobin, with no change (10.5 +/- 0.5% to 11.2 +/- 0.5%; P = NS) over 2.2 +/- 0.3 years. Ten-year risk of coronary events (Framingham cohort parametric regression) calculated for 61 patients with known untreated blood pressures (169 +/- 3/98 +/- 1 mm Hg) was 21.0 +/- 1.7%, with a skewed distribution reaching high values (66%) and attributable in large part (72%) to modifiable risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suboptimal outcome of management of metabolic cardiovascular risk factors in Hispanic patients with essential hypertension. 749 72

The Bogalusa Heart Study now establishes that precursors of adult cardiovascular diseases begin in childhood. The clearest evidence comes from autopsy studies that show coronary atherosclerotic lesions occur in early life and are strongly associated with very-low-density lipoprotein cholesterol, systolic and diastolic blood pressure, and obesity, and have an inverse relationship with high-density lipoprotein cholesterol. Observations of cardiovascular risk factors span a period of life from birth to 31 years of age, and longitudinal studies span a 15-year period. Risk factor variables tend to persist over time, "track." Although tracking is best for height and weight, low-density lipoprotein cholesterol and serum total cholesterol track at a high order; blood pressure tends to track at a lower order. Obesity and body fatness have an adverse influence on risk factors in children, just as noted in adults, with central obesity becoming more obvious after puberty, and having a greater adverse effect on risk factors. The emergence of abnormal levels of risk factors by adult criteria begins to occur in young adults, and is not evident in childhood. Retrospective studies, interestingly, for obesity, higher blood pressure, and dyslipidemia reveal evidence of their presence already in childhood. These findings have strong implications for undertaking prevention in early life.
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PMID:Rationale to study the early natural history of heart disease: the Bogalusa Heart Study. 750 19


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