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

Oxyhemoglobin dissociation curves (ODC) were performed on blood from diabetic and nondiabetic subjects with and without hypertriglyceridemia. P50 at in vivo pH was slightly lower than normal in normolipemic diabetics (25.7 versus 26.6 mmHg, p less than 0.05), in spite of increased red cell 2,3-diphosphoglycerate concentration (15.4 versus 14.4 mumole/g Hg, p less than 0.025). P50 at in vivo pH in diabetics with moderately elevated very low density lipoproteins (VLDL)--Type IV hyperlipoproteinemia (HLP)--was likewise found to be slightly lower than normal (25.5 versus 26.6 mmHg, p less than 0.05). In contrast, diabetics with pronounced hyperlipemia due to accumulation of chylomicrons (type I HLP) or due to accumulation of chylomicrons (type I HLP) or due to accumulation of chylomicrons as well as VLDL (type V HLP) showed markedly increased hemoglobin--oxygen affinity (P50:21.1 versus 26.6 mmHg, p less than 0.001). The change in the ODC of normolipemic diabetics is considered to be an expresssion of the presence of an increased proportion of a hemoglobin fraction (Hb Alc) with increased oxygen affinity. The additional change in the ODC of the hyperlipemic patients is thought to be secondary to accumulation of triglyceride-rich particles for the following reasons: (1) a similar increase in oxygen affinity of hemoglobin was demonstrated in familial type I HLP of nondiabetic subjects; (2) normal red cells increased their oxygen affinity when incubated in lactescent plasma; (3) in both acquired types I and V HLP the disappearance of HLP was followed by a normalization of the ODC.
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PMID:Hyperlipoproteinemia, diabetes, and oxygen affinity of hemoglobin. 1 60

We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas. Twelve young, healthy men were given 1 g of tolbutamide by mouth before and after 12 days of double-blind treatment with 1 g per day of halofenate, or placebo. There was a significant increase in serum tolbutamide at eight, 10 and 12 hours (P less than 0.01) and a significant (P less than 0.01) decrease in serum glucose at one, four and six hours after halofenate treatment, but not after placebo. In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both. No appreciable decrease in serum glucose levels was noted in diabetic patients receiving sulfonylurea and clofibrate. This interaction between halofenate and sulfonylureas is clinically important, especially in view of the association of hyperlipemia and diabetes.
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PMID:Potentiation of hypoglycemic effect of sulfonylureas by halofenate. 17 74

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27

Among 74 hypertriglyceridemic patients who were referred for study because of hypertriglyceridemia, family investigations detected 19 with familial hypertriglyceridemia and 24 with familial combined hyperlipidemia. The frequency of myocardial infarction among adult living hyperlipidemic relatives of patients with familial combined hyperlipidemia was 17.5% (10/57). Five of these relatives had their infarct between the ages of 40 and 50 yr of age, and five before the age of 40 yr. The frequency of myocardial infarction in living hyperlipedemic relatives with familial hypertriglyceridemia was 4.7% (2/43) and was similar to the frequency of myocardial infarction among normolipidemic relatives (4.5%) or among spouse controls (5.2%). Mortality data due to myocardial infarction among relatives of index patients failed to contribute meaningful information.
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PMID:Myocardial infarction in the familial forms of hypertriglyceridemia. 125 Jan 65

Hypertriglyceridemia is not a common finding in well controlled patients with insulin dependent diabetes; however, in noninsulin dependent, or Type II diabetes, hypertriglyceridemia and coronary heart disease are a well recognized clinical triad. In the latter setting, hypertriglyceridemia is usually the result of an associated inherited hyperlipidemia, most commonly familial hypertriglyceridemia but also familial combined hyperlipidemia. In the former, one sees elevated triglycerides and a low HDL-cholesterol, in the latter the same phenotype may be present but often there is a high LDL-cholesterol. Irrespective of the pathogenesis of the primary hypertriglyceridemic disorder, the occurrence of poorly controlled diabetes will enhance the hypertriglyceridemia and even in the Type II diabetic, with triglycerides in the thousands, dietary and glycemic control, alone, will strikingly ameliorate the hypertriglyceridemia. In contrast to patients with hypercholesterolemia, no national guidelines have been proposed for the treatment of patients with hypertriglyceridemia. Yet both experimental and clinical data support an algorithm in which dietary and glycemic control are optimized with a resultant major improvement in triglycerides, followed by the introduction of drug therapy. Three agents are particularly useful in correcting the hypertriglyceridemia: gemfibrozil, niacin, and fish oils, with the first two having the added benefit of increasing HDL levels. Lovastatin is also useful in treating these patients, but primarily for lowering LDL-cholesterol while triglycerides are independently being brought under control. Correction of hyperlipidemia in diabetic patients can generally be achieved with judicious use of dietary, glycemic and drug therapy; however, maintenance of a favorable response requires a high level of patient compliance, which is usually difficult to sustain.
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PMID:Hypertriglyceridemia in diabetes. An approach to management. 176 54

The familial aggregation of lipids [total cholesterol (CH) and triglyceride (TG)] and lipoproteins [high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL)] was investigated in families ascertained through both random and nonrandom probands in the Minnesota Lipid Research Clinic Family Study. Nonrandom proband ascertainment was based on single selection through truncation for hyperlipidemia at an earlier screening. A path model was used to investigate the nature of familial resemblance using appropriate adjustments for ascertainment and to determine whether random and hyperlipidemic samples are heterogeneous with regard to the multifactorial model. The results suggest that parameter estimates are consistent with those from previous studies in which only random families were used and that random and nonrandom samples are homogeneous with regard to the path model for CH and LDL. However, for TG and HDL the random and hyperlipidemic samples are significantly heterogeneous. This heterogeneity would be observed if familial hypertriglyceridemia and/or familial hypoalphalipoproteinemia segregates predominantly in the hyperlipidemic rather than in the random sample, as on might expect.
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PMID:Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Minnesota Lipid Research Clinic Family Study. 188 94

The hyperlipoproteinemias are disturbances in the metabolism of lipoproteins. Elevated levels of total and low density lipoprotein-cholesterol, and low levels of high density lipoprotein-cholesterol are proven risk factors for atherosclerosis. The significance of hypertriglyceridemia as an independent risk factor for atherosclerosis is controversial, however, at high levels triglycerides are a major risk factor for pancreatitis. Lipoprotein abnormalities can be divided into dietary, primary (genetic), and secondary disorders. The major causes of moderate and severe hypercholesterolemia are familial hypercholesterolemia, familial combined hyperlipidemia, severe primary (polygenic) hypercholesterolemia, and familial dysbetalipoproteinemia. Causes of hypertriglyceridemia include familial hypertriglyceridemia, familial lipoprotein lipase deficiency, sporadic hypertriglyceridemia, and secondary causes.
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PMID:Hyperlipoproteinemias: Part I. Lipoprotein classification and abnormalities. 194 97

In order to learn whether patients with diabetic ketosis who had very severe hypertriglyceridemia had underlying genetic hyperlipidemia, the authors measured plasma lipids in 211 episodes. They report the findings in the 15 patients who had initial plasma triglyceride concentrations above 11.3 mmol/L (1,000 mg/dL). These patients were detected during a prospective study of 155 episodes of ketoacidosis and 56 episodes of ketosis. Eleven of the 15 patients had definite or probable insulin-dependent diabetes mellitus (IDDM), but eight of the 15 were not acidemic despite their ketosis. Twelve of the 15 patients (80%) were men, a far higher percentage of men than the 53.6% in the base population of 211 episodes. Plasma triglyceride concentrations returned to normal levels either during the acute episode (seven cases) or well within a year (two more cases) in most of the patients. From that and other considerations, the authors infer that at least ten, and perhaps 12 of the 15 patients did not have an underlying genetic hyperlipidemia contributing to their original severe hypertriglyceridemia. That contrasts with the findings of others who reported that most patients with severe hypertriglyceridemia associated with noninsulin-dependent diabetes mellitus (NIDDM) (usually without ketosis) did have coexisting familial hypertriglyceridemia.
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PMID:Severe hypertriglyceridemia in diabetic ketosis. 212 81

We have studied the lipoproteins, apolipoproteins, and postheparin lipase activities in an extended pedigree with familial hepatic lipase deficiency. A deficiency of hepatic lipase was found in three of five brothers and in one of their children. Triglyceride enrichment of low density and high density lipoproteins was identified as the constitutive phenotype. beta-very low density lipoprotein was observed in hepatic lipase-deficient subjects, but it was absent when the plasma triglyceride concentration was less than 1 mM/l. The hepatic lipase-deficient subjects had normal or elevated low density lipoprotein cholesterol and high density lipoprotein cholesterol concentrations. Hyperprebetalipoproteinemia, hyperbetalipoproteinemia, and hyperalphalipoproteinemia were observed in both affected and unaffected family members. Compared with the unaffected family members, the hepatic lipase-deficient subjects had no significant differences in very low density lipoprotein cholesterol, very low density lipoprotein triglyceride, or low density lipoprotein cholesterol. These observations are consistent with the presence of additional genes causing hyperlipidemia in this family, independent of the deficiency of hepatic lipase.
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PMID:Plasma lipoproteins in familial hepatic lipase deficiency. 229 46

The objectives of this study were (1) to determine the incidence of dominantly inherited hyperlipoproteinemia in children referred to our medical center because of hyperlipidemia associated with a family history of premature coronary artery disease and (2) to assess the degree of expression in childhood of the most common inherited hyperlipoproteinemia, familial combined hyperlipidemia. Among 129 families referred to us by area pediatricians, we identified a dominantly inherited hyperlipoproteinemia in 97 of them. Twenty had familial hypercholesterolemia, 65 familial combined hyperlipidemia, 11 hyperapobetalipoproteinemia, and one familial hypertriglyceridemia. As expected, almost half (9/20) of the siblings of probands with familial hypercholesterolemia were affected. Although we expected incomplete gene penetrance in the siblings of the probands with familial combined hyperlipidemia, we found 43 affected and 40 unaffected among the 83 siblings of the 65 probands. Our findings suggest that hyperlipidemia in children, caused by familial combined hyperlipidemia, occurs more than three times as frequently as familial hypercholesterolemia and that in families identified by a child proband, the penetrance is complete. Pediatricians should identify this primary hyperlipidemia in childhood and attempt to prevent the associated risk of premature coronary artery disease by prescribing appropriate diet and life-style modifications.
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PMID:Prevalence and expression of familial combined hyperlipidemia in childhood. 231 96


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