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)

The metabolism of lipids in CAPD has not been fully elucidated. To further clarify the behavior of dyslipidemia in this setting we followed the values of total cholesterol (TC), HDL-cholesterol (HDL-C) and apolipoprotein (apo) parameters over time (12-24 months) in 40 patients and correlated these values and their ratios with clinical (age, gender, race, weight, diabetes, etc.) and biochemical (multiphastic screen) information. Mean HDL-C was lower in men (p less than 0.04), in whites, (p less than 0.03) and in diabetic patients (p less than 0.05), but there were no group differences for mean total cholesterol, mean apolipoprotein values, the atherogenic risk ratio TC/HDL-C, or the anti-atherogenic ratio apo A-I/apo B. Total months on CAPD was found to correlate positively with TC/HDL-C (p less than 0.05), an atherogenic risk factor, and to correlate negatively with HDL-C (p less than 0.02), an anti-atherogenic index. There was also a negative correlation with another anti-atherogenic index, apo A-I/apo B, which did not reach statistical significance (r = -0.41, p = NS). Counterbalancing this apparently increased atherogenic risk is the stability of individual parameters for each patient over time in this study. In fact, the good news appears to be that TC, HDL-C, apolipoproteins and the risk ratios TC/HDL-C and apo A-I/apo B all remained stable over 12-24 months (p = NS by paired t-test for all). Thus, we find no evidence for worsening of the uremic dyslipidemia over time with CAPD treatment.
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PMID:The impact of CAPD treatment on lipid metabolism and cardiovascular risk. 198 15

Epidemiologic research indicates that glucose intolerance and hypertension are interrelated phenomena, each powerfully predisposing to atherosclerotic cardiovascular disease. Both diabetic and hypertensive patients have greater amounts of atherogenic risk factors, including dyslipidemia, hyperuricemia, elevated fibrinogen, and left ventricular hypertrophy. Diabetic persons have an increased prevalence of hypertension (50%), and glucose intolerance is more common in hypertension (15% to 18%). Both share a strong relationship to excess weight, but the excess of hypertension in diabetic persons occurs in both lean and obese subjects. Diabetes doubles the risk of hypertension associated with overweight. The risk of coronary disease, stroke, and peripheral arterial disease increases with increasing blood pressure to the same degree in diabetic persons as in nondiabetic persons, but at any level of blood pressure, diabetic persons have a doubled risk of these outcomes. Both diabetic and hypertensive patients are particularly prone to silent or unrecognized myocardial infarctions. Greater efforts at primary prevention of both hypertension and diabetes are clearly needed, including efforts at weight control, exercise, limitation of salt intake, and control of blood lipid levels. In either diabetic or hypertensive candidates for cardiovascular disease, optimization of the chances of avoiding sequelae requires a comprehensive multifactorial approach. Prevention requires more than normalization of either the blood sugar or blood pressure. Rational preventive measures must also include weight reduction, a fat-modified diet, cessation of smoking cigarettes, raising high-density lipoprotein, lowering low-density lipoprotein, and reduction of fibrinogen. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol tend to coexist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of impaired glucose tolerance and hypertension. 200 55

Investigations of lipid metabolism in patients with disturbed GTT and manifest diabetes mellitus revealed in most cases dyslipidemia, decreasing significantly in the time course of therapy. The results of the investigations showed that the blood levels of cholesterol (CS), beta-lipoproteins, total lipids (TL) and free fatty acids (FFA) in patients with disturbed GTT were significantly increased as compared to healthy persons. In patients with DM of type I, CS, beta-lipoproteins, TL and FFA were significantly lowered after achieving compensation, and in patients with type II DM the above indices except CS and alpha-CS were also lowered. The detected lipid metabolic derangements were noted at the preclinical stage, i.e. in persons with disturbed GTT and were preserved at the stage of manifest forms of DM, necessitating adequate therapy.
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PMID:[The blood serum lipid spectrum in diabetes mellitus]. 208 Jan 39

We performed a prospective study in 106 patients with acute stroke. The main purpose was to evaluate the associated diseases and to determine their prevalence and incidence in two different types of cerebrovascular disease: the intracerebral hemorrhage (HI) and ischaemic events (AI). The studied population included 54 men and 52 women with a mean age of 66.8 +/- 10.3 years. A clinical examination was performed in all patients by different specialists and all were submitted to diverse complementary tests, including a computed tomography scan of the brain (TAC) and an echocardiogram (ECO). We found 24 (23%) HI and 82 (77%) AI. In the past history, previous stroke were more prevalent in AI (p less than 0.01). Heart disease was present in 87 (82%) patients but, among them, only atrial fibrillation which was found in 19 (18%) patients, was significantly more frequent in AI (p less than 0.02). Hypertension (HTA) existed in 79 (75%) patients, respiratory complications and periferic vascular disease in 9 (8%), diabetes in 44 (42%) and dyslipidemia in 31 (29%) patients. No significant difference was found between the two groups of stroke regarding these diseases; however, there was a tendency for HTA and diabetes to be more prevalent in HI and for periferic vascular disease in AI. In the blood tests, high haematocrit was found in 35 (33%) patients, anemia in 21 (20%), hypercholesterolemia in 17 (16%), hypertrigliceridemia in 18 (17%) and uremia or creatinemia or ionic alteration in 32 (30%) patients, without any difference in their prevalence and incidence in the two groups of stroke. In conclusion, in this prospective study of patients with an acute stroke, there was 23% of HI and 77% of AI, a high prevalence of previous stroke, heart disease and HTA, but only the previous stroke and, within heart disease, the atrial fibrillation were significantly more frequent in the AI group. Also, periferic vascular disease had a tendency to be more frequent in AI, as well as diabetes and HTA had in HI.
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PMID:[The patient with acute cerebrovascular disorders: assessment of associated diseases]. 208 57

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.
Diabetes Care 1990 Feb
PMID:Management of dyslipidemia in NIDDM. 219 Jul 70

Human arterial hypertension is likely a multifactorial trait resulting from multiple measurable monogenes, blended polygenes, shared family environment, and individual environment. Familial aggregation of hypertension and familial correlation of blood pressure appears to be more due to genes than to shared family environment. Total genetic heritability of 80% with some recessive major gene effects have been found for several traits associated with hypertension including urinary kallikrein excretion, intraerythrocytic sodium, and sodium-lithium countertransport. Other interesting factors regarding hypertension genetics include: non-modulation of the renin angiotensin system, intralymphocytic sodium, ionized calcium, and several genetic markers such as haptoglobin, HLA, and MNS blood type. Probably the most clinically useful information regarding the genetics of hypertension is evolving in several studies reporting a strong association of hypertension with dyslipidemia, diabetes, and obesity.
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PMID:Genetics of hypertension: what we know and don't know. 220 56

The chronic hyperglycemia of non-insulin-dependent diabetes mellitus (NIDDM) evolves gradually and is usually preceded by more transient hyperglycemia, classified as impaired glucose tolerance (IGT). Already in this phase, there is an increased risk of cardiovascular complications, and many IGT subjects, like NIDDM patients, often display several of the metabolic and circulatory disturbances that are associated with hyperglycemia, e.g., insulin resistance, hyperinsulinemia and/or hyperproinsulinemia, delayed insulin release, dyslipidemia, and hypertension. Therefore, and because untreated hyperglycemia is a self-perpetuating condition, early detection and early intervention may be necessary to prevent the progression and complications of NIDDM. This in turn would necessitate screening procedures, and the therapeutic goal should include both euglycemia and normalization of plasma insulin, plasma lipids, and blood pressure. A study in the German Democratic Republic indicated that the mortality in screening-detected NIDDM patients did not differ from that in patients detected in routine care. In a Swedish study on screening-detected NIDDM subjects, only those who had IGT rather than manifest NIDDM could maintain fasting blood glucose less than or equal to 6 mM for 5 yr by hypocaloric dietary regulation alone. In those with screening-detected NIDDM, the delayed acute insulin release and net postprandial hyperglycemia were improved by addition of glipizide, and most managed to attain and maintain fasting blood glucose less than or equal to 6 mM for approximately 2 yr after such addition. However, after 4 yr, there was an increase in blood glucose, suggesting that preventive intervention either may not be possible or may have to start in the IGT phase.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care 1990 Aug
PMID:Will sulfonylurea treatment of impaired glucose tolerance delay development and complications of NIDDM? 220 45

The authors have studied 30 patients with transient global amnesia aged between 49 and 76 years (median age of 63 years), without focal neurologic signs that have been followed for periods varying between 6 months and 10 years. Three of the patients had recurrent attacks of transient global amnesia, and another three had a stroke, although at some distance from the amnesia attack. Association was noted with certain risk factors including high blood pressure, and angiopathic changes of the eye fundus (in 50% of the patients), dyslipidemia (in 30%), diabetes (in 10%), and essential polyglobulia (in 7%). Coagulation studies including thrombelastograms were carried out in 22 patients, and demonstrated hypercoagulability in 50% of them. Changes in the arterial wall were noted in 85% of the 14 patients in whom carotid sphygmograms were recorded. The presence of these risk factors could explain the occurrence of cerebrovascular accidents in patients with transient global amnesia. Electroencephalograms performed immediately or a short time after the amnesia attack have evidenced in 18 patients rapid-type dysrhythmia, or diffuse theta waves, predominantly located in the deep layers of the left and right temporal areas. The EEG tracings were either flat or normal in the remaining 12 patients. Of the 30 patients presenting with global transient amnesia only two had migraine in antecedents, and another six had headache during the evolution of amnesia. The neurologic examination did not reveal any abnormality in 27 of the patients. Sequelar signs of neurological deficits were noted in the remaining three patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transient global amnesia (a study of 30 cases)]. 223 8

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.
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PMID:Plasma apolipoprotein E, high density lipoprotein1 (HDL1) and urinary mevalonate excretion in pancreatectomized diabetic dogs: effects of insulin and lovastatin. 224 16


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