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

Severe pancreatic exocrine insufficiency was demonstrated in a 41 year old man with familial type I hyperlipoproteinemia (fat-induced hyperlipemia). Plasma triglyceride concentration failed to increase significantly with increased dietary fat intake, and fecal fat excretion was markedly increased. Indices of intestinal function were normal. Pancreatic enzyme therapy resulted in reduced fat excretion and increased plasma triglyceride concentration. Secretin stimulation tests revealed impaired duodenal fluid volume, bicarbonate and pancreatic enzyme responses. Insulin-dependent diabetes mellitus had been diagnosed three years earlier. No attacks of acute pancreatitis had occurred in the preceding 20 years, and it is suggested that pancreatic damage may have resulted from repeated subclinical pancreatic insults due to elevated plasma lipid levels. This report is the first to indicate that pancreatic exocrine insufficiency may occur as a late complication of hyperlipemic disorders in the absence of recurrent acute pancreatitis. Steatorrhea may not be apparent because of therapeutic restriction of dietary fat, and the first manifestation of pancreatic exocrine disease may be an amelioration of fat-induced hyperlipemia.
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PMID:Subclinical chronic pancreatitis in type I hyperlipoproteinemia. 83 83

Cholesterol, triglyceride, and lipoprotein levels were determined in serum from 40 children with diabetes and from controls. Mean cholesterol levels in the children with diabetes (205 +/- 78 mg/dl) were statisically higher than for controls (155 +/- 27 mg/dl), as were mean triglyceride levels (120 +/- 63 vs 85 +/- 23 mg/dl). Eight of the children with diabetes had hypercholesterolemia, five had hypertriglyceridemia, and nine had combined hypercholesterolemia and hypertriglyceridemia. Low-density lipoprotein levels were statistically higher and high-density lipoprotein levels statistically lower for children with diabetes compared with control children. Increased urine glucose spillage was found to correlate with higher serum triglyceride levels, suggesting that the elevated triglyceride levels may have been related to diabetes control. With the known association between hyperlipidemia and coronary heart disease (CHD) and between diabetes and CHD, the results of the present study indicate that all children with juvenile diabetes mellitus should have a serum lipid analysis annually.
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PMID:Juvenile diabetes mellitus and serum lipids and lipoprotein levels. 97 14

1. Increased erythrocyte sodium-lithium countertransport activity has been reported to be associated with nephropathy in type 1 diabetes and linked to a family history of essential hypertension. 2. This study aimed to determine the mechanism of increased sodium-lithium countertransport activity. Sodium-lithium countertransport kinetics were measured in uncomplicated and hyperlipidaemic type 1 diabetic patients. 3. In the nine out of 31 uncomplicated type 1 diabetic patients who had high sodium-lithium countertransport activity, the sodium affinity (Km) was normal but the maximum velocity (Vmax) was increased. 4. Hyperlipidaemia, when present in diabetic patients, was associated with increased sodium-lithium countertransport activity, but could not explain the high activity in uncomplicated type 1 diabetic patients in whom plasma lipid concentrations were normal. 5. Sodium-lithium countertransport activity is increased in type 1 diabetes by a mechanism different to that in essential hypertension, where the mechanism is a low Km (increased sodium affinity). Hence familial hypertension cannot explain the raised sodium-lithium countertransport activity in type 1 diabetes.
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PMID:Kinetics of sodium-lithium countertransport activity in patients with uncomplicated type 1 diabetes. 131 14

The activity of serum paraoxonase, an enzyme located on high-density lipoprotein, has been investigated in familial hypercholesterolaemia (FH) and insulin dependent diabetes mellitus (IDDM). Increases in total serum cholesterol and apolipoprotein B were present in both FH and IDDM compared to healthy controls and in the patients with IDDM, serum triglycerides were also raised. The serum HDL-cholesterol concentrations in controls and patients with FH and IDDM did not differ significantly. Serum paraoxonase activity was significantly lower in both the FH and IDDM populations than in controls (P less than 0.001 and P less than 0.01, respectively). 72% of the FH population and 67% of the IDDM population were in the lower half of the frequency distribution for serum paraoxonase (activity of less than 112 U/l). It is likely that the common factor related to low paraoxonase activity is hyperlipidaemia. It is possible that paraoxonase has a physiological role in lipid metabolism and that decreases in its activity may accelerate atherogenesis.
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PMID:Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus. 165 32

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
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PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

The effects of a sustained-release preparation of bezafibrate (Bezalip Mono) 400 mg once daily and placebo administered for 3 months were compared in 36 patients with stable type 1 diabetes and hypercholesterolemia and/or hypertriglyceridemia. There was a significant decrease in fasting glucose levels with bezafibrate, but not in glycosylated hemoglobin. The serum cholesterol concentration decreased on bezafibrate [from 7.1 +/- 0.2 (mean +/- SEM) to 6.3 +/- 0.3 mmol/L; p less than 0.05] predominantly due to a reduction in low-density lipoprotein (LDL) cholesterol [from 4.8 +/- 0.3 to 4.2 +/- 0.3 mmol/L; p less than 0.05. There was also a decrease in fasting serum triglycerides with bezafibrate [1.82 to 1.26 mmol/L (geometric mean)] and in very-low-density lipoprotein (VLDL) cholesterol. Plasma fibrinogen decreased significantly with bezafibrate (from 4.1 +/- 0.2 to 2.9 +/- 0.2 g/L; p less than 0.001). Serum apolipoproteins B and A showed no statistically significant changes. Overall, there was no change in high-density lipoprotein (HDL). However, in patients who were initially hypertriglyceridemic, there was a significant increase in the cholesterol content of total HDL and the HDL2 subfraction (both p less than 0.05). It is concluded that in insulin-dependent diabetic patients with hyperlipidemia, bezafibrate is effective in lowering both serum VLDL and LDL. In addition, it has a potentially important action in decreasing plasma fibrinogen levels.
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PMID:Bezafibrate retard in patients with insulin-dependent diabetes: effect on serum lipoproteins, fibrinogen, and glycemic control. 171 Jul 43

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

In the last years, a plasmatic fibrinogen increase, a fibrinolytic system activity reduction and platelet activation, seemed to play a significant role on the genesis and progression of atheromatous plaques, especially when combined to a plasmatic lipoprotein increase. The results obtained in normolipidaemic patients (2000 asymptomatic subjects, 364 non-insulin diabetic patients randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 69 nifedipine-30 mg/daily-treated subjects, and 38 patients submitted to nifedipine-30 mg/daily-combined to indobufen-400 mg/daily-therapy), are reported. The results obtained in hyperlipidaemics (blood cholesterol level > 240 mg/dl; 356 patients, randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 56 patients with simvastatin 40 mg/daily and 85 with low saturated fat and low cholesterol diet), are also reported. Follow-up of all the patients was 4 years, but the simvastatin group followed-up only 1 year. An ultrasound examination of carotid and femoral arteries was performed in all the patients by means of a Duplex Scanner ATL Ultramark 5, with a high resolution probe (10 MHz). Subjects were graded into I-VI classes, according to the vessel progressive atherosclerotic impairment. In normolipidaemics, wall atheromatous changes were seen with increasing frequency with age, and a significant relationship among plaque progression rate and developed cerebrovascular symptoms, developed symptomatic peripheral symptoms, increased cardiovascular events and mortality rate, was evidenced. Non-insulin dependent diabetes, combined to normal levels of blood lipoproteins, appears an independent risk factor, superimposable to hyperlipidaemia. In this group of patients, bezafibrate therapy significantly reduced plaque progression, acting on blood coagulation factors and similar results were obtained in nifedipine and nifedipine plus indobufen groups. Also in hyperlipidaemics treated with diet, simvastatin and bezafibrate, the plaque progression was significantly reduced with respect to control group, especially when blood lipoproteins and coagulation were normalized. In conclusion, hyperlipidaemia, Ca++ and blood coagulation disorders, appear to be the main factors affecting the plaque progression, and the prevalence of each factor in the atheroma development must be well evaluated in the single patients to establish an adequate therapeutic strategies.
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PMID:[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]. 184 88

Gemfibrozil, a lipid lowering agent, was administered to two patients with familial hyperlipidaemia and one patient with insulin dependent diabetes mellitus. It was partially effective in familial hyperlipidaemia. It dramatically reduced triglyceride and cholesterol levels in the patient with Type V hyperlipidaemia and insulin dependent diabetes mellitus. Patients with familial and Type V hyperlipidaemias should be given a trial of gemfibrozil therapy.
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PMID:Gemfibrozil in familial and type V hyperlipidaemias. Report of 3 cases. 207 73

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11


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