Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of pravastatin (CAS 81131-70-6) on serum lipid levels in 91 type 2 diabetic patients with mean glycosylated hemoglobin of 8.5% was investigated up to 12 weeks. Oral administration of 10 to 20 mg/d of pravastatin significantly decreased total cholesterol by 18.4 +/- 1.5% after 4 weeks. When analyzed separately in type IIa and IIb hyperlipidemia, the reduction of total cholesterol by pravastatin was more prominent in the former. Low-density lipoprotein cholesterol were also significantly decreased 22.2 +/- 2.7% after 4 weeks. The effect of pravastatin in reducing triglyceride was more prominent in patients with higher triglyceride compared to those with lower triglyceride before the administration of the drug. High-density lipoprotein cholesterol showed a slight but significant increase by 4.2 +/- 1.9% after 4 weeks. Among the apolipoproteins examined, apolipoprotein B was significantly decreased after 4 weeks. Atherogenic index and apolipoprotein B/apolipoprotein A-I ratio were also significantly decreased after 4 weeks. The efficacy of pravastatin was also observed after 12 weeks to the same extent as after 4 weeks. No major side effects or abnormalities of laboratory parameters have been observed. These data lead to the conclusion that pravastatin is useful for the treatment of hyperlipidemia in type 2 diabetic patients with poor glycemic control without major adverse effects.
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PMID:Clinical efficacy of pravastatin for hyperlipidemia in patients with type 2 diabetes mellitus. 764 75

We report a method for assaying magnesium in serum and urine involving only one enzyme, isocitrate dehydrogenase (NADP+)(EC 1.1.1.42), which requires magnesium ion for activity. The enzymatic reduction of NADP+ by isocitrate increases in rate linearly up to at least 20 mmol/L magnesium in the presence of appropriate concentrations of the two metal-chelating reagents, EDTA and glycol ether diamine-N,N,N',N'-tetraacetate. Within-run (n = 20) CVs and day-to-day (n = 10) CVs for sera are < or = 1.5% and < or = 2.6%, respectively. Analytical recovery of magnesium in sera averages 96-100%. This method is not affected by bilirubin, hemoglobin, or lipemia. The method (y) gives the following results correlating with atomic absorption spectrophotometry (x): y = 1.03x + 0.06 mmol/L (n = 62, r = 0.995, Sylx = 0.03) for sera, and y = 1.03x - 0.10 mmol/L (n = 62, r = 0.989, Sylx = 0.19) for urines; with the calmagite method (x): y = 0.99x + 0.04 mmol/L (n = 62, r = 0.991, Sylx = 0.03) for sera, and y = 0.98x + 0.03 mmol/L (n = 62, r = 0.999, Sylx = 0.02) for urines.
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PMID:Assay of magnesium in serum and urine with use of only one enzyme, isocitrate dehydrogenase (NADP+). 765 41

Patients with diabetes mellitus are more frequently hypertensive than age-matched non-diabetic subjects. They are confronted with a markedly increased risk of coronary vascular disease, of progressive nephropathy and renal end-stage diseases. The most common type of hypertension in type I and type II diabetics is essential hypertension, probably as a consequence of insulin resistance and hyperinsulinemia. Hyperglycemia and hypertension are both significantly involved in the progression of diabetic nephropathy. Hence, the modern therapeutic concept consists of optimal blood glucose control and strict blood pressure control. Progression of the nephropathy may be halted in most of the cases by adhering to set limits in mean arterial blood pressure, glycated hemoglobin and urinary albumin excretion rate. Furthermore, a significant decrease in cardiovascular mortality may be achieved. In case the blood pressure targets cannot be met by non-drug therapies and life-style modifications, antihypertensive drug therapy has to be initiated. The selection of antihypertensives should be based on the concomitant diabetes mellitus with its additional cardiovascular risk factors hyperlipidemia and hyperinsulinemia. In general, preference should be given to so-called metabolic neutral substances such as ACE inhibitors or calcium antagonists or to alpha-blockers which may have positive metabolic effects. Meanwhile, data from several prospective studies claim that ACE inhibitors and calcium antagonists exert nephroprotective effects beyond their beneficial blood pressure lowering effects, thereby preventing the progression of diabetic nephropathy. However, these drugs should not be uncritically used and we should be aware of their potential adverse effects. The differential therapy of hypertension in diabetes mellitus requires mature consideration before initiation of therapy, an individualized concept of therapy, and careful monitoring during treatment.
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PMID:[Hypertension, microalbuminuria and insulin resistance in diabetes mellitus]. 784 97

Progression of atherosclerotic lesion of the carotid artery is suggested to induce the development of cerebrovascular events. We evaluate the risk factors related to carotid artery, wall thickness by ultrasonography. A total of 159 patients, who had received no medication for hypertension or hyperlipidemia were enrolled in this study. The wall thickness of carotid artery was evaluated as an intima-media (IM) complex measured by B-mode ultrasonography with a 7.5 MHz probe. Simple regression analysis demonstrated significant correlation between the IM complex and both age and systolic blood pressure, but not with fasting levels of plasma glucose, hemoglobin A1c, total and HDL cholesterol, triglyceride or gender. Stepwise regression analysis showed age and systolic blood pressure contribute to IM thickness (r = 0.623). However, in patients aged 60 or over, blood pressure did not contribute to the IM wall thickness. Smoking was not a risk factor for IM thickness, but the Brinkman Index (daily consumption of cigarettes x years smoking) was significantly higher in patients with plaques in the carotid artery than those without it. These results suggest that high blood pressure is a risk factor for mild atherosclerotic lesions of the carotid artery for those aged under 60. Smoking may contribute to the formation of plaque, which may consequently lead to the ischemic cerebrovascular disease.
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PMID:[Risk factors related to the wall thickness of carotid artery assessed by ultrasonography]. 804 Oct 25

We evaluated a turbidimetric method for the estimation of apo A1 and apo B on the Ciba Corning 550 EXPRESS using Ciba Corning reagents. Interference due to bilirubin, hemoglobin, lipemia, triglycerides, and uremia was minimal, with apolipoproteins (apo) A1 and B results usually within +/- 4% of expected values. Within-run and day-to-day imprecision (coefficients of variation) ranged from 1.96 to 3.60% and 2.63 to 3.39% for apo A1 and 1.02 to 1.74% and 2.08 to 3.66% for apo B, respectively. Accuracy was determined by participation in the IFCC apolipoprotein standardization project in which results obtained on 50 patient samples were compared to those obtained by the reference laboratory. Apo A1 and apo B showed an average bias of +3.7% and +2.0% and correlation coefficients of 0.986 and 0.977, respectively. Results were also compared to those obtained on the Behring Turbitime system and showed a bias of +7.5% and -8.8% for apo A1 and apo B, respectively. The Ciba Corning automated method was rapid and gave good accuracy, precision, linearity, and parallelism and was relatively unaffected by raised triglyceride values.
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PMID:Evaluation of a turbidimetric procedure for apolipoproteins A1 and B on the Ciba Corning 550 EXPRESS. 812 63

Most traditional hypoglycemic treatments for non-insulin-dependent diabetes mellitus (NIDDM) are of considerable antiquity. What we would now call a low-carbohydrate diet was first used in 1796; insulin was introduced in 1922; the (toxic) biguanide synthalin was used sparingly from 1926 until the Second World War; and tolbutamide and chlorpropamide were marketed in the late 1950s. Amphetamine was available as an anorectic agent in the 1950s. Hence, representatives of all our present treatments for NIDDM have been available for over 30 y, but there is still great uncertainty about how to use them best. This uncertainty is reflected in major variations in prescription rates from country to country. In spite of this formidable pharmacological armamentarium, we have to face the fact that glycemic control is unsatisfactory in the majority of patients with NIDDM; irrespective of the mode of treatment, less than a quarter have a normal glycated hemoglobin. We clearly need new approaches to control glycemia in NIDDM. Furthermore, in addition to high blood glucose, many patients with NIDDM also have hypertension, hyperlipidemia, and other atherogenic abnormalities that need to be tackled if mortality (predominantly from atherosclerotic vascular disease) is to be reduced. It seems improbable that a single drug will be found to cure the many metabolic abnormalities. Polypharmacy thus seems inevitable for many patients.
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PMID:Traditional pharmacological management of non-insulin-dependent diabetes. 854 15

Hyperlipidemia is a known cause for acute pancreatitis. Hyperlipidemia may also produce multiple spurious laboratory results that may complicate the diagnosis and management of pancreatitis. We encountered such a patient who had the following spurious laboratory results: normal serum amylase activity, hyponatremia, and high hemoglobin levels. These laboratory artifacts were previously described, mostly separately. In addition, our patient had artifactual thrombocytopenia. The patient improved dramatically following plasmapheresis, which enhanced reduction of serum lipids.
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PMID:Multiple spurious laboratory results in a patient with hyperlipemic pancreatitis treated by plasmapheresis. 886 33

Diuretics are among the first drugs offered to the hypertensive patient. However, they can induce metabolic changes resulting in cardiovascular insult. Especially noteworthy are increased levels of glucose and lipids. Indapamide is a diuretic and vasodilator that does not raise blood glucose or lipid levels. We therefore investigated its use as a substitute diuretic in patients whose treatment had resulted in hyperglycemia and/or hyperlipidemia. In 24 hypertensives, Indapamide, 2.5 mg daily, replaced the diuretic therapy they were receiving. Blood pressure, blood glucose, hemoglobin A1C and lipid profile were measured before and every month during the 6 months of Indapamide treatment. Replacement of diuretics with Indapamide significantly reduced blood glucose from 148 +/- 53 mg/dl to 127 +/- 37, p = 0.05 HbA1C from 8.42 +/- 0.4 mg/dl to 7.7 +/- 2.0, p = 0.05; total cholesterol from 253 +/- 45 mg/dl to 228 +/- 43, p < 0.05; and triglycerides from 224 +/- 145 mg/dl to 176 +/- 91, p < 0.05. Blood pressure was better controlled with Indapamide than with previous medications. It was reduced from an average of 155 +/- 1 systolic and 89 +/- 8 diastolic (mm Hg), to 142 +/- 13 and 83 +/- 7, respectively, p < 0.05. We conclude that Indapamide is safe and effective in lowering blood pressure and contributes to better control of blood glucose and lipid levels in diabetic and dyslipidemic patients, compared to standard diuretics.
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PMID:[Indapamide--a substitute diuretic for hypertensives with hyperglycemia and/or dyslipidemia]. 894 May 16

Data on 746 patients with non-insulin-dependent diabetes mellitus (NIDDM) were collected from the Internal Medical Association in Himeji by questionnaire, and the patients were divided into six groups according to the duration of illness. Frequencies of various complications according to the duration of illness and risk factors of complications were compared between men and women. Although the number of male patients was 417, significantly more than the 329 female patients, many female patients were elderly, and the age at initial onset was about 10 years older than that of the male patients. Fasting blood sugar and hemoglobin A1c levels increased with the duration of illness. The female patients showed a greater tendency to suffer from hypertension, hyperlipidemia and obesity than the male patients. There was positive correlation between the incidence of complications and duration of illness. This tendency was more marked in the female patients than in the male patients. Both male and female patients showed a tendency for microangiopathy to appear earlier than macroangiopathy. The increase in the frequency of complications accompanying the increase in the duration of illness was more marked for microangiopathy than for macroangiopathy.
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PMID:The frequencies of diabetic complications in elderly non-insulin dependent diabetic patients in Himeji. 901 74

Troglitazone (TRG) is an orally active antidiabetic agent that increases insulin sensitivity in models of non-insulin-dependent diabetes mellitus (NIDDM), subsequently reducing hyperinsulinemia and hyperglycemia. We examined the effects of TRG on the development and severity of diabetes in the Goto-Kakizaki (GK) rat, a spontaneous, non-obese model of NIDDM. TRG was administered at a dose of 30 mg/kg/d beginning at 4 weeks of age. TRG-treated GK rats were evaluated against Wistar and untreated GK rats at 8, 12, and 16 weeks of age. Untreated GK rats were nonketotic, normolipidemic, hyperglycemic, and had normal fasting insulin levels compared with Wistar rats. TRG treatment decreased glycosylated hemoglobin levels in the GK rat independently of its effects on plasma insulin. In untreated GK rats, intravenous glucose tolerance tests (IVGTTs) showed a hyperglycemic response to glucose loading with severely impaired glucose disposal relative to Wistar controls. TRG treatment was successful in decreasing the glucose area under the curve (AUC) (P < .03) but did not improve glucose disposal, suggesting a direct hepatic effect. Ex vivo evaluation of hepatic glucose output (HGO) further supported a direct hepatic action, with 50% reduction in HGO in TRG-treated GK rats (P < .004). A euglycemic-hyperinsulinemic clamp performed at 16 weeks of age showed severe insulin resistance in the untreated GK rat, with a glucose infusion rate (GIR) 33% lower than in Wistar rats (P < .004). TRG treatment had no effect on this insulin resistance. These results indicate that TRG selectively decreases hepatic glucose production in this unique model of NIDDM independently of its action on peripheral insulin sensitivity or hyperlipidemia.
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PMID:Metabolic effects of troglitazone in the Goto-Kakizaki rat, a non-obese and normolipidemic rodent model of non-insulin-dependent diabetes mellitus. 903 Aug 28


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