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

Experimental, epidemiological and clinical evidence indicates that salt plays a major role in the pathogenesis of arterial hypertension. Endocrine and membrane ion transport studies suggest a genetic disposition with regard to salt susceptibility. In the industrialized countries sodium intake in children probably exceeds the physiological needs. However, a reduction of salt consumption in the general paediatric population cannot be recommended as the longterm risk benefit ratio is currently unknown. In children with manifest arterial hypertension sodium intake should be reduced below 2 mval/kg/day. Diuretic therapy is an important part of antihypertensive treatment. Thiazides and in renal insufficiency furosemide are the drugs of choice. The side effects of diuretic therapy, such as hypokalemia, hyperuricemia, and hyperlipidemia, in children require further investigation.
 ...
PMID:[Reduction of table salt and diuretic therapy in arterial hypertension in childhood]. 357 12

To investigate the effect of long-term acetate administration on uremic and nonuremic rats, the blood lipid level, the incorporation of [14C]acetate into exhaled 14CO2 and into tissue lipids, and morphological changes were studied. Experimental chronic uremia was caused by partial nephrectomy, and sodium acetate of NaC1 was given intraperitoneally for approximately 12 weeks. Controls were sham-operated rats given acetate or NaC1. Hyperlipidemia was found in the uremic rats; it was more severe in the rats given acetate. Incorporation of [14C]acetate into 14CO2 was lower in uremic rats given acetate than in other groups, and incorporation into liver lipids was not different in different groups. Small fat droplets had accumulated diffusely in the hepatocytes of nonuremic and uremic rats, but accumulation was more severe in the former. Large fat droplets were found in rats given acetate, mostly in the periphery of liver lobules. Uremic rats given NaC1 did not have such changes. The results suggested that chronic acetate administration may contribute to hyperlipidemia in uremic rats and to lipid accumulation in hepatocytes in both uremic and nonuremic rats, causing fatty degeneration of the liver.
 ...
PMID:Effect of acetate administration on rats with chronic uremia. 361 95

Dichloroacetate (DCA) reduces blood glucose, lactate and lipids in diabetes or during fasting. Chronic use of DCA, however, is limited by toxicity, probably due in part to its rapid conversion to oxalate in vivo. In theory, therefore, DCA's efficacy may be retained and its toxicity minimized by controlling its rate of metabolism. We attempted to alter DCA pharmacokinetics and bioavailability by synthesizing various derivatives comprising DCA esters with polyols and DCA ionic complexes. Twenty-four hour fasted, nondiabetic rats received single, orogastric doses of saline (control) sodium DCA (100mg/kg) or the following derivatives (D1-4): the esters D1-D3: potassium tetra (dichloroacetyl) glucuronate (D1), inositol-monophosphate-tetradichloroacetate (D2), inositol-hexadichloroacetate (D3) and inositol-hexa [N-methylnicotinate] hexadichloroacetate salt (D4). Each derivative was administered at a dose that would ultimately provide 100 mg/kg DCA as the anion. All derivatives were orally effective in significantly decreasing blood glucose and lactate. D4 exerted the most potent and long-lasting glucose- and lactate-lowering effects, yet increased plasma DCA concentrations less than an equivalent dose of the sodium salt. When administered to reverse light-cycled rats, D4 markedly inhibited the incorporation of tritiated water into cholesterol and triglycerides. We conclude that derivatives of DCA retain the biological activity of the parent compound, but may exhibit different pharmacokinetics. They may eventually prove useful in the treatment of diabetes mellitus, hyperlipidemia and lactic acidosis in man.
 ...
PMID:Dichloroacetate derivatives. Metabolic effects and pharmacodynamics in normal rats. 366 16

Pseudohyponatremia should be distinguished from true hyponatremia lest injudicious therapy be instituted. Pseudohyponatremia is caused by a displacement of serum water by elevated concentrations of serum lipids or proteins. Only two (flame photometry and indirect potentiometry) of the three current methods available for measuring serum sodium involve sample dilution and may consequently produce spuriously low sodium values. The third method (direct potentiometry) involves no sample dilution, and sodium measurements are unaffected by hyperlipidemia and hyperproteinemia. As all three methods for sodium measurements may coexist in a clinical laboratory, it is important for the physician to be aware not only of the serum value but also the method employed.
 ...
PMID:Pseudohyponatremia. 399 1

Six patients had apparent hyponatremia associated with hyperlipidemia and acute pancreatitis. To our knowledge, only one such patient with acute pancreatitis has previously been described, although the association of hyperlipidemia with "pseudohyponatremia" had been well documented. One of the above patients, whose condition was hemodynamically unstable on admission, developed dangerous symptoms of hyperosmolarity and cerebral dysfunction following aggressive resuscitation with hypertonic saline solution. The pseudohyponatremia results from displacement of water in the serum by the lipids, with sodium existing only in the aqueous phase. This volume displacement results in errors of sodium measurement when the latter is determined by flame photometry or indirect potentiometry, but not when determined by ultracentrifugation and direct potentiometry.
 ...
PMID:Pseudohyponatremia in acute hyperlipemic pancreatitis. A potential pitfall in therapy. 402 58

In 48 patients with early stage renal disease and mild to moderate hypertension, control of high blood pressure and metabolic alterations during long-term diuretic treatment (mean duration, 71 months) were assessed. Compared to the untreated state, administration of thiazide-potassium sparing diuretics, a single table per day, supplemented by dietary sodium restriction, led to normalization of high blood pressure. Renal function was preserved. Gross abnormalities in electrolyte metabolism did not occur. Deterioration of glucose tolerance was noted in 3 patients. Preexisting hyperlipidemia was aggravated by the diuretics in men and postmenopausal women, but premenopausal women were protected. Long-term diuretic treatment was well tolerated, and caused remarkably few significant untoward reactions. The unfavorable metabolic response to diuretic treatment may, however, cancel part of the potential benefit of blood pressure control in certain patients. During long-term diuretic treatment of renal patients, attention should be given to monitoring of metabolic parameters and the introduction of specific dietary treatment may become the cornerstone of patient management.
 ...
PMID:Clinical efficacy and safety of long-term diuretic treatment in renal parenchymal hypertension. 407 9

Fifty Type II diabetic patients with mild hypertension were treated by a high cereal fibre, low fat and low sodium diet in a controlled trial for a 3-month period. The modified diet and control diet groups were well matched although the control group had significantly increased levels of HDL2-cholesterol (p less than 0.05). The modified diet group had a significant reduction of mean serum triglyceride (p less than 0.05) and elevation of HDL2 (p less than 0.05) levels. There was also a reduction of systolic (p less than 0.001) and diastolic blood pressure (p less than 0.001), weight (p less than 0.01) and glycosylated haemoglobin (p less than 0.001). No changes were observed in the control group. In those patients with added hyperlipidaemia, dietary therapy resulted in a significant decrease of mean serum cholesterol (p less than 0.02), triglyceride (p less than 0.01) and glycosylated haemoglobin levels (p less than 0.01). The control group had a significant reduction of HDL-cholesterol (p less than 0.02). We conclude that a high cereal fibre, low fat and low sodium dietary regimen is associated with improvement in cardiovascular risk over a 3-month period, especially in those with hyperlipidaemia. Contrary to previous reports, no deleterious effect on serum triglyceride, HDL- and HDL2-cholesterol levels were recorded in this study. These data add further support to the recent dietary recommendations of several Diabetic Associations.
 ...
PMID:Effect of a high fibre, high carbohydrate dietary regimen on serum lipids and lipoproteins in type II hypertensive diabetic patients. 609 30

In studies concerning risk factors for cardiovascular diseases, a number of reports have emphasized the influence of lipids, but the role of dietary minerals other than sodium has been less studied. However, epidemiological studies have suggested that dietary intake of magnesium and potassium may be involved in such pathogenesis. Studies of the influence of magnesium deficiency on arteriosclerosis include its effect on the initial lesion, altered metabolism of elastin, proliferation of collagen, calcification, lipid metabolism, platelet aggregation and hypertension. Magnesium and potassium metabolism are closely related and magnesium is required for maintaining the level of cellular potassium. As a consequence, magnesium and potassium deficiency frequently occur together and potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular magnesium and potassium. Experimental magnesium deficiency induces arterial damage, a loss of magnesium and potassium and an increase in the calcium and sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that magnesium deficiency may affect several different stages involved in arteriosclerosis and that potassium deficiency may exacerbate this. Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid. Magnesium and potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Role of magnesium and potassium in the pathogenesis of arteriosclerosis. 639 44

We evaluated the Kodak Ektachem multilayer ion-selective electrolyte slides. For various types and concentrations of control material the precision (CV) within- and between-day ranged from 0.5 to 1.3% (1.7-2.1%) for sodium, 1.2 to 2.2% (2.7-2.9%) for potassium, 2.9 to 4.6% (5.9-6.7%) for carbon dioxide, and 0.7 to 1.6% (1.3-1.4%) for chloride. For all these analytes, analytical recovery was about 100%, except in the supra-physiological ranges, for which carbon dioxide recovery was about 110-120%. Either serum or heparin-treated plasma can be used, interchangeably, for analysis; use of serum treated with lithium iodoacetate is unacceptable. Comparisons with results by continuous-flow procedures demonstrated good correlation for sodium, potassium, and chloride; carbon dioxide comparisons indicate an Ektachem calibrator change may be required. Abnormally low protein concentrations or lipemia had no observed effects on results for electrolytes. Abnormally high protein concentrations affect sodium results slightly (approximately 5 mmol/L).
 ...
PMID:Multilayer film analysis: evaluation of ion-selective electrolyte slides. 640 Dec 31

Persons with either borderline or established hypertension should always be instructed in a series of general measures. These include a reduction of overweight, dietary salt restriction, no smoking, whenever possible discontinuation of oral contraceptives, appropriate physical exercise, and treatment, primarily by diet, of a coexisting hyperlipidemia. Such non-pharmacologic measures may often improve the potential risk constellation and in some persons with borderline or mild hypertension even normalize the blood pressure. Pharmacotherapy is recommended only in selected cases with persistent borderline blood pressure elevation but, on a partly empirical basis, appears usually to be indicated for established hypertension of greater than or equal to 160/95 mm Hg. The coexistence of diabetes mellitus or renal functional impairment and advancing age of a patient deserve special consideration in the choice and/or dosage of antihypertensive drugs. Failure to achieve satisfactory blood pressure control through general measures and appropriately dosed triple drug therapy (including a diuretic, a betablocker or other sympatholytic or calcium antagonist, and (di)hydralazine, prazosin or endralazine) calls for thorough reevaluation of the situation. Causes which may simulate or induce resistant hypertension include technical problems with measurement, oral contraceptives, insufficient patient cooperation, sodium fluid volume retention, insufficient pharmacotherapy, drug interactions, "office hypertension" with satisfactory blood pressure in the patient's daily environment, and potentially operable causes such as renal artery stenosis or pheochromocytoma. If none of these factors is present, persistent uncontrolled hypertension can very often be treated satisfactorily with newer potent drugs such as the convertase inhibitor captopril as first choice agent in women, or the direct vasodilator minoxidil as the preferred agent in men. Together with the necessary steps to improve patient compliance, including increased blood pressure measurements by the patient himself, practitioners can now rely upon effective therapeutic tools. The present social and economic burden resulting for the individual and the public from neglected therapeutic opportunities, from excess morbidity and early death due to inadequately treated hypertension, can and must be reduced in the interests of the community at large.
 ...
PMID:[Long-term treatment of hypertension in 1983]. 641 60


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>