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)

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

We describe the performance of a colorimetric reagent kit (Diagnostic Systems Laboratories, Inc., Webster, TX 77598) for measuring calcium directly in urine, serum, and ultrafiltered serum, and compare the results with those obtained with atomic absorption spectrophotometry. The CV for within-run precision was 2.8 and 2.1% for urine and whole serum, respectively (n = 10 each). Between-run precision for urine, whole serum, and ultrafiltered serum was 1.9, 1.6, and 2.2%, respectively (n = 8 to 10). Analytical recovery of added calcium from three different urine and serum specimens, to which three different concentrations of calcium had been added, was 101.9 (SD 0.3%) for urine and 100.9 (SD 0.2%) for serum. Assay of 30 urine specimens, 15 ultrafiltered serums, and 20 whole serums by both the kit and atomic absorption spectrophotometry demonstrated correlation coefficients of 0.993, 0.828, and 0.751, respectively. Mg2+, hemolysis, or lipemia does not interfere. Compared with atomic absorption spectrophotometry, the calcium kit procedure is rapid and simple.
 ...
PMID:New rapid kit for determining calcium in serum and urine evaluated. 669 96

A case of subcutaneous fat necrosis (S.F.N.) with hypercalcemia and hyperlipemia in a newborn infant is reported. On the basis of previous reports it is impossible to definite the pathogenesis of hypercalcemia and hyperlipemia in subcutaneous fat necrosis. Moreover the Authors point out that in a newborn with S.F.N. plasma levels of calcium and lipids and, if it is possible, urinary prostaglandin E and serum PTH and 250HD3 should be determined.
 ...
PMID:[Fat necrosis in the newborn infant associated with hypercalcemia and dyslipidemia (description of a case)]. 692 59

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
 ...
PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

The chemical measurements on our Technicon SMAC of lipemic sera before and after clearing lipemia by ultracentrifugation showed that uric acid, creatinine, carbon dioxide, calcium, phosphorus, potassium, and alkaline phosphatase were not affected significantly by lipemia, whereas sodium, urea, glucose, chloride and total protein showed small but significant increases with averages of less than 1.9 percent. Albumin showed a significant decrease of 1.2 percent. In contrast, the results for the enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) showed striking differences between pre- and post-centrifuged sera in a number of specimens. With lactate dehydrogenase, thirty-two of fifty specimens registered an increase in activity while with the aminotransferases, thirty-five and forty-one out of fifty specimens showed a decrease in aspartate aminotransferase and alanine aminotransferase activities, respectively. Although much of the lipemic interference can be explained by the volume displacement of serum by lipids or by interference by lipemia with colorimetry, the anomalous effects observed with the enzymes indicate the possibility of other, as yet, undetermined factor(s).
 ...
PMID:The effect of hyperlipidemia on Technicon SMAC measurements. 712 23

Naturally occurring kidney stones are rare in animals. The Japanese strains of spontaneously hypertensive rats (SHR) are normotensive at birth but develop high blood pressure, hyperglycaemia and hyperlipidaemia as they mature. The SHR strain is prone to develop kidney stones. A unique sub-strain of SHR has been developed in which some animals develop hypothalamic obesity concomitantly with their rising blood pressure, i.e. Obese/SHR. The Obese/SHR characteristically develop microscopic kidney stones which become detached at an early stage of formation, migrate to the bladder, and grow by concretion into huge, rounded calculi. The stone nidus starts as a subepithelial cyst-like focus containing oedema, colloidal acidic mucoprotein, and red and white blood cells suspended on a delicate network of fibrils. THe nidi grow by concretion of an admixture of calcium and acidic protein in a lamellar arrangement. The disparate morphogenesis and anatomic location of kidney stones in Obese is opposed to non-obese/SHR suggest that calculus formation may be governed by specific differences in genetic programming. The incidence of kidney stones parallels the severity and chronicity of the hypertension in SHR, non-obese and Obese/SHR, and the Cushingoid habitus in the Obese/SHR.
 ...
PMID:Kidney and bladder calculi in spontaneously hypertensive rats. 729 30

The pathogenesis of acute pancreatitis is poorly understood, despite well-recognised precipitating factors. Current evidence suggests that the earliest abnormalities of acute pancreatitis arise within acinar cells, but the key intracellular trigger has yet to be identified. Within the pancreas, physiological concentrations of secretagogues bind to G-protein-linked cell-surface receptors on acinar cells, evoking short, oscillatory spikes of acinar cytosolic-free ionised calcium ([Ca2+]i), an ubiquitous intracellular messenger. Specific effects within acinar cells include initiation of enzyme release through the phosphorylation cascades of stimulus-secretion coupling. Low resting levels of [Ca2+]i are restored by Ca(2+)-ATPase, which pumps calcium into the endoplasmic reticulum and out of the cell. If high concentrations of [Ca2+]i persist, toxicity results, intracellular signalling is disrupted, and cell damage occurs. Sustained elevations in acinar [Ca2+]i result from exposure to high concentrations of secretagogues, high doses of which also induce acute pancreatitis. Similarly, sustained elevations of [Ca2+]i may result from ductal hypertension, alcohol, hypoxia, hypercalcaemia, hyperlipidaemia, viral infection, and various drugs--all factors known to precipitate acute pancreatitis. We suggest that these factors precipitate acute pancreatitis by causing either excessive release of acinar [Ca2+]i, or damage to the integrity of mechanisms that restore low resting levels of [Ca2+]i, and that the consequent calcium toxicity is the key trigger in the pathogenesis of acute pancreatitis.
 ...
PMID:Is an elevated concentration of acinar cytosolic free ionised calcium the trigger for acute pancreatitis? 747 53

Diuretics have been used to treat hypertension since 1958. The doses used were relatively high. Dose-dependent side effects and the increasing availability of other drugs such as beta- and alpha-blockers, calcium-entry blockers, and angiotensin-converting enzyme (ACE) inhibitors, with equal antihypertensive efficacy but additional effects in cardiovascular diseases, led to a decrease in diuretic use. In controlled trials, little or no protection against coronary artery disease (CAD) was discussed as being due to the diuretics' side effects. The main side effects are hypokalemia, hyperglycemia, and hyperlipidemia. Hypokalemia occurs most often (up to 30%) in thiazide-treated hypertensive patients, and may cause arrhythmias in patients with CAD. This side effect is clearly dose-dependent and may be avoided by comedication with antikaliuretics. Glucose intolerance may develop in about 3% of diuretic-treated men and is reversible after discontinuation of the diuretic. This side effect is functionally correlated with hypokalemia and therefore is not seen when patients are given a comedication (for example, spironolactone prevents hypokalemia). Hypercholesterolemia was first reported in 1964 during long-term diuretic treatment. During the first 12 weeks of treatment, low-density lipoprotein (LDL) cholesterol increased 5-15% in men and postmenopausal women. After 1 year of therapy, the levels decreased to pretreatment values. However, in placebo-controlled trials, the placebo groups exhibited cholesterol levels falling below the diuretic group. Although the mechanisms and the clinical implications of these side effects are not completely understood, the perception grew that diuretics per se may have been at least partially responsible for the lack of protection against CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The role of low-dose diuretics in essential hypertension. 750 54

The number of women affected by postmenopausal osteoporosis is likely to continue to increase substantially as the population ages. Furthermore, the therapeutic options for such patients are likely to increase. In this brief review, we outline the use of the currently available medications for the management of osteoporosis--namely, estrogen, calcitonin, calcium, and vitamin D. In addition, we discuss the next generation of drugs that are likely to become available in the future--the bisphosphonates and estrogen analogues. As these options become available, the prevention and treatment of osteoporosis will become similar to the management of other common disorders such as hypertension or hyperlipidemia, in which the most appropriate medication may differ for individual patients. Thus, the treatment of osteoporosis is likely to evolve from a decision of whether to initiate estrogen replacement therapy to a more complex decision of the best agent to use for an individual patient.
 ...
PMID:Treatment options for osteoporosis. 756 51

This chapter focuses on the biochemical mechanisms that mediate glucose-stimulated insulin secretion (GSIS) from beta-cells of the islets of Langerhans and the potentiating role played by fatty acids. We summarize evidence supporting the idea that glucose metabolism is required for GSIS and that the GLUT-2 facilitated glucose transporter and the glucose phosphorylating enzyme glucokinase play important roles in measuring changes in extracellular glucose concentration. The idea that glucose metabolism is linked to insulin secretion through a sequence of events involving changes in ATP:ADP ratio, inhibition of ATP-sensitive K+ channels, and activation of voltage-gated Ca2+ channels is critically reviewed, and the relative importance of ATP generated from glycolytic versus mitochondrial metabolism is evaluated. We also present the growing concept that an important signal for insulin secretion may reside at the linkage between glucose and lipid metabolism, specifically the generation of the regulatory molecule malonyl CoA that promotes fatty acid esterification and inhibits oxidation. Finally, we show that in contrast to its short term potentiating effect on GSIS, long-term exposure of islets to high levels of fatty acids results in beta-cell dysfunction, suggesting that hyperlipidemia associated with obesity may play a causal role in the diminished GSIS characteristic of non insulin-dependent diabetes mellitus (NIDDM).
 ...
PMID:Metabolic coupling factors in pancreatic beta-cell signal transduction. 757 98


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