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)

1. Hypertriglyceridemia and hyper beta-lipoproteinemia are closely related to the pathophysiologic status of the cerebrovascular patients. 2. The electrophoretic analysis of serum lipoprotein is the usefull method for the study on hyperlipidemia in the cerebrovascular disease. 3. The electrophoretic analysis of the serum lipoprotein gives close relation to the clinical features in the patients with normal serum lipid levels as well as in those with the hyperlipidemia. 4. Hyperlipidemia relates closely to the renal impairment, which is supposed to originate from the sclerotic changes of renal artery.
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PMID:Hyperlipidemia in cerebrovascular diseases. 16 33

The effect of lovastatin on the hyperlipidemia induced in rats with experimental nephrotic syndrome was investigated; toxicity and the effects on common blood chemistry parameters were also assessed. Hyperlipoproteinemia in this particular model is associated with an increase in hepatic synthesis of lipoproteins, and treatment with lovastatin could be the most suitable, since the drug inhibits cellular cholesterol synthesis. Lovastatin treatment resulted in a considerable reduction in plasma cholesterol and triglyceride levels. The decrease in cholesterol levels with treatment was mainly confined to the low-density lipoproteins (LDL) although there was a reduction in the nephrotic-syndrome-induced incremental level of high-density lipoprotein cholesterol. Other lipoprotein fractions were unaffected by lovastatin. LDL apoprotein B was increased in both groups of rats, but to a lesser degree in the lovastatin-treated group, suggesting a double effect, inhibition of both, cholesterol and apoprotein synthesis. Both groups of rats showed a certain degree of renal impairment as shown by significant elevations in plasma urea and creatinine levels. Hepatic damage was also observed, chemically and microscopically, in both groups of rats, being more pronounced in those rats treated with lovastatin in which a 50% mortality ensued after 2 weeks of treatment. At the dosage used this may have some implications in its therapeutic use in certain conditions.
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PMID:Toxicity of lovastatin in rats with experimentally induced nephrotic syndrome. 207 99

The drug treatment of mild hypertension has been shown to afford protection against fatal and nonfatal strokes, congestive heart failure, progression to more severe levels of hypertension, and all-cause mortality, but not against the complications of coronary artery disease. The lack of benefit against coronary artery disease may result from failure to reduce other risk factors or because the drugs employed increased coronary risk. It can be taken as axiomatic that effective preventive antihypertensive therapy is more likely with drugs with mechanisms and sites of action that are focused on the underlying pathophysiology than with drugs that lower blood pressure by means unrelated to the hypertensive process. Adrenergic predominance plays a major role in the initiation and maintenance of essential hypertension and, consequently, the alpha-adrenergic receptor inhibitors were among the first substances to receive serious consideration as antihypertensive agents. However, since these drugs are nonselective, feedback control of transmitter norepinephrine was lost and, consequently, the clinical expectations of the early alpha-adrenergic receptor inhibitors in the treatment of high blood pressure were not fulfilled. The discovery of selective postjunctional alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, which preserve feedback control of transmitter norepinephrine release, was the crucially important step in the development of specific drugs to combat the hyperactivity of adrenergic vasoconstrictor nerves in hypertension. These drugs have been shown to normalize hemodynamics in hypertensive patients. They lower blood pressure through a reduction in peripheral resistance at rest and during exercise, independent of changes in heart rate and blood pressure, with minimal reflex activation or tolerance development. Alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, represent an attractive choice for initial therapy in all grades of hypertension and are especially appropriate in hypertensive patients with congestive heart failure, asthma and chronic obstructive airways disease, renal impairment, diabetes mellitus, hyperlipidemia, benign prostatic hyperplasia, or gout, and in those involved in vigorous work, sports, or exercise. There are no known contraindications to these drugs, except in patients who are sensitive to quinazolines.
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PMID:Pharmacologic basis for the use of doxazosin in the treatment of essential hypertension. 256 23

In any therapeutic situation, the choice of drug therapy depends on an estimation of relative risk and benefit. With respect to moderate hypertension, and with less certainty, mild hypertension, the use of drug therapy has resulted in a decrease in overall mortality, a decrease in the incidence of stroke and renal impairment, but little or no change in the incidence of ischemic heart disease. For several years, the choice of first drug in these situations has rested between thiazide diuretics and beta-adrenoceptor blocking agents. There is probably little to choose between these two groups in terms of efficacy, and equally there is little evidence that patient response to one or other agents can be predicted either on demographic or biochemical evidence. There are, however, several studies both in Africa and America suggesting that black patients have a relatively greater hypotensive response to thiazides than to beta-blockers. The adverse reaction profile of these two groups is quite different. There is currently much debate whether the administration of large doses of thiazide diuretics (for example, 10 mg bendrofluazide per day) may cause a constellation of metabolic side effects (hyperlipemia, hypokalemia, abnormal glucose tolerance, and hyperuricemia) which may result in an increase of the risk of developing coronary artery disease in spite of lowering blood pressure. Further, there is no good evidence that the hypotensive effect of diuretics is dose dependent. On the other hand, the evidence that beta-blockers when used as antihypertensive agents have a primary preventive effect for ischemic heart disease is currently very small.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin converting enzyme inhibition in clinical practice. Re-examination of step care: choice of first drug. 258 Jan 63

Lipids are transported in plasma as lipoproteins, and an increase in 1 or more classes of lipoprotein underlies all forms of hyperlipidaemia. Physiological influences on lipoprotein metabolism are age, gender, bodyweight, diet and exercise. Pathological influences include genetic abnormalities, endocrine dysfunction, renal impairment and iatrogenic effects. Three inherited forms of hyperlipidaemia which predispose to atherosclerosis are familial hypercholesterolaemia (FH), type III hyperlipoproteinaemia and familial combined hyperlipidaemia (FCH), each of which has its own distinctive metabolism defect. In FH, deficiency of low density lipoprotein (LDL) receptors results in the accumulation in plasma of LDL-cholesterol because of a reduction in the receptor-mediated component of LDL catabolism. In type III hyperlipoproteinaemia, the presence of an abnormal apo E isoform (apo E2) in remnant particles leads to their accumulation in plasma, through nonrecognition by remnant receptors and a consequent reduced rate of hepatic uptake. In contrast, there is no primary catabolic defect in FCH, in which increased levels of very low density lipoprotein (VLDL) and LDL are largely the result of increased synthesis.
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PMID:Normal and pathological lipoprotein metabolism. 307 22

Various renal abnormalities have been reported in Alagille's syndrome (arteriohepatic dysplasia), usually as single case reports. The renal findings at autopsy of four patients with Alagille's syndrome, ranging in age from 4 1/2 months to 7 years, 2 of whom had evidence of renal dysfunction, are described and are compared with kidneys from patients with other cholestatic liver diseases of childhood. Two of the Alagille's patients had histologic findings suggestive of membranous nephropathy and special stains revealed accumulation of lipid in the glomerular and tubular basement membranes. Immunofluorescence of 1 revealed extensive accumulation of IgG and IgM. One patient had medullary cysts and mild interstitial fibrosis, and the fourth had a large subcapsular cyst and mild tubulointerstitial nephritis. All 4 cases, when examined with the electron microscope, revealed varying degrees of basement membrane thickening, splitting, and vacuolation with dense osmiophilic particles, most prominent in the patients with membranous nephropathy. These ultrastructural findings did not correlate with the degree of hyperlipidemia, but rather with the patient's age, and were also observed in other cholestatic diseases. The findings suggest that Alagille's syndrome is frequently associated with renal abnormalities, including lipid deposition, which may in some instances, lead to clinically significant renal impairment.
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PMID:Renal histopathology in Alagille's syndrome. 332 21

We have investigated the activity and kinetics of sodium-lithium countertransport (SLC) in patients with IgA nephropathy and their relationship to plasma lipids. Standard SLC activity, the Michaelis constant (Km) and maximum velocity (Vmax) were measured in patients who had IgA nephropathy with either normal serum creatinine (IgA-NRF), or raised serum creatinine (IgA-IRF), and normal subjects (NC). The standard SLC activity was raised in hypertensive patients with IgA-NRF due to a raised Vmax in association with hyperlipidaemia. The Km was significantly lower and Vmax also tended to be lower in IgA-IRF. Km and Vmax were not different in IgA-NRF compared with the NC. There was no difference in the mean standard SLC activity between all three groups. The low Km and low Vmax resulted in a normal standard SLC activity being observed in IgA-IRF which is similar to the situation we have observed in a proportion of diabetic patients with nephropathy. The low Km in patients with IgA nephropathy may be due to inheritance associated with familial essential hypertension or to an acquired change of the kinetics related to a change in the environment of the plasma membrane during the development of renal impairment.
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PMID:Sodium-lithium countertransport kinetics in IgA nephropathy: relation to plasma lipids and renal impairment. 777 2

Liver transplantation poses enormous and complex medical problems. Of the infective complications, bacterial infections are the commonest overall, but the single commonest is cytomegalovirus and the most deadly are the fungal infections. Therapeutic options and possibilities for prophylaxis are improving. Rejection, both acute and chronic, is the other major cause of mortality, and the balance between immunosuppression and infection is difficult. Cyclosporin treatment contributes to renal impairment, hypertension, and multitudinous potential neurological problems. The risk of long-term neoplasia is unclear. Relatively more minor is the potential for osteoporosis and metabolic complications, such as diabetes and hyperlipidaemia. Hepatitis B disease has a sizable risk of recurrence, but the most recent prophylaxis regimes have improved relapse rates. Having survived the physical problems following transplantation, most of which occur in the first 6 months, there are considerable psychosocial adjustments to be made particularly in the case of children where growth and development may have been delayed. Despite all these difficulties, liver transplantation is an expanding and optimistic area with enormous potential.
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PMID:Medical complications of liver transplantation. 833 63

Hypertension, diabetes and hyperlipidemia are risk factors for life-threatening complications such as end-stage renal disease, coronary artery disease and stroke. Why some patients develop complications is unclear, but only susceptibility genes may be involved. To test this notion, we studied crosses involving the fawn-hooded rat, an animal model of hypertension that develops chronic renal failure. Here, we report the localization of two genes, Rf-1 and Rf-2, responsible for about half of the genetic variation in key indices of renal impairment. In addition, we localize a gene, Bpfh-1, responsible for about 26% of the genetic variation in blood pressure. Rf-1 strongly affects the risk of renal impairment, but has no significant effect on blood pressure. Our results show that susceptibility to a complication of hypertension is under at least partially independent genetic control from susceptibility to hypertension itself.
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PMID:Renal disease susceptibility and hypertension are under independent genetic control in the fawn-hooded rat. 852 50

The effect of hyperlipidemia on the progression of chronic renal failure was investigated in 104 chronic renal failure patients, aged 39.3 +/- 2.9 years. The follow up period was 4.1 +/- 2.9 years. The serum creatinine level was 2.1 +/- 1.1 (mean +/- SD) mg/dl at the beginning of study and increased to 8.7 +/- 4.4 mg/dl at the end of the study. The reciprocal serum creatinine concentration (1/Cr) was plotted against the observation time, and the slope was calculated. The absolute value of the slope was used as the progression rate of renal impairment. The progression rate was positively related to total cholesterol level or urinary protein score, while it was negatively related to total protein level. Without the influence of urinary protein score, the progression rate correlated with total cholesterol level. The result suggests that hypercholesterolemia may be an independent aggravating factor in the progression of renal dysfunction in chronic renal failure patients.
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PMID:Hypercholesterolemia and the progression of the renal dysfunction in chronic renal failure patients. 900 82


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