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)

Sixteen monoclonal antibodies (MAbs) directed against toxic shock syndrome toxin-1 (TSST-1) were generated by immunization of mice with purified TSST-1 and subsequent fusion of spleen cells with myeloma cells. Antibody-producing clones, identified by an enzyme-linked immunosorbent assay, were maintained as ascites tumors, and MAbs were purified by protein A chromatography. High-titered clones were further characterized and tested for the ability to neutralize several biological activities of TSST-1. The MAbs, which are of several immunoglobulin subtypes, reacted specifically with purified TSST-1 and TSST-1 present in Staphylococcus aureus culture supernatants. Three MAbs neutralized TSST-1-induced mitogenesis in a dose-dependent manner. Three of eight MAbs tested were able to neutralize induction by TSST-1 of interleukin-1 production by human monocytes. One neutralizing MAb, 8-5-7, was tested for the ability to protect rabbits from a constant infusion of TSST-1. Rabbits given the MAb had an attenuated clinical illness and were protected from the hypocalcemia, lipemia, and hepatic and renal insufficiency seen in control rabbits. Six of seven control rabbits died, compared with only one of seven rabbits treated with MAb 8-5-7. These experiments suggest that MAb 8-5-7 is directed against an antigenic determinant critical to the toxicity of TSST-1 and that the MAbs should be useful as probes in structure-function analyses of the TSST-1 molecule.
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PMID:Neutralization of toxic shock syndrome toxin-1 by monoclonal antibodies in vitro and in vivo. 325 1

The diversity of its causes, the unpredictability of its clinical course, and our expanding knowledge of the conditions that may exacerbate or retard its progression suggest that glomerular sclerosis cannot be attributed to a single aberration in glomerular physiology. Nonetheless, the welter of clinical and experimental observations is beginning to yield a pattern. Agents or conditions injurious to glomerular epithelium tend to cause glomerular sclerosis. Agents or conditions that induce short-term or long-term activation of mesangial cells may lead to glomerular sclerosis. Indeed, one contribution of the healthy epithelium may be to serve as a tonic inhibitor of the intraglomerular processes arising from mesangial-cell activation. Long-term activation of the mesangium is associated with the proliferation and infiltration of cells and with the expansion of the mesangial matrix--the antecedents of sclerosis. We anticipate that different diseases associated with glomerular sclerosis will be found to depend to varying extents on these two potential mechanisms of sclerosis. Beyond a certain threshold of glomerular injury, glomerular diseases share an additional factor: the capacity of both intrinsic cells and infiltrating cells to alter the microenvironment of the glomerulus so that sclerosis progresses inexorably long after the disappearance of the initiating insult. Several potential risk factors may contribute to the progression of chronic renal disease. These factors include systemic hypertension, proteinuria, hyperlipidemia, high protein intake, and probably conditions that lead to glomerular hypertrophy. Interventions designed to minimize the potential contribution of these factors to the progression of renal insufficiency may halt or slow the loss of function of the kidney. Clinical trials designed to examine the effects of these factors on the progressive course of renal insufficiency will help to establish their role and relative importance in humans.
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PMID:The progression of renal disease. 328 63

Chronic renal insufficiency is often accompanied by hyperlipidaemia and subsequent coronary heart disease. Two groups of 15 patients with serum creatinine greater than 2 mg/100 ml and serum cholesterol less than 250 mg/100 ml were given 3 x 50 mg magnesium pyridoxal 5-phosphate glutamate (MPPG) or placebo for 12 weeks in a double-blind, randomised study. Total cholesterol in the MPPG group (282.4 mg.100 ml-1) was lower than in the placebo group (354.3 mg.100 ml-1) after 12 weeks of treatment. Triglycerides in the MPPG group were 265.1 mg.100 ml-1 compared to 361.9 mg.100 ml-1. After 12 weeks on MPPG the LDL/HDL ratio of 3.56 was lower than in the placebo group-6.83. Side effects in the MPPG group were similar to those in the placebo group. Thus, MPPG was an effective antihyperlipidaemic agent in patients with renal insufficiency.
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PMID:Magnesium pyridoxal 5-phosphate glutamate reduces hyperlipidaemia in patients with chronic renal insufficiency. 338 85

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.
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PMID:[Reduction of table salt and diuretic therapy in arterial hypertension in childhood]. 357 12

Certain physiological and pathological conditions in women require choice of a contraceptive method that will not aggravate the condition or exacerbate known side effects. IUDs and oral contraceptives (OCs) are not appropriate for the immediate postpartum. Low dose progestins appear best suited and can be started on the 5th day after delivery. IUDs and high dose discontinuous progestins are the best choices for the menopausal period, but contraindications to them must be respected. Contraception with a dominant progestational climate is required in case of benign breast disease. Low dose progestins may cause luteal insufficiency and low dose combined OCs may allow endogenous estradiol secretion poorly balanced by the progestin. All progestin-dominant formulations and discontinuous 19-norsteroids may be used. 19-norsteroids appear suitable for women with breast cancer because of their antiestrogenic activity. High dose progestins are advisable for women with precancerous or cancerous endometrial pathology. Estrogens should be avoided in such cases. Cervical cancer has never been proven to be hormonodependent, and at present the use of hormonal contraception in cervical dysplasia is not contraindicated except after pelvic radiation for invasive cancer. Use of the IUD has the same indications as for the general population after lesions have been treated. In cases of hyperlipidemia, low doses of continuously administered 19-norsteroids cause a decline of high density lipoprotein (HDL) cholesterol but are considered to be without longterm metabolic effects. The new progestin desogestrel does not diminish HDL cholesterol. Many cases of hyperlipidemia and hypercholesterolemia contraindicate OCs at the usual dose and require mechanical contraception, although low dose progestins may be considered. Derivatives of 17-hydroxyprogesterone are without effects on lipid metabolism but are less reliable. No contraceptive method is fully satisfactory for diabetics. Hormonal contraception is risky because of possible metabolic and vascular effects. Low dose progestins have the fewest side effects but are often poorly tolerated. IUDs are often used for diabetics despite possible increased risks of infection and failure. Hypertensive women should not use combined OCs or high-dose 19-norsteroids, but low dose progestins carry no risk of hypertension. Women at vascular risk are advised to use IUDs if no specific contraindications are found. Otherwise low-dose progestins are an acceptable choice. Low dose progestins are often the only possibility for cardiac patients. Nonhypertensive women with renal insufficiency can use OCs under careful supervision if there are no contraindications. Combined OCs are contraindicated when there is any disturbance of hepatic function, but low dose progestins or mechanical means are acceptable. Chronic use of certain drugs which act as enzymatic inductors is incompatible with hormonal contraception.
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PMID:[Contraception at risk]. 365 96

The incidence of arterial hypertension in patients with gouty nephropathy was studied. A reverse correlation dependence was established between the clearance of uric acid and the values of systolic and diastolic pressure, directing the clinicians to controlling the hyperuricemia, in parallel with the prescription of hypotensive agents. Attention is drawn to the higher incidence of hyperlipidemia in patients with gouty nephropathy and hence--the possibility of more frequent coronary incidents. Renal insufficiency advanced earlier in the patients with gouty nephropathy and arterial hypertension.
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PMID:[Arterial hypertension in gouty nephropathy]. 376 79

The development of experimental atherosclerosis was studied in subtotally nephrectomized rats which were subjected to preimmunization with horseradish peroxidase and subsequent feeding with atherogenic diet. Both in sham-operated pair-fed control animals and in uremic animals, the atherogenic diet caused hyperlipemia which was more pronounced in uremic than in control animals (control animals: triglycerides 1.11 +/- 0.04 mmol/l; cholesterol 5.82 +/- 0.21 mmol/l; uremia: triglycerides 1.33 +/- 0.06; cholesterol 10.9 +/- 0.31). An increase of cholesterol was seen both in the VLDL and in the LDL fractions. Despite more pronounced hyperlipemia, lipid concentration in the aortic wall was not increased nor were more marked histological abnormalities encountered in the aorta of uremic animals (cholesterol-fed control: cholesterol 95.4 +/- 4.4 micrograms/mg protein; phospholipids 2.42 +/- 0.9 micrograms/ml protein; cholesterol-fed uremia: cholesterol 96.8 +/- 4.9; phospholipids 2.52 +/- 0.8). The results suggest that despite hyperlipemia short-term experimental renal insufficiency does not promote atherogenesis.
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PMID:Atherogenesis in experimental uremia. 733 7

Patients with analgesic nephropathy are reported to have a higher risk of atherosclerosis. One possible reason for this is a high incidence of hyperlipaemia in patients with analgesic nephropathy. In a retrospective study, serum cholesterol and serum triglyceride concentrations of patients with analgesic nephropathy and moderately restricted renal function were significantly higher compared to a control group with other renal diseases of similar age and degree of renal insufficiency. Hyperlipaemia in analgesic nephropathy is not explained by end-stage renal failure on one side or protein loss as in nephrotic syndrome on the other side. Some possible mechanisms for hyperlipaemia in analgesic nephropathy are discussed.
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PMID:Hypercholesterolaemia and hypertriglyceridaemia in patients with analgesic nephropathy. 741 66

This review describes categories of renal function (normal, renal insufficiency, end-stage renal failure), types of treatment modalities (renal insufficiency management, dialysis, transplantation), and corresponding dietary parameters (protein, energy, fiber, sodium, fluid, potassium, phosphorus, calcium, vitamins, minerals). The focus is directed toward general and nonrenal specialty practitioners, who are encountering a growing number of geriatric patients and patients who have undergone renal transplantation or are in early renal failure. The findings indicate that early intervention may delay or prevent rapid progression of renal disease in some patients, that treatment modalities continue to need individualized dietary support to maintain nutritional status, and that transplant goals should include control of obesity and hyperlipidemia to reduce cardiovascular mortality.
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PMID:Which diet for which renal failure: making sense of the options. 861 54

A choice of many antihypertensive strategies is now offered for the treatment of the hypertensive patient with renal insufficiency. Angiotensin-converting enzyme (ACE) inhibitors appear to be the drugs of choice since they not only lower blood pressure but also reduce some important risk factors that may cause progressive loss of renal function, such as intraglomerular hypertension, angiotensin II (Ang II)-induced glomerular growth, proteinuria and hyperlipidemia. Indeed, several clinical studies now show that ACE inhibitors offer renal protection beyond the lowering of systemic blood pressure. The new class of Ang II receptor antagonists and its first representative losartan has not yet been tested clinically for its renal protective efficacy. The first signs, however, look promising, since losartan appears to induce changes in several identified risk factors to the same extent as ACE inhibitors, such as renal vasodilation, and a fall in proteinuria and serum lipids. The challenge will be to discover the differences between ACE inhibitors and Ang II receptor antagonists and to use them to the future advantage of the renal patient.
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PMID:Losartan in patients with renal insufficiency. 766 17


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