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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the incidence of clinical and autopsy arteriosclerosis (AS) was studied in over 300 renal transplant patients (RTP) followed in our clinic up to 13 years post-transplant. Of 45 RTP followed a mean of 10.45 years, the incidence of clinical AS was 6% or 0.58% per year at risk. The incidence of death from AS was 2.2% over 10 years or 0.22% per year at risk. There was no apparent tendency for increase of the risk incidence with increasing time post-transplantation up to 13 years. This incidence of clinical and death-related AS in long term RTP contrasts sharply with a quite high incidence of both clinical and death-related AS in long-term dialysis patients as reported by Scribner's group and both the European and U.S. Dialysis Registry. Of our RTP surviving a decade or more, 77% have normal serum triglycerides and 92% are normotensive, again contrasting sharply with a 70-80% incidence of hyperlipidemia and a 60-80% incidence of hypertension in long-term dialysis patients. These studies suggest that the high rate of accelerated AS in dialysis patients is largely reversed by successful renal transplantation, probably due to a lowering of both blood pressure and hyperlipidemia in the long-term RT patients. Practically, these results suggest that the superior survival of transplant patients over dialysis patients already evident at 10 year mark will widen further during the second post-transplantation decade.
Ann Surg 1976 Sep
PMID:Factors in the differential rate of arteriosclerosis (AS) between long surviving renal transplant recipients and dialysis patients. 78 91

Serum lipids in 58 renal transplant recipients were related to duration of follow-up, relative body weight, steroid medication, proteinuria and graft performance. Hyperlipidemia was observed between the 4th month and the end of the first year after transplantation in 83% of the patients. Thereafter, the frequency of hyperlipidaemia appeared to decrease: at 4 to 7 years only 61% of the subjects continued to exhibit abnormal high serum lipids. Three mechanisms leading to hyperlipidaemia were identified: 1) overweight, 2) steroid mediation, 3) proteinuria. A forth apparent mechanism was impaired transplant function.
Klin Wochenschr 1976 Sep 15
PMID:Hyperlipidemias in patients with kidney transplants. 78 55

The risks of the use of oral contraceptives (OC) or intrauterine devices (IUD) to the woman with significant cardiac disease are discussed. An increased risk of thromboembolic events, a hypertensive street, the retention of body fluids and water resulting in weight gain, and hyperlipidemia are some of the adverse effects of OCs reported in the literature. With the IUD, the risk of pelvic infection and the occurrence of the vagal syndrome at, or immediately after, insertion have serious implications for the woman with cardiac disease. It is concluded that OCs containing 50 mcg or more of estrogen should not be prescribed to women with cardiac disease, though combination OCs containing 20-30 mcg estrogen may be tried with caution. Very little risk is posed by the insertion of an IUD accompanied by antibiotic treatment. The conventional methods of contraception may be offered, but the greater risk of pregnancy should be carefully considered.
Clin Obstet Gynecol 1975 Sep
PMID:Contraception for the woman with significant cardiac disease. 80 65

Vitamin E deficiency in two species of monkeys (capuchins and cynamolgus) reduced the in vitro cholesterol esterification by plasma lecithin-cholesterol acyltransferase. The reduction was greates in the most deficient species and in animals fed a diet rich in polyunsaturated fat (safflower oil) stripped of vitamin E. The best correlate of total esterification was the plasma concentration of free cholesterol which reflected the degree of hyperlipidemia, found to be greatest in capuchins fed coconut oil. A logical explanation for the decreased LCAT activity in vitamin E deficiency would be peroxidative damage of substrate (the PUFA of lecithin) or of sulfhydryl sited on lecithin-cholesterol acyltransferase itself. However, neither case was fully supported by the data suggesting that additional information concerning the nature of the reaction and the role of vitamin E is required.
Am J Clin Nutr 1975 Sep
PMID:Depression of lecithin-cholesterol acyltransferase esterification in vitamin E-deficient monkeys. 80 56

These studies provide new insight into the complex mechanisms wherby hyperlipidemia causes progressive atherosclerosis. It has been shown that physical injury to the endothelial lining of arteries sets off a process which probably is an attempt at healing the injury but which can lead to atherosclerosis. It has also been found that chemical agents such as homocystine can produce a similar series of events leading to atherosclerosis. These events include focal loss of endothelium, exposure of subendothelial connective tissue, and adherence of platelets followed by release of factors that stimulate intimal smooth muscle proliferation. The present studies indicate that the effects of chronic hyperlipidemia are complex in that the condition results not only in the deposition of lipids in the atheromatous lesions but that it may produce the primary endothelial injury that initiates the process of atherosclerosis as well.
Science 1976 Sep 17
PMID:Hyperlipidemia and atherosclerosis. 82 15

Plasma linoleic acid levels were found to be low in the atherosclerosis patients investigated. In contrast, platelet arachidonic acid levels were decreased only when atherosclerosis was combined with diabetes or mixed hyperlipidemia. In acute vascular thrombosis, a marked decrease in platelet arachidonic levels occurrrd, irrespective of whether the patient had atherosclerosis or not.
Clin Chim Acta 1977 Sep 15
PMID:[Platelets fatty acid variation in patients with atherosclerosis (author's transl)]. 89 Sep 91

A rapid method for estimating glucose concentrations in serum and in fluoride-, iodoacetate-, heparin-, and EDTA-treated plasma and whole blood is described. The procedure requires about three minutes to perform and utilize a tungstic acid precipitant solution and urine glucose dipsticks. Test results correlate with those of a reference quantitative glucose method at levels from 25 to 500 mg/dl (1.38 to 27.5 mmol/l). Hemolysis, lipemia and bilirubin levels as high as 20 mg/dl (342 mmol/l) do not interfere with the procedure. The simplicity and adaptability of the method make it useful in emergency situations.
Am J Clin Pathol 1977 Sep
PMID:A rapid screening method for blood glucose estimation. 90 68

We report the case of a 5-year-old girl who died two years after onset of the idiopathic nephrotic syndrome, which failed to respond to treatment with corticosteroid and cyclophosphamide. Severe atherosclerotic changes were noted in both coronary arteries. Prolonged hyperlipidemia in patients with long-standing nephrotic syndrome may represent a major risk factor predisposing to premature coronary atherosclerosis in children who are also destined to develop chronic renal failure.
Am J Dis Child 1977 Sep
PMID:Premature coronary atherosclerosis in a 5-year-old with corticosteroid-refractory nephrotic syndrome. 90 86

A patient is described with acute pancreatitis which was probably caused by furosemide. Administration of furosemide on two separate occasions was associated with increases in serum amylase concentrations and recurrence of abdominal pain. This case is of further interest because of the presence of hyperlipemia in the absence of an underlying lipid abnormality. Following recovery from pancreatitis, the lipoprotein pattern evolved from type V to type III, type IIA, and finally to normal.
Am J Dig Dis 1977 Sep
PMID:Acute pancreatitis secondary to furosemide with associated hyperlipidemia. 90 Jan 1

The catabolism of chylomicrons was investigated in genetically obese rats and their nonobese littermates, and was compared with catabolism in older Sprague-Dawley rats with body weights similar to the obese rats and their younger controls. Labeled thoracic-duct lymph was collected from donor rats and the catabolism of the labeled chylomicrons was studied after a single intravenous injection or during steady intravenous infusion in unanesthetized, nonfasting, recipient rats. In the genetically obese rats clearances from the plasma of chylomicron triacylglycerol and cholesteryl ester were less than in their nonobese littermates. Fractional clearance rates were reduced for both triacylglycerol and cholesteryl ester but triacylglycerol turnover rate (mg min(-1)) was greater than controls. Chylomicron triacylglycerol clearance was more efficient than cholesteryl ester clearance so that radioactivity remaining in the plasma was relatively depleted in triacylglycerol. The large-bodied old Sprague-Dawley rats showed no reduction in clearance of chylomicron radioactivity in comparison with younger controls. These results suggest that hyperlipidemia in genetically obese rats may be due in part to an accumulation of chylomicron remnants in the plasma. Flotation characteristics of plasma lipoproteins in the obese rats were consistent with this interpretation. However, separate experiments showed that genetically obese, fasting rats also accumulated more triacylglycerol in the plasma after injection of Triton WR 1339. The enlarged plasma triacylglycerol pool appears to derive from a mixture of hepatic and intestinal triacylglycerol-rich lipoproteins which, together, overload their common removal mechanism. Addition of cholesterol to the diets of the obese rats exacerbated their hyperlipemia and hepatic steatosis whereas their nonobese littermates and the large-bodied Sprague-Dawley rats were unaffected.
J Lipid Res 1977 Sep
PMID:Catabolism of chylomicron triacylglycerol and cholesteryl ester in genetically obese rats. 90 8


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