Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year-old male was admitted with an acute myocardial infarction. A coronarography showed 90% occlusion in of the descendent anterior artery. A coronary angioplasty was done with excellent response. As coronary risk factors he had diabetes mellitus for 5 years and dyslipidemia with a phenotype IIb and hypo-alpha-lipoproteinemia. The case is discussed in regard to the possible etiopathogenic causes for his premature atherosclerosis.
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PMID:[Premature atherosclerosis in a 17-year-old male with diabetes mellitus and familial dyslipoproteinemia]. 163 17

The cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl esters from high-density lipoproteins (HDL) into very-low-density lipoproteins (VLDL) with a reciprocal exchange of triglycerides. Plasma CETP is mainly bound to HDL and is involved in the interconversion of these lipoproteins. In experimental models such as transgenic mice, CETP activity decreases HDL cholesterol and increases the cholesteryl ester content of apo B-containing lipoproteins. In humans, CETP activity and concentration are positively correlated with VLDL-LDL cholesterol. Clinical studies suggest that the effect of CETP on HDL cholesterol depends on the amount of acceptor lipoproteins. CETP activity is negatively correlated with HDL cholesterol only in hypertriglyceridemic states. Various CETP gene mutations have been reported, they induce hyper-alpha-lipoproteinemia. On the other hand, the impact of the variability of CETP gene on HDL cholesterol variations in Caucasians is controversial. CETP is often involved in secondary dyslipidemia and is susceptible to modify the composition of plasma lipoproteins in an atherogenic way. The real impact of CETP activity on atherosclerosis is still unknown. CETP is susceptible to play a proatherogenic role since it mediates a redistribution of plasma cholesterol from lipoproteins associated with a protection against atherosclerosis into the proatherogenic apo B-containing lipoproteins. However, CETP mediates one of the steps of the reverse cholesterol transport, an antiatherogenic process that channels cholesterol from peripheral tissues back to the liver.
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PMID:Cholesteryl ester transfer protein: an enigmatic protein. 896 91

We studied the coronary risk factors of hospitalized patients with coronary artery disease (CAD) in the Department of Cardiovascular Internal Medicine of Kobe University Hospital in 1993, 1996, 1999 and 2003, and examined trends in the factors over the past decade. The prevalences of diabetes mellitus (DM) (24.7%, 33.6%, 41.1% and 44.7%, respectively) and impaired glucose tolerance (IGT) (5.9%, 8.0%, 9.3% and 11.0%, respectively) steadily increased, whereas dyslipidemia (high total cholesterolemia, high triglyceridemia, or low high-density lipoproteinemia) and hypertension remained unchanged. We also revealed an increase in hemoglobin A1c levels (5.8%, 5.9%, 6.2% and 6.4%, respectively), in contrast to modest improvements in lipid levels and blood pressure levels. Additionally, patients with multi-vessel disease (MVD, stenosis in more than two major coronary vessels) significantly increased from 44.7% in 1993 to 58.8% in 2003 (p < 0.01). In 1993, DM and dyslipidemia were significant predictors for MVD (Odds Ratio: 2.72 and 2.68, respectively). On the other hand, in 2003, the significant predictor for MVD shifted to DM alone (Odds Ratio: 2.38). In conclusion, the prevalence rate of DM among CAD patients significantly increased in this decade, and the consequent increase in the prevalence of MVD should be recognized as the most important problem clinically.
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PMID:Impact of increasing diabetes on coronary artery disease in the past decade. 1555 9

This paper reports a rare case of elevated lipoproteinemia(a) that evolved into thrombosis during the neonatal period. During the first days of life, the patient presented with an intracardiac thrombus, pulmonary thromboembolism and a hemorrhagic stroke. Initially, the results of the blood tests performed to screen for thrombophilic diseases were normal for the patient's age. The maternal dyslipidemia and the family's positive history of thromboembolism drew attention to an underlying, inherited, thrombophilic defect. Upon further investigation of the thrombophilia, the increase in lipoprotein(a) levels found in the mother and infant enabled the diagnosis of hyperlipoprotein(a) and the administration of appropriate therapy.
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PMID:Elevated lipoprotein(a) in a newborn with thrombosis and a family history of dyslipidemia. 2324 86

Lipoprotein apheresis (LA) is an extracorporeal technique which permits the unselective or specific removal of lipoproteins, namely Low Density Lipoproteins (LDL), as well as other apolipoprotein B100-containing lipoproteins from plasma. LA represents a selective upgrade (with both clinical and metabolic advantages) from conventional forms of extracorporeal therapy such as plasma-exchange (PEX) which was used in the seventies to treat severe hypercholesterolemia. The primary reason for using is the treatment of homo-, double- (or compound) and heterozygous familial hypercholesterolemia (Hoz-, DHtz,- Htz,-FH). This technique has also been shown to be efficacious in the treatment of other severe forms of hyperlipoproteinemia such as: hyperLp(a)lipoproteinemia, the familial combined hyperlipoproteinemia and other varieties associated with an elevated cardiovascular risk (CVR) when used in patients who are poor- or non-responders to pharmacological treatment following specific guidelines for the reduction of cholesterol in plasma. Patients with these severe forms of dyslipidemia and, particularly, those affected by FH are subject to coronary ischemic events and thus require an intensive, efficacious, continuous, and personalized form of therapy. A therapy based solely on current available drugs does not achieve the desired results in the Hoz- and DHtz forms of FH or in approximately 10-20% of the Htz form. For the aforementioned clinical conditions, LA treatment offers a necessary therapeutic approach. LA can also be applied in the prevention of secondary recurrence of coronary ischemic events and of arterial stenosis which appears, rather frequently after vascular surgery (coronary by-pass, percutaneous transluminal angioplasty). Clinical trials have shown that statins provide a major reduction in cardiovascular morbidity and mortality, but often fail to attain desirable LDL-cholesterol target level in Hoz- and DHtz- (Compound) FH high cardiovascular risk patients. Intolerance to statins is also relatively frequent in Htz-FH and non-FH patients. LA has effectively replaced pharmacological cholesterol-lowering therapy for decades. Young high CVR risk patients survived to adulthood thanks only to LA. More recently, promising novel compounds aimed at other molecular targets are being studied for the treatment of severe dyslipidemia: Lomitapide, Mipomersen, PCSK9 inhibitors and HDL-enhancers. It is expected that these potent new agents will be combined with LA in the treatment of the most severe forms of hyperlipidemia.
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PMID:Lipoprotein apheresis: state of the art and novelties. 2335 36

Obesity-associated dyslipidemia is characterized as hyper-triglyceridemia and hypo-high-density lipoproteinemia. Visceral fat accumulation results in the dysregulation of various adipocytokines as well as the elevation of portal free fatty acid and glycerol levels. The latter cause hepatic overproduction of very-low-density lipoprotein, and the adipocytokine dysregulations impair the transfer of cholesterol from extra-hepatic tissues to the liver. In addition, obesity disease associates with the elevated atherogenic remnant lipoprotein as a result of increased lipid absorption and decreased lipoprotein hydrolysis due to insulin resistance. It is important to further elucidate the regulatory mechanisms of adipocytokines on lipid metabolism for the prevention of atherosclerosis.
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PMID:[Dyslipidemia]. 2363 Dec 6