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)

Current topics and new developments in risk factors for ischemic stroke were reviewed. Hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, cigarrette smoking, and heavy alcohol drinking have been established as being common treatable risk factors for stroke. Recent studies have clarified that homocysteine, various cardiac sources of embolism such as patent foramen ovale, antiphopholipid antibodies, lipoprotein (Lp) abnormalities including Lp(a) and remnant-like particle, insulin resistance or hyperinsulinemia, infectious diseases such as Chlamydia Pneumoniae, and CRP are additional risk factors for stroke. In addition, genetic studies using single nucleotide polymorphisms have suggested that many gene polymorphisms are significant risk factors for certain subpopulations of stroke, which is recognized to be a polygenic disease. Management of these risk factors is crucial for primary prevention of stroke, which is the leading cause of death or disability all over the developed countries.
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PMID:[Risk factors for cerebral infarction: current topics and new developments]. 1278 67

Apolipoprotein E2, which has an R158 for C substitution, has reduced affinity for the LDL receptor and is associated with type III hyperlipoproteinemia in humans. Consistent with these observations, we have found that following adenovirus-mediated gene transfer, full-length apoE2 aggravates the hypercholesterolemia and induces hypertriglyceridemia in E-deficient mice and induces combined hyperlipidemia in C57BL/6 mice. Unexpectedly, the truncated apoE2-202 form that has an R158 for C substitution when expressed at levels similar to those of the full-length apoE2 normalized the cholesterol levels of E-deficient mice without induction of hypertriglyceridemia. The apoE2 truncation increased the affinity of POPC-apoE particles for the LDL receptor, and the full-length apoE2 had a dominant effect in VLDL triglyceride secretion. Hyperlipidemia in normal C57BL/6 mice was prevented by coinfection with equal doses of each, the apoE2 and the apoE2-202-expressing adenoviruses, indicating that truncated apoE forms have a dominant effect in remnant clearance. Hypertriglyceridemia was completely corrected by coinfection of mice with an adenovirus-expressing wild-type lipoprotein lipase, whereas an inactive lipoprotein lipase had a smaller effect. The findings suggest that the apoE2-induced dyslipidemia is not merely the result of substitution of R158 for C but results from increased secretion of a triglyceride-enriched VLDL that cannot undergo lipolysis, inhibition of LpL activity, and impaired clearance of chylomicron remnants. Infection of E(-)(/)(-)xLDLr(-)(/)(-) double-deficient mice with apoE2-202 did not affect the plasma cholesterol levels, and also did not induce hypertriglyceridemia. In contrast, apoE2 exacerbated the hypercholesterolemia and induced hypertriglyceridemia, suggesting that the LDL receptor is the predominant receptor in remnant clearance.
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PMID:Molecular mechanisms of type III hyperlipoproteinemia: The contribution of the carboxy-terminal domain of ApoE can account for the dyslipidemia that is associated with the E2/E2 phenotype. 1292 33

The time to failure of a renal allograft is determined by the initial function achieved after transplantation, the number and severity of insults to the graft, and a number of tissue characteristics. The insults a graft usually encounters include ischaemia/reperfusion injury, acute rejection episodes, drug-related nephrotoxicity, hypertension and hyperlipidaemia. Important tissue characteristics include susceptibility to injury and the ability of the tissue to repair damage. Elderly transplant recipients are considered poor immune responders but if a single acute rejection episode occurs this is more likely to significantly shorten graft and patient survival in this age group. Two issues have been identified with the use of old (>50 years of age) donor kidneys. First, compared with kidneys from younger donors, they have an increased incidence of acute interstitial rejection. Secondly, once a rejection episode occurs, the ability to mount a tissue repair process seems impaired. An explanation for the increased loss of grafts from old donors that have experienced acute rejection episodes is that such kidneys have fewer nephrons that function adequately and that the cumulated effect of damage results in an earlier demise of the graft compared with younger donor kidneys. Alternatively, graft parenchymal cells may undergo premature senescence or aging as a result of multiple injuries and repair. If progressive loss of renal mass or senescence is the mechanism responsible for increased graft loss, then it is expected that grafts from older donors will show a progressive decrease in function over time and that the rate of decline of function will correlate with donor age. We have suggested that increased graft loss of older donor kidneys results from increased incidence of acute rejection episodes in the early post-transplantation months together with a partly impaired ability to repair the tissue. Drug pharmacokinetic parameters are generally little influenced by age. However, the degree to which drugs suppress the immune system, and the extent to which kidneys from older donors are susceptible to the nephrotoxic effects of certain drugs, are unpredictable. There appears to be a more delicate balance between adequate immunosuppression and excess nonimmune toxicity in patients receiving older kidneys. Outcome parameters in elderly renal transplant recipients are currently dominated by increased death from infectious disease and drug-related (cardiovascular) causes. Increased susceptibility to nephrotoxic drugs, and to calcineurin inhibitors in particular, may be related to the increased risk of allograft failure experienced by the elderly as a surrogate for chronic allograft nephropathy.
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PMID:The impact of age on rejection in kidney transplantation. 1590 55

At one time, atherosclerosis was thought to be a simple lipid storage disease. However, it is now recognized as a chronic and progressive inflammation of the arterial wall. Gene deletion experiments in murine models of atherosclerosis that reduce the inflammatory process also reduce disease severity. Identifying the initiators and mediators of that inflammation can provide promising avenues for prevention or therapy. Two prominent risk factors, hyperlipidaemia and infectious disease, point to innate immune mechanisms as potential contributors to proatherogenic inflammation. The TLRs (Toll-like receptors), pro-inflammatory sensors of pathogens, are potential links between inflammation, infectious disease and atherosclerosis. A mechanism for hyperlipidaemic initiation of sterile inflammation can be postulated because oxidized lipoproteins or their component oxidized lipids have been identified as TLR ligands. Moreover, infectious agents are correlated with atherosclerosis risk. We have identified a role for TLR2 in atherosclerosis in mice deficient in low-density lipoprotein receptor. We observed that proatherogenic TLR2 responses to unknown endogenous or unknown endemic exogenous agonists are mediated by non-BMDC (bone-marrow-derived cells), which can include endothelial cells. In contrast, the proatherogenic TLR2 responses to the defined synthetic exogenous agonist Pam3 CSK4 are mediated at least in part by BMDC, which can include lymphocytes, monocytes/macrophages and dendritic cells. TLR2-mediated cell activation in response to endogenous and exogenous agents is proatherogenic in hyperlipidaemic mice.
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PMID:Toll-like receptors in atherosclerosis. 1803 Dec 44

At one time, atherosclerosis was thought to be a simple lipid storage disease. However, it is now recognized as a chronic and progressive inflammation of the arterial wall. Gene deletion experiments in murine models of atherosclerosis that reduce the inflammatory process also reduce disease severity. Identifying the initiators and mediators of that inflammation can provide promising avenues for prevention or therapy. Two prominent risk factors, hyperlipidemia and infectious disease, point to innate immune mechanisms as potential contributors to proatherogenic inflammation. The Toll-like receptors (TLR), proinflammatory sensors of pathogens, are potential links between inflammation, infectious disease and atherosclerosis. There is increasing evidence that TLRs also recognize host-derived ligands and this also connects TLRs to diseases that may not have an etiology that is associated directly with infection. A mechanism for hyperlipidemic initiation of sterile inflammation can be postulated because oxidized lipoproteins or their component oxidized lipids have been identified as TLR ligands. Moreover, infectious agents are correlated with atherosclerosis risk. There are multiple published reports that TLR4 activation is relevant to the inflammation of atherosclerosis in mice and humans. In addition, we have identified a role for TLR2 in atherosclerosis in low density lipoprotein receptor-deficient (LDLr-/-) mice. Proatherogenic TLR2 responses to unknown endogenous or unknown endemic exogenous agonists are mediated by non-bone marrow-derived cells, which can include endothelial cells, adventitial fibroblasts and vascular smooth muscle cells. This is in contrast to the proatherogenic TLR2 response to defined synthetic exogenous agonists, which is mediated at least in part by bone marrow-derived cells, which can include lymphocytes, monocytes/macrophages, NK cells and dendritic cells. Thus, TLR2-mediated cell activation in response to endogenous and exogenous agents is proatherogenic in hyperlipidemic mice.
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PMID:The toll of Toll-like receptors, especially toll-like receptor 2, on murine atherosclerosis. 1822 Jul

Smoking has been known to cause endothelial dysfunction and is an important risk factor for ischemic stroke. In our study we investigated whether chronic cigarette smoking affects the cerebral blood flow velocity response to a physiological, visual stimulus. By using a visual cortex stimulation paradigm, the flow velocity response in the posterior cerebral arteries (PCA) was measured bilaterally, in 32 young healthy adults (16 smokers, 16 nonsmokers). The stimulation protocol consisted of 10 cycles with a resting phase of 20 s and a stimulating phase of 40 s for each cycle. Besides functional transcranial Doppler (TCD), laboratory tests and measurement of intima-media-thickness (IMT) were also performed. Repeated-measure analysis of variance (ANOVA) was used to detect differences in visually evoked relative flow velocity time courses between smokers and nonsmokers. Repeated-measure ANOVA revealed marked difference in the peak systolic flow velocity time courses between smokers and nonsmokers (p< .001). Maximum percent change of visually evoked flow velocity after visual stimulation was 19+/-4% and 30+/-3% in smokers and nonsmokers, respectively (p< .0001). IMT values did not indicate atherosclerosis in young smokers. Infectious disease and hyperlipidemia were also ruled out by measurement of sensitive C-reactive protein and serum lipids. This is the first functional TCD study demonstrating impaired visually evoked flow velocity response caused by chronic cigarette smoking in otherwise healthy, young subjects. The impaired cerebral vasodilatory mechanism together with atherosclerosis may influence stroke occurrence and outcome in chronic smokers.
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PMID:Visually evoked cerebral vasomotor response in smoking and nonsmoking young adults, investigated by functional transcranial Doppler. 1823

To compare adherence to published primary care guidelines by general internal medicine and infectious diseases (ID) specialist physicians treating HIV-positive women we conducted a retrospective patient record review of 148 female HIV-positive patients seen at the Nathan Smith Clinic in New Haven, Connecticut, in 2001 and 2002. Four quality measures were defined to evaluate physician practices: annual cervical cancer screening, influenza vaccination and hyperlipidemia screening, and biennial mammography. Main outcome was the frequency of meeting each measure by generalist and ID-specialist physicians, and the two physician types were compared after controlling for patient clustering, age, and CD4 cell count. Among all measures, the rates of cervical cancer screening in 2001 were lowest among generalists (55%) and ID-specialists (47%) but not significantly different (odds ratio [OR] 1.26, 95% confidence interval [CI] 0.78 to 1.90), and the rates of hyperlipidemia screening in 2002 were highest for both generalists (98%) and ID-specialists (93%), but again not significant (OR 2.86, CI 0.30 to 27.6). No statistically significant differences were found between physician types for any quality measure, nor were significant differences found in the CD4 cell counts of patients of each physician type who received each service. Our results show potential for improvements in care among both generalist and ID-specialist physicians treating HIV-positive women.
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PMID:Physician specialization and women's primary care services in an urban HIV clinic. 1837 14

Since 1965, more than 2000 renal transplantations (including more than 100 living-donor transplantations) have been performed at the University of Brussels. An end-stage renal disease patient candidate to renal transplantation will be therefore followed from his enrolment on the waiting list to the long-term post-transplant period. Improvement in the outcome of renal transplantation is achieved due to better knowledge in many fields of medicine, such as immunology, infectious disease, metabolic diseases (hyperlipemia, diabetes mellitus), pharmacology, use of immunosuppressive regimen, a more adequate cardiovascular prevention and treatment. If the best results were achieved with kidneys from living donors, the graft survival rate at the University of Brussels was nearly 80% for the last period (2000-2006). Unfortunately, renal transplantation cannot cure certain comorbid conditions and even may promote them: infectious diseases, neoplasia, metabolic disorders (e.a diabetes mellitus, hyperlipemia). Many efforts have to be done to develop less toxic and more immune selective therapeutic strategies. Living donation and extension of the pool of cadaveric donors will reduce the length of time spent on the waiting list and will significantly impact on mortality and morbidity after kidney transplantation.
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PMID:[Experience about more than 2000 renal transplantations at the university of Brussels]. 1849 18

No epidemiological studies on cardiovascular disease (CVD) were conducted on Hmong refugees arriving to the U.S. from 1970s to 1990s. This study measured prevalence of CVD and CVD risk factors in Hmong refugees newly arriving from Wat Tham Krabok, Thailand 2004-2006. Cross-sectional study of 1,462 Hmong refugees who received refugee screening exams at seven primary care clinics in St. Paul MN, June 2004-March 2006. In younger age group (N = 988, 0-20 years old), overweight equaled 13.7%, hypertension = 8.2%, pre-hypertension = 9.6% and in a subset, hyperglycemia equaled 20.7% and hyperlipidemia = 13.5%. In older age group (N = 448, >20 years old), overweight equaled 33.4%, obese = 14.8%, hypertension = 16.5%, and pre-hypertension = 36.2%. In a subset, diabetes mellitus = 2.8%, hyperglycemia = 31.7%, hyperlipidemia = 25.8%, renal insufficiency = 9%, and hyperuricemia = 11.7%. Hmong refugees had significant CVD risk factors on arrival. Healthcare providers and public health officers must identify CVD in addition to infectious diseases when refugees arrive in the U.S. and must address long-term care in order to forestall the development of CVD.
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PMID:Cardiovascular disease risks in Hmong refugees from Wat Tham Krabok, Thailand. 1910 3

High dose glucocorticoids (GC) are commonly used for the treatment of autoimmune diseases. The frequencies, occurrence day and dose-dependency for side effects may be different among the events such as diabetes mellitus, hyperlipidemia, infectious disease, osteoporosis, and peptic ulcer. We investigated GC-induced side effects in 68 patients treated with GC for autoimmune diseases. Initial dose of GC (prednisolone equivalent) was 0.67+/-0.35 mg/kg/d. Hypercholesterolemia (66%), hypertension (62%), insomnia (50%), hypertriglyceridemia (44%), excessive appetite (38%), hyperglycemia (18%), digestive symptom (16%), moon-shaped face (13%) and oral candidiasis (12%) were observed in 63 patients treated with GC. Hypercholesterolemia, excessive appetite, digestive symptom, moon-shaped face, and oral candidiasis were associated with the initial dose of prednisolone greater than 0.80 mg/kg/d. Insomnia [median 6 days (range 1-88)], excessive appetite [7 days (2-57)], hypertension [8 days (1-37)], digestive symptom [15 days (1-87)] and hypercholesterolemia [19 days (3-77)] were observed early after 6-19 days starting GC. On the other hand, hypertriglyceridemia [33 days (2-131)], oral candidiasis [35 days (7-52)] and hyperglycemia [60 days (4-134)] were developed after 33-60 days starting GC. Since the frequencies, dose-dependency and occurrence day were different among the side effects of GC, medical staffs including physicians and pharmacists should pay attention such features of the events in the treatment of autoimmune diseases.
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PMID:[Investigation of glucocorticoid-induced side effects in patients with autoimmune diseases]. 1933 98


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