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)

Alterations in lipid parameters occur during many acute infections. Different studies suggest that variations in lipid parameters can be used as markers of the progression of human immunodeficiency virus (HIV) infection. Hypocholesterolemia is observed in asymptomatic HIV+ subjects, then hypertriglyceridemia appears in patients with AIDS. Several hypotheses have been raised concerning the potential causes and consequences of these modifications. Cytokine effects on different enzymes of lipid metabolism, studied in vitro and in vivo, are thought to be partially responsible for the dyslipidemia. Hypertriglyceridemia could participate in cachexia and dementia could be facilitated by the changes in cholesterol metabolism. The use of the lipid parameters is proposed in HIV positive subjects, especially during anti-viral treatment.
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PMID:[Lipoprotein anomalies in HIV infections]. 903 36

A 45-year-old nondiabetic man presented with features resembling diabetic triopathy. He worked in a rayon manufacturing plant and was exposed to toxic levels of carbon disulfide (CS(2)). Clinical abnormalities included peripheral and central nervous system abnormalities as well as retinopathy, dyslipidemia, cardiovascular disease, and nephrotic syndrome. He later developed focal sclerosing glomerulonephritis. The latter has not previously been described in cases of CS(2) exposure. Terminally, he developed end-stage renal disease and progressive dementia, both of which were thought to be consequences of CS(2) exposure earlier in life.
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PMID:Carbon disulfide nephropathy. 1097

Atypical antipsychotics have the potential to cause weight gain and derangement of glucose metabolism. These side effects can lead to obesity, diabetes mellitus, and dyslipidemia and should be considered in the management of the behavioral and psychological symptoms of dementia.
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PMID:Adverse effects of atypical antipsychotics. 1158 88

In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be non-specific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, non-pharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and renin-angiotensin-II-aldosterone modulators.
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PMID:Mechanisms and consequences of large artery rigidity. 1273 19

Vascular dementia (VaD) and Alzheimer's disease (AD) are the most common causes of dementia in the elderly. The aim of this study was to investigate carotid atherosclerosis, serum lipid profiles, and atherogenic hormone levels in nondiabetic Japanese men with VaD or AD. Carotid artery intima-media thickness (IMT) and plaque, serum lipid and lipoprotein profiles, including low-density lipoprotein (LDL) particle size, as well as insulin-like growth factor-I (IGF-I, somatomedin C) and testosterone levels, were determined in 34 patients with AD, 37 patients with VaD, and 63 healthy male controls. Age, body mass index, systolic and diastolic blood pressure, and fasting plasma glucose, hemoglobin A(1c) (HbA(1c)), triglyceride, high-density lipoprotein (HDL)-cholesterol, and apolipoproteins (apo) A-I, B, and E levels did not differ significantly among the 3 groups. However, the mean value of carotid IMT, the frequency of atherosclerotic plaque deposition, the serum levels of LDL-cholesterol, lipoprotein(a), and lipid peroxides, and the incidence of small dense LDL (particle diameter </= 25.5 nm) were increased significantly in VaD patients compared with AD patients or controls. VaD patients had a close reverse correlation between carotid IMT and LDL particle diameter, which were statistically proven independent risk factors for VaD. In contrast, AD patients had significantly lower serum levels of IGF-I and testosterone than either VaD patients or controls. Our results indicate that VaD is associated with atherogenic dyslipidemia, in particular, small dense LDL and carotid atherosclerosis, whereas AD is associated with hyposomatomedinemia and hypogonadism rather than atherosclerosis.
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PMID:Small dense low-density lipoprotein and carotid atherosclerosis in relation to vascular dementia. 1504 95

Type 2 diabetes in the elderly is associated with increased incidence of vascular disease, particularly, atherosclerosis of large blood vessels. Together with other risk factors such as dyslipidemia, atherosclerosis increases the risk for coronary heart disease and stroke. Most studies that have examined the impact of type 2 diabetes and other heart disease risk factors on cognitive functions do not provide evidence that heart disease risk factors (with the possible exception of triglycerides) further increase the likelihood of observing cognitive deficits in diabetic patients. However, none of these studies used imaging techniques to evaluate atherosclerosis or evidence of cerebrovascular disease, such as infarctions. The few studies that have included brain imaging suggest that evidence of cerebrovascular disease further increases the risk for dementia in diabetic patients. The results of longitudinal studies suggest that diabetes is an independent risk factor for cognitive decline and dementia. The pattern of neuropsychological performance observed in type 2 diabetic patients appears to be the result of multiple interacting processes developing over time. In addition to the detrimental effects of protracted impaired glucose regulation on the central nervous system, type 2 diabetes pathology also encompasses the detrimental effects of associated complications such as cerebrovascular disease, which is likely the main cause of the observed processing speed/reaction time decrements.
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PMID:The relationships between atherosclerosis, heart disease, type 2 diabetes and dementia. 1526 76

Increasingly, data from epidemiologic studies suggest diabetes is a risk factor in old age for brain aging, including cognitive impairment and dementia. These associations may reflect a direct effect on the brain of hyperglycemia, or the effects of the diabetes-associated comorbidities of hypertension, dyslipidemia, or hyperinsulinemia. Epidemiologic data on diabetes and brain aging are reviewed. A brief overview is also given of the physiologic mechanisms supporting the epidemiologic data.
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PMID:Diabetes and brain aging: epidemiologic evidence. 1566 19

Although hyperlipidemia is known to contribute to vascular disease and it may play a role in dementia, specific studies for elderly are limited. The aim of this study is to examine the relationship between dyslipidemia and dementia. In this study, 1251 patients admitted to the Hacettepe University Division of Geriatric Medicine were enrolled. On the basis of the mini mental state examination (MMSE), the clock drawing test (CDT) scores, the APA DSM-IV and the NINCDS-ADRDA criteria and the Hachinski ischemic score (HIS), the subjects were divided into four groups: Alzheimer's disease (AD), vascular dementia (VD), mild cognitive impairment (MCI) and normal cognitive status (NCS). The lipoprotein levels were measured, and we analyzed the data using chi2 and the one-way analysis of variance methods. Among the subjects, 14.8% had low high-density lipoproteins (HDL), 58.5% had high triglyceride (TG), 73.6% had high low-density lipoproteins (LDL), and 21.6% had high lipoprotein-a (Lp(a)) of our study population. There was no difference between the dementia subgroups and the NCS group in the lipoprotein levels. The only significant relationship was between high TG levels and the AD, as well as the MCI groups. Low HDL and high LDL are important problems in elderly. Although serum lipid levels, especially of Lp(a), has recently been thought to be related with dementia, our study suggests the absence of such a relationship. The national data regarding the elderly population should be evaluated on the basis of genetic and environmental factors in each country. The present study showing no significant relationship between Lp(a) and the cognitive status adds new information to the available literature.
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PMID:Are serum lipid and lipoprotein levels related to dementia? 1591 Oct 36

Identification of genetic polymorphisms as risk factors for complex diseases affecting older people can be relevant for their prevention, diagnosis and management. The -1131T-->C polymorphism of the apolipoprotein A-V gene (APO A-V) is tightly linked to lipid metabolism and has been associated with increased triglyceride levels and familial dyslipidemia. The aims of this study were to analyze the allele and genotype frequencies of this polymorphism in a Brazilian elderly population and to investigate any association between the polymorphism and major morbidities affecting elderly people. This polymorphism was investigated in 371 individuals, aged 66-97 years, in a Brazilian Elderly Longitudinal Population Study. Major morbidities investigated were: cerebrovascular diseases (CVD); myocardial infarction (MI); type 2 diabetes; hypertension; obesity; dementia; depression; and neoplasia. DNA was isolated and amplified by PCR and its products were digested with restriction enzyme Tru1I. T and C allele frequencies were 0.842 and 0.158, respectively. Our population showed allele frequencies that were similar to European and Afro-American and different from Asiatic populations. Genotype distributions were not within Hardy-Weinberg equilibrium only for the obesity subject sample. On the other hand, a significant association between the C allele and obesity in the presence of CVDxdepression interaction was observed. Logistic analysis showed no association of the polymorphism with each morbidity group. Therefore, the C allele in elderly Brazilian subjects may represent a risk factor for these morbidity interactions, which may lead to better comprehension of their pathophysiology.
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PMID:APO A-V-1131T-->C polymorphism frequency and its association with morbidity in a Brazilian elderly population. 1637 82

Vascular cognitive impairment encompasses a spectrum of clinically defined syndromes ranging from vascular cognitive impairment-no dementia, to vascular dementia. The underlying cerebrovascular pathology includes both overt infarction as well as rarefaction of gray and white matter. Alzheimer's pathology may coexist with vascular pathology. Diagnosis rests on identifying acquired cognitive impairment in the setting of documented cerebrovascular disease, based on clinical presentation and neuroimaging; MRI is more sensitive than CT. The course can be stepwise or gradually progressive. The clinical picture is typically dominated by deficits in executive function rather than the short-term memory deficit typical of Alzheimer's disease. No specific therapies exist, but treatment with anticholinesterase agents and N-methyl-d-aspartate antagonists may result in clinical improvement. Prevention remains paramount, with early recognition of populations at risk and early and aggressive management of risk factors, including hypertension, dyslipidemia, diabetes, and tobacco use as well as antithrombotic therapy, in appropriate populations.
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PMID:Vascular cognitive impairment. 1663 44


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