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

Pancreatitis caused by chylomicronaemia was diagnosed in three patients, two men of 36 and 51 years and a woman of 33 years. All three patients had a combined hyperlipidaemia, with severely elevated levels of triglycerides and cholesterol. Secondary causes of hypertriglyceridaemia such as uncontrolled diabetes mellitus, alcohol abuse, and non-compliance with diet and lipid lowering drug therapy caused aggravation of the lipid disorder. It is important to consider chylomicronaemia as a possible cause of pancreatitis, as treatment of the lipid disorder with diet and, if necessary, drugs can prevent recurrence of pancreatitis.
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PMID:[Acute pancreatitis caused by chylomicronemia syndrome]. 856 9

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

Although the treatment of acute ischemic stroke has improved, the greatest reductions in stroke mortality and morbidity may possibly be achieved through more effective prevention strategies. Toward this goal, risk factor profiles for initial and recurrent stroke have been identified through longitudinal epidemiologic studies. Nonmodifiable risk markers for initial ischemic stroke include age, sex, family history, and race/ethnicity. Modifiable risk factors for first ischemic stroke include hypertension, cardiac disease (particularly atrial fibrillation), diabetes, hyperlipidemia, cigarette smoking, alcohol abuse, physical inactivity, asymptomatic carotid stenosis, and transient ischemic attack. As improved acute treatments increase survival after a first stroke, the threat of increased morbidity from stroke recurrence will have greater significance. The risk and specific determinants of early and late stroke recurrence are the subject of ongoing investigations. Age, stroke syndrome, hypertension, cardiac disease (particularly congestive heart failure), hyperglycemia, and alcohol abuse have been identified as predictors of late stroke recurrence. Now that many risk factors are established, greater emphasis should be placed on identifying high stroke-risk patient populations for intensive risk factor modification and antithrombotic treatments. Better understanding and management of stroke risk factors will undoubtedly improve our ability to prevent first and recurrent ischemic stroke.
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PMID:Identifying patient populations at high risk for stroke. 974 29

Benign symmetric lipomatosis of the pseudoathletic type was identified in a woman with a positive family history for the disorder and a past history of alcohol abuse. She had an exceptionally high number of additional diseases such as arthropathy with degenerative osteoporosis, hyperuricemia, hyperlipidemia, psoriasis, neuropathy, muscular atrophy, arteriosclerosis and increased cardiovascular risk factors.
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PMID:[Benign symmetrical Launois-Bensaude type II lipomatosis with market systemic involvement and psoriasis]. 1090 59

Stroke places a tremendous burden on health resources throughout the world. Improved detection and modification of risk factors could reduce the impact of this disease. Important non-modifiable risk factors for ischemic stroke include age, gender, ethnicity, and heredity. Modifiable risk factors include hypertension, cardiovascular disease, diabetes, hyperlipidemia, asymptomatic carotid stenosis, cigarette smoking, and alcohol abuse. Data from the Northern Manhattan Stroke Study provide new insights into these stroke risk factors. In this study, African-Americans and Hispanics had a greater incidence of stroke, with almost a twofold increase compared with Caucasians. The protective effect of physical activity and moderate alcohol consumption was confirmed and further established as modifiable risk factors. The independent effects of lipids, apolipoproteins, and lipoprotein were also clarified. High-density lipoprotein was shown to be protective against ischemic stroke (particularly atherosclerotic stroke subtypes). Conversely, lipoprotein-a increased the risk for stroke. The ratio of apolipoprotein b to apolipoprotein a-1 was shown to be associated with carotid atheroma. In addition, newer risk factors, including homocysteine and chronic infection (Chlamydia pneumoniae and periodontal disease), are being studied as predictors of ischemic stroke. With these recent advances in the understanding of risk factors, the ability to detect or modify the risk for ischemic stroke should lead to a substantial reduction in the number of people killed or disabled by stroke each year.
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PMID:Newer risk factors for stroke. 1155 52

The liver steatosis is a frequent human disease. The most frequent cause of the process is the alcohol consumption. But it also may arise without significant alcohol abuse. This pathogenetic process is called non-alcoholic steatohepatitis (NASH), that is characterized by the same conditions like the alcoholic steatohepatitis. In the pathogenesis of the NASH various factors participate i.e. obesity, diabetes mellitus type II, hyperlipidaemia, pregnancy, variable chemotoxins, parenteral nutrition, jejunoileal bypass, chronic inflammatory diseases, protein deficient nutrition and inborn metabolic diseases. Pathobiochemically the process consists of oxidative stress and lipid peroxidation. This condition comes from the progressive accumulation of the free fatty acids in mitochondria and from the induction of cytochrome P450, CYP 2E1 isoform in hepatocytes and Kupffer cells. The free fatty acids and ketons can cause the induction of CYP 2E1 system, that is why diabetes mellitus and obesity are the two most important factors in the NASH pathogenesis. This article is concerned mainly in the explanation of NASH pathomechanism.
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PMID:[Role of lipid peroxidation in non-alcoholic steatohepatitis]. 1511 15

A 65-year-old woman was admitted to our hospital for an investigation of liver dysfunction. She had mild obesity with hyperlipidemia, but no history of alcohol abuse. Other known causes of liver dysfunction, such as viruses, autoimmunity and drug effects, were excluded. The liver histology was consistent with nonalcoholic steatohepatitis (NASH). After diagnosis of NASH, the patient started diet and exercise therapy and, in parallel with weight reduction, her liver function improved. One year after the therapy, a liver biopsy showed that steatosis, necroinflammation and even fibrosis were improved. Hence, here we report a case of NASH in which weight reduction was effective in improving both biochemical and histological findings.
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PMID:Nonalcoholic steatohepatitis with improved hepatic fibrosis after weight reduction. 1516 70

Hypertriglyceridemia (HTG) is a rare but well known cause of acute pancreatitis (AP), which can be a life- threatening complication if the degree of HTG is severe enough. It might be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, or drugs. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is the identifiable risk factor. HTG-induced AP typically presents as an episode of AP or recurrent AP. The clinical course of HTG-induced AP is not different from other causes. Routine management of HTG-induced AP should be similar to other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. The mainstay of treatment includes dietary restriction of fatty meal and lipid-lowering medications (mainly fibric acid derivatives). Although there are limited experiences with plasmapheresis, lipid apheresis, heparinization and insulin application, these can support the treatment of HTG- induced AP. We report two cases of HTG-induced AP which were successfully treated by plasmapheresis.
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PMID:Acute pancreatitis due to hypertriglyceridemia: report of 2 cases. 1637 23

Nonalcoholic fatty liver disease is a common condition associated with metabolic syndrome. It is the most common cause of elevated liver enzymes in U.S. adults, and is diagnosed after ruling out other causes of steatosis (fatty infiltration of liver), particularly infectious hepatitis and alcohol abuse. Liver biopsy may be considered if greater diagnostic and prognostic certainty is desired, particularly in patients with diabetes, patients who are morbidly obese, and in patients with an aspartate transaminase to alanine transaminase ratio greater than one, because these patients are at risk of having more advanced disease. Weight loss is the primary treatment for obese patients with nonalcoholic fatty liver disease. Medications used to treat insulin resistance, hyperlipidemia, and obesity have been shown to improve transaminase levels, steatosis, and histologic findings. However, no treatments have been shown to affect patient-oriented outcomes.
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PMID:Nonalcoholic fatty liver disease. 1677 Sep 27

Survivors of ischemic stroke are at significant risk for recurrent stroke. Appropriate therapy for stroke prevention is needed given the significant morbidity and mortality associated with stroke, the high financial costs, and the neurologic disability associated with treatment failure. A treatment strategy based on assessed risk represents an appropriate use of medical resources and results in improved outcomes. This approach requires evaluation of major risk factors, the most serious of which is a history of ischemic stroke or transient ischemic attack. The annual risk for recurrent stroke is 6% during the first 5 years after an initial stroke. Non-modifiable risk factors include age, race, ethnicity, gender, family history, and geography. The most important modifiable risk factor is hypertension. Diabetes mellitus, hyperlipidemia, left ventricular hypertrophy, atrial fibrillation, and lifestyle factors such as smoking, alcohol abuse, and obesity contribute to stroke risk. Antihypertensive, lipid-lowering, and antiplatelet therapies have been successful in reducing the incidence of secondary stroke. Clinical trials validate the benefits of statin therapy in reducing the risk for secondary stroke. Studies of antiplatelet agents, including aspirin, clopidogrel, and aspirin combined with extended-release dipyridamole, have evaluated the risk reduction in recurrent stroke and have been concerned particularly with the risk for hemorrhage. Therapy for stroke prevention based on risk stratification can identify patients who are appropriate targets for aggressive intervention.
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PMID:Secondary prevention of ischemic stroke: evolution from a stepwise to a risk stratification approach to care. 1796 Oct 80


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