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

Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2 subfraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides; omega-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLch levels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
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PMID:Nutritional management of plasma lipid disorders. 255 90

Hyperlipidaemia is a major cause of coronary heart disease (CHD) and is especially prevalent in Britain. Prior to lipid-lowering therapy it is necessary to define the type of lipoprotein abnormality present and whether it is primary or secondary. Diet forms the initial treatment but additional drug therapy may be necessary in patients with established CHD or considered to be at high risk of developing CHD or rarely, in the case of severe hypertriglyceridaemia, acute pancreatitis.
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PMID:Current management of hyperlipidaemia. 231 9

A patient with Werner's syndrome and acute pancreatitis due to severe hyperlipidaemia is reported. Special attention is paid to early recognition of the syndrome and the prevention of complications of the several metabolic disorders that occur in this syndrome.
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PMID:Acute pancreatitis in a case of Werner's syndrome with severe hyperlipidaemia. 272 98

Diabetic lipemia with and without acute pancreatitis in chronic alcoholism. A report of 4 cases. Diabetic lipemia was observed in 4 chronic alcoholic men after ingestion of high doses of alcohol and/or sugar-rich beverages, including one patient who was treated for insulin-dependent diabetes. None had a previous history of serum lipid disturbances. All had marked hyperglycemia, hyperosmolality and hypertriglyceridemia (mean: 60.8 mmol/l), 2 of undetermined type and 2 of type IV with eruptive xanthomas. Factitious hyponatremia was present in 3 cases, but true serum sodium was normal (138 mmol/l) or elevated (154, 156, 182 mmol/l) after correction. Three patients developed acute pancreatitis ascribed to high serum triglyceride levels and/or to alcohol ingestion. Serum and urine amylase activity was inhibited by hypertriglyceridemia. The diagnosis of pancreatitis was assessed twice by echography and computed tomographic scan, and once by tomographic scan and an elevation of the amylase on creatinine clearance ratio. It is likely that hypertriglyceridemia predisposed these patients to develop pancreatitis, alcoholism being a precipitating factor. We suggest that the diagnosis of acute pancreatitis should be systematically considered in any case of diabetic lipemia without true hyponatremia.
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PMID:[Diabetic hyperlipemia with or without acute pancreatitis in patients with chronic alcoholism. A study of 4 cases]. 274 Jun 61

Like the liposomes of certain intravenous fat emulsions associated with embolic effects in acutely ill patients, chylomicrons and very low density lipoproteins (VLDL) show calcium-dependent agglutination by C-reactive protein (CRP). It is suggested that non-traumatic fat embolism may be caused by agglutination of chylomicrons and VLDL by high levels of plasma CRP. This mechanism may also cause acute pancreatitis in patients with types I, IV, and V hyperlipidaemia, and avascular necrosis of bone in patients with corticosteroid-induced hyperlipidaemia.
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PMID:Pathogenesis of non-traumatic fat embolism. 289 46

Eleven evaluators from nine laboratories in five countries evaluated a new immunoinhibition method for pancreatic isoamylase determination that is as simple to perform as that for total amylase. The precision at low and intermediate activity concentrations was superior, and at high concentrations it equalled that of the wheat-germ inhibitor method. The test was linear to approximately 2000 U/L, depending on the instrumentation used. The percentage salivary isoamylase activities remaining in specimens after reaction with two monoclonal antibodies ranged from 2 to 4.4%. Comparative studies showed good correlation with the wheat-germ inhibitor (r greater than 0.978) and electrophoresis methods (r = 0.920). Hemolysis, lipemia, and bilirubinemia have no effect on results. Interlaboratory studies demonstrated excellent transferability of the method, if instruments are calibrated with the same calibrator. Reference intervals for pancreatic isoamylase are 13 to 64 U/L (25 degrees C), 13 to 83 U/L (30 degrees C), and 17 to 115 U/L (37 degrees C). A clinical evaluation of patients with acute pancreatitis showed that pancreatic isoamylase has a greater clinical sensitivity than total amylase.
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PMID:Multicenter evaluation of a specific pancreatic isoamylase assay based on a double monoclonal-antibody technique. 304 84

Hyperlipidaemia is a common and important clinical entity which frequently has a genetic basis. The chief features of severe hypertriglyceridaemia are eruptive xanthomata and acute pancreatitis, whereas most forms of hypercholesterolaemia are associated with premature coronary heart disease. This applies especially to familial hypercholesterolaemia, which is also characterized by tendon xanthomata. Better recognition of hyperlipidaemia allied to recent improvements in treatment should help reduce the frequency of its disabling and sometimes fatal consequences.
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PMID:Clinical consequences of hyperlipidaemia. 314 83

Hypertriglyceridemia is a recognized complication of pregnancy. In patients with familial hypertriglyceridemia, the biochemical changes are greatly enhanced during pregnancy and may be associated with acute pancreatitis, a potentially fatal triad. Three patients were studied, in one of whom previously undiagnosed hyperlipidemia resulted in a fatal attack of fulminant acute pancreatitis. In the other two patients, this complication was avoided by close monitoring and restriction of dietary facts. A history of episodic abdominal cramps, often beginning in early childhood, or the presence of lipemic fasting plasma should alert the clinician to the presence of severe familial hypertriglyceridemia. Early diagnosis allows for the institution of relatively simple management strategies, which diminish the risk of pancreatitis.
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PMID:Hyperlipidemia, pregnancy and pancreatitis. 318 71

Chylomicrons show calcium-dependent agglutination by C-reactive protein (CRP). This has been suggested as a mechanism by which fat embolism may occur in the absence of trauma. It may also play a role in the pathogenesis of acute pancreatitis in patients with types I and V hyperlipidaemia.
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PMID:Fat macroglobule formation from chylomicrons and non-traumatic fat embolism. 323 65

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328


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