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

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.
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PMID:Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease. 178 37

In 27 (78%) of 36 patients with massive hemolysis (defined as a fall in hematocrit of more than 12% within 12 h due to intravascular red cell destruction), hypertriglyceridemia (plasma triglycerides greater than 175 mg/dl) was present or appeared within two days after the hemolytic crisis. Eighteen subjects with triglycerides exceeding 300 mg/dl (peak 516 +/- 39 mg/dl) were further analyzed. The development of hyperlipidemia was independent of the etiology of hemolysis (microangiopathic hemolytic disease 7, toxicemia 3, parainfectious complications 3, autoimmune hemolysis 2, glucose-6-phosphate dehydrogenase deficiency 2). Factors known to increase plasma triglycerides, such as shock, infections, or pancreatitis, were present in only a few cases. Hemolysis-associated complications were activation of intravascular coagulation (16), coma (13), acute renal failure (13), and respiratory insufficiency (5), organ dysfunctions indicating diffuse microvascular injury. Plasma triglycerides fell within a few days if the cause of red cell destruction was eliminated. In 5 of the 8 patients presenting with triglycerides below 175 mg/dl, severe hepatic dysfunction was present. We conclude that hemolysis causes transient hyperlipidemia, either directly by red cell destruction or indirectly by inducing intravascular coagulation, and possibly due to both increased triglyceride synthesis and decreased catabolism.
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PMID:Hyperlipidemia in acute hemolysis. 194 54

The hyperlipoproteinemias are disturbances in the metabolism of lipoproteins. Elevated levels of total and low density lipoprotein-cholesterol, and low levels of high density lipoprotein-cholesterol are proven risk factors for atherosclerosis. The significance of hypertriglyceridemia as an independent risk factor for atherosclerosis is controversial, however, at high levels triglycerides are a major risk factor for pancreatitis. Lipoprotein abnormalities can be divided into dietary, primary (genetic), and secondary disorders. The major causes of moderate and severe hypercholesterolemia are familial hypercholesterolemia, familial combined hyperlipidemia, severe primary (polygenic) hypercholesterolemia, and familial dysbetalipoproteinemia. Causes of hypertriglyceridemia include familial hypertriglyceridemia, familial lipoprotein lipase deficiency, sporadic hypertriglyceridemia, and secondary causes.
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PMID:Hyperlipoproteinemias: Part I. Lipoprotein classification and abnormalities. 194 97

The control of coronary artery disease depends primarily on its prevention at an early stage. Researchers generally agree that early prevention depends on the elimination or treatment of known risk factors, among which hyperlipidemia occupies a central position. Two European Consensus Conferences have concluded that therapy of hyperlipidemia should always start with dietary counseling. First, subjects with body mass indexes (weight/height) greater than 27 should lose weight. Second, the lipid-lowering diet should provide 55% of calories from carbohydrates; 10 to 15% from protein; and up to 30% from fat comprising 10% each of saturated, monounsaturated and polyunsaturated fatty acids; less than 300 mg/day cholesterol; 35 g/day of fiber derived largely from legumes and other vegetables; and fruit. Further reduction of fat consumption (to 20 to 25% of total energy) and of cholesterol (to less than 150 mg/day) may be attempted when patients respond inadequately to the standard diet. The goal of treatment is to minimize the risk of coronary artery disease and of pancreatitis. Where possible, a low-density lipoprotein cholesterol level of 135 mg/dl (3.5 mmol/liter) should be the goal in hypercholesterolemic patients with multiple or severe risk factors and a level of 155 mg/dl (4 mmol/liter) in the absence of other risk factors. Also, high-density lipoprotein cholesterol greater than 35 mg/dl and triglycerides less than 200 mg/dl are considered important goals of treatment. Some patients with hyperlipidemia do not respond adequately to diet and correction of underlying causes; drug treatment should then be instituted, but careful attention to diet should be continued.
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PMID:At what levels of total low- or high-density lipoprotein cholesterol should diet/drug therapy be initiated? European guidelines. 218 Feb 66

Acquired hyperlipidemia (secondary dyslipoproteinemias) results from underlying disorders that lead to alterations in plasma lipid and lipoprotein metabolism. Secondary dyslipoproteinemias may mimic primary forms of hyperlipidemia and can have similar consequences. They may result in increased predisposition to premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to the development of pancreatitis and other features of the chylomicronemia syndrome. Diabetes mellitus and use of drugs such as diuretics, beta blockers, and estrogens are commonly encountered causes of secondary dyslipoproteinemia. Other conditions leading to acquired hyperlipidemia include hypothyroidism, renal failure, nephrotic syndrome, alcohol usage, and some rare endocrine and metabolic disorders. When secondary and familial forms of hypertriglyceridemia coexist, triglyceride removal mechanisms may be saturated and marked hypertriglyceridemia with fasting chylomicronemia might ensue. Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.
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PMID:Acquired hyperlipidemia (secondary dyslipoproteinemias). 219 73

Type II diabetes mellitus may affect as many as 20% of the elderly US population. In the absence of data to support the need to maintain a specific level of glucose beyond that necessary to relieve symptoms, choice of therapy is problematic. Clearly, supervised dietary therapy for the obese type II diabetic patient represents a safe and cost-effective treatment. For those patients who fail dietary therapy because they fail to lose weight or regain lost weight, or because blood glucose levels remain high despite weight loss, further therapy must be individualized. The only rational criteria for drug treatment supportable by currently available data are (1) persistent symptoms associated with hyperglycemia, (2) ketonuria in the unstressed state, and (3) certain cases of hyperlipidemia, especially with triglyceride levels greater than 1000 mg/dl. In these clinical settings, drug therapy is necessary to eliminate symptoms, prevent development of ketoacidosis, and reduce the risk of pancreatitis, respectively. Consideration of drug therapy should also be made in the case of very elevated blood glucose levels, even in the absence of symptoms, when dehydration and risk of severe hyperosmolarity exist. The issues regarding insulin versus sulfonylureas have not been examined specifically in the elderly population. Extrapolating from published studies that generally include patients older than 65 years leads to the following conclusions: Caution regarding adverse side effects of insulin (hypoglycemia, theoretic risk of hyperinsulinemia) and sulfonylureas (hypoglycemia, drug interactions, increased risk of cardiovascular death) must be balanced against the theoretic benefit of treatment in the absence of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in the elderly diabetic patient. 222 55

Acute pancreatitis is a disease characterized by abdominal pain, low-grade fever, abdominal tenderness and rigidity, and moderate elevation of the white blood cell count. A widely used revised classification of pancreatitis is that proposed in 1984 at Marseille. It only distinguishes between acute and chronic pancreatitis. In 61 cases were 40 men and 21 women. The mean age in the total series was 52.5 years. The etiology of the acute condition was alcoholism in 32.8% and biliary tract disease in 23%. In 9.8% the acute pancreatitis is associated with alimentary tract diseases (adipositas, hyperlipidemia). The severity of acute pancreatitis is pathological anatomy determined by three stages. In pathogenesis the process of digestion is caused by activated pancreatic enzyme with acinar cell injury. The acinar cell is normally protected from the action of its own enzymes by elaborate intracellular compartmentation of enzymes. Acute pancreatitis is triggered by pancreatic phospholipase A leading to necrosis of lipolytically active fat cells with release of membrane-toxic fatty acids with following destruction of adjacent tissue. Fat necrosis initiates an acute inflammatory reaction with immigration of granulocytes and liberation of kinins, which activate pancreatic enzyme. Pancreatic enzymes are similar to lysosomal enzymes with regard to substrate specificity. Activation will be also triggered by lysosomal enzymes of necrotic acinar cells.
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PMID:[Acute pancreatitis--etiology, pathological anatomy and pathogenesis]. 226 Mar 61

Chronic "idiopathic" pancreatitis (CP) in a 7 year-old-boy, whose father has suffered from CP, and whose former grandfather had suffered from pains possibly of pancreatic origin, led us suspect a hereditary etiology. An analysis, extended in a control fashion to the relatives of the healthy spouse of the affected grandfather, surprisingly revealed 2 more proven and 3 more suspected CP, giving the overall number of 8 affected members in this 35-member 3 generation kindred and revealed a maternal heredity instead of paternal heredity (which was first thought to be apparent). We therefore recommend that in a family suspected to suffer from hereditary CP (HCP), a screening should be extended to cover even the unaffected spouse's family--the present extended study revealed for 23 new members them to belong in an affected family. Without an extensive screening advises for family planning, alcohol consumption etc. can not be given. Plain abdominal X-ray accompanied with epigastric ultrasonographic are suitable for screening, which might be extended to every individual in smaller families, but may be safely restricted to the members ever suffered from epigastric pains in the case of a huge family. Pancreatic duct anomalies, hyperlipidaemia, hypercalcaemia, aminoaciduria or hyperimmunoglobulinaemia, all of which have been seen to accompany HCP, were not present in this family. Neither was any linkage found between the penetrance of HCP and ABO/Rh blood groups or HLA haplotypes.
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PMID:Screening a family for hereditary chronic pancreatitis. 226 97

The majority (about 75%) of patients who suffer from acute pancreatitis do so as a consequence of gallstones or alcohol abuse. The other 25% of patients often present difficult diagnostic problems. Over several years the author has accumulated a series of patients with remedial causes of pancreatitis. They include a group of congenital conditions such as pancreas divisum, choledochal cysts and congenital abnormalities of the pancreatic ductal system. Patients who have had pancreatitis and who have an intact gallbladder often have stones that are difficult to identify. Repeated attacks of pancreatitis in the absence of any other apparent cause justifies cholecystectomy, which will often identify the cause so that recurrence can be prevented. A group of nonanatomic causes are also known. They include hyperlipidemia, drugs and toxins, certain systemic illnesses such as systemic lupus erythematosus, pregnancy, hypercalcemia, hereditary causes and occasionally cancer. In his lecture the author reviews the various etiologies of acute pancreatitis and describes an algorithm that can be used when the diagnosis is difficult.
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PMID:Recurrent acute pancreatitis--rarely idiopathic: 1989 Du Pont lecture. 226 8

In most patients presenting with acute pancreatitis, the cause can be established on the basis of initial history, physical examination, laboratory studies, and abdominal sonography. Patients with unexplained pancreatitis at that point are often considered to have idiopathic disease. However, a cause and, often, effective treatment to prevent recurrent pancreatitis are possible in many of these patients if an aggressive diagnostic approach is taken to discover undiagnosed hyperlipidemia, occult gallstones, abnormalities of the bile and pancreatic ducts, sphincter of Oddi dysfunction, pancreatic cancer and other tumors, and cystic fibrosis (in children and young adults).
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PMID:Idiopathic acute pancreatitis. 226 20


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