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)

Infected pancreatic necrosis is a devastating and lethal complication of acute pancreatitis. Late death is usually a result of sepsis. W.A. Altemeier and J.W. Alexander established in 1963 that open drainage of the necrotic pancreas is mandatory for survival (Arch Surg 1963;87:96-105). In 1981, E.D. Davidson and E.L. Bradley III concluded that "marsupialization" is the most effective method of open drainage (Surgery 1981;89:252-6). At our institution, we have a series of 10 patients who have undergone marsupialization for treatment of infected pancreatic necrosis. Our mortality rate was 30 per cent. One death resulted from sepsis after an infected necrotic pancreas was found with a colonic anastomotic leak at emergency exploratory celiotomy. Of note, further debridement was not performed. A second death occurred in a female with idiopathic pancreatitis and leukocytopenia, and we are uncertain whether that played a role in the failure of surgical intervention. The third death was in a young alcoholic with hyperlipidemia and severe pancreatitis who was septic 8 days before surgery. The patient died on postoperative day 1. Of the survivors, some were old, many were septic, and all but one returned for further debridement. Our series supports open debridement of infected pancreatic necrosis as a life-saving maneuver and marsupialization as an effective means of open drainage.
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PMID:Marsupialization of the pancreas for infected pancreatic necrosis. 903 96

A severe hyperlipemia in mink, with a pattern that suggested recessive inheritance, was observed at a farm in Norway. On a normal mink diet, affected animals had grossly elevated levels of plasma triglycerides which decreased towards normal on a low-fat diet. Normal minks had the main part of their plasma cholesterol in the HDL fraction. Affected minks, although severely hypertriglyceridaemic, had almost normal levels of both LDL and HDL. Affected minks frequently had lipogranulomas in the mesentery and the pancreas. The lipogranulomatous tissue contained spaces filled with an amorphous, sudanophilic substance with many foamy macrophages in the fibrous tissue between the lesions. Separation of postheparin plasma on heparin-agarose revealed that the affected minks had no detectable lipoprotein lipase activity but normal activity of hepatic lipase. Both normal and affected minks had inactive lipoprotein lipase protein in pre- and post-heparin plasma. This protein, which eluted before the active lipase from heparin-agarose, probably corresponds to lipase monomers. The presence of lipoprotein lipase mass in the affected minks, but no activity, indicates that there might be a point mutation in the lipase gene. The minks provide a new animal model for studies on pancreatitis induced by hypertriglyceridemia and on lipoprotein metabolism in the lipoprotein lipase-deficient state and show features similar to those found in human hyperlipoproteinemia type I.
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PMID:Lipoprotein lipase deficiency with pancreatitis in mink: biochemical characterization and pathology. 918 2

Three women, aged 52, 54 and 30 years, presented with severe hypertriglyceridaemia. One had suffered pancreatitis. All three used oral oestrogens as replacement therapy or as anticonceptive agent. After cessation of the oral oestrogen mild hypertriglyceridaemia persisted, indicating a pre-existent abnormality in their triglyceride metabolism, in these cases non-insulin-dependent diabetes mellitus, familial combined hyperlipidaemia and familial hypertriglyceridaemia, respectively.
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PMID:[Hypertriglyceridaemia following oestrogen use]. 938 Jan 63

Severe hypertriglyceridemia is an uncommon pathological finding in pregnant women if there is no prior history of hyperlipidemia. A partial reduction in lipoprotein lipase (LPL) activity due to a mutation in the LPL gene, is often an associating factor. Here we report a novel LPL gene mutation (Glu421Lys), in a previously healthy primigravid woman who died from hypertriglyceridemia-induced pancreatitis during the last trimester of pregnancy. The patient was heterozygous for this mutation which a charge inversion in the C-terminal domain of LPL resulting in a moderate reduction in catalytic activity, both in vivo and in vitro. These data support the role of partial LPL deficiency in the pathogenesis of severe gestational hypertriglyceridemia.
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PMID:A novel Glu421Lys substitution in the lipoprotein lipase gene in pregnancy-induced hypertriglyceridemic pancreatitis. 949 99

Chronic pancreatitis (CP), a disease described only in 1946 by Comfort and colleagues is currently a global disease. Chronic alcoholism, albeit is the most frequent etiologic factor for the disease in most of the affluent nations, a form of CP of undetermined etiology, tropical calculous pancreatitis (nutritional pancreatitis, Afro-Asian pancreatitis, or tropical calculous pancreatopathy) has been recognized to be prevalent in many developing nations. Hereditary pancreatitis inherited as an autosomal dominant disease is reported from all parts of the world. A landmark is the recent discovery of a gene that transmits the disease. Nearly 10% of cases of CP are truly "idiopathic" with no identifiable cause. Recent studies indicate that the idiopathic variety of CP has two subsets--a juvenile form and a senile or late onset form, with distinct clinical features. It is extremely rare to see CP secondary to hyperlipidemia or hypercalcemia. These etiologic associations appear to be overemphasized. Epidemiological studies indicate that alcoholism is growing in incidence all over the world along with an increase in all alcohol-associated disorders such as cirrhosis of the liver or pancreatitis. A genetic predisposition to alcoholic pancreatitis is suspected based on population studies, but not proven. The influence of cigarette smoking in enhancing alcohol-induced injury to the pancreas underscores the health hazard associated with alcoholism and cigarette smoking--two habits that often coexist in many individuals. The recent finding that all forms of CP are premalignant further emphasizes the need to enforce preventive measures. The hope is that CP is a preventable disease. The despair is that alcoholism is increasing and spreads across geographic and religious boundaries.
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PMID:Chronic pancreatitis: a historical and clinical sketch of the pancreas and pancreatitis. 953 Nov 14

The results of treatment of 319 patients with acute pancreatitis are analyzed, 48 from them (15.1%)--with pancreanecrosis. Etiologic factors in destructive pancreatitis were alcohol addiction (41.67%), cholelithiasis (37.5%), hyperlipidemia (10.41%), hypercalcemia (4.17%), postoperative (4.17%). Location of the necrosis in parapancreatic fat cellular tissue was detected in 6 patients, in pancreatic head--in 8 and both in pancreatic head and corpus--in 11, in corpus and in tail--in 10; total pancreo-necrosis was observed in 5 patients. Therapeutic measures were conservative and only in cholelithiasis cholecystectomy was performed as well as drainage of the choledochus and abdominal cavity. Intensive care was aimed at blocking pancreatic and gastric secretion, inhibition of pancreatic enzymes ferments and suppressing mediators of inflammation, immunocorrection, prophylaxis of infection in the necrotic tissues. Desintoxication was carried out by combination of infusion therapy with forced diuresis, usage of extracorporeal methods and laparoscopic sanation of the abdominal cavity with subsequent lavage. Surgical interventions were carried out in far-off period only for complications of pancreanecrosis. Mortality rate in pancreanecrosis made up 20.85% and in total number of patients with acute pancreatitis--3.13%.
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PMID:[The clinical picture and treatment of destructive pancreatitis]. 968 Aug 11

Hyperlipidemia is recognized as one of the major risk factors for the development of coronary artery disease and progression of atherosclerotic lesions. Dietary therapy together with hypolipidemic drugs are central to the management of hyperlipidemia, which aims to prevent atherosclerotic plaque progression, induce regression, and so decrease the risk of acute coronary events in patients with pre-existing coronary or peripheral vascular disease. In patients at high risk of coronary artery disease but without evidence of atherosclerosis, treatment is designed to prevent the premature development of coronary artery disease, whereas in those with hypertriglyceridemia, treatment aims to prevent the development of hepatomegaly, splenomegaly, and pancreatitis. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are the most potent lipid-lowering agents currently available, and their use in the treatment of hyperlipidemia provides the focus for this review. Particular emphasis is given to cerivastatin, a new HMG-CoA reductase inhibitor that combines potent cholesterol-lowering properties with significant triglyceride-reducing effects. Recently completed primary and secondary intervention trials have shown that the significant reductions in low-density lipoprotein (LDL) cholesterol achieved with statins result in significant reductions in morbidity and mortality associated with coronary artery disease as well as reductions in the incidence of stroke and total mortality. Such benefits occur early in the course of statin therapy and have led to suggestions that these drugs may possess antiatherogenic effects over and above their capacity to lower atherogenic lipids and lipoproteins. Experimental studies have also shown statin-induced improvements in endothelial function, decreased platelet thrombus formation, improvements in fibrinolytic activity, and reductions in the frequency of transient myocardial ischemia.
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PMID:Current and future treatment of hyperlipidemia: the role of statins. 973 40

It was reported that free fatty acids degraded from triglycerides by lipase may play a major role in acute necrotizing or hyperlipidemia-induced pancreatitis. We hypothesized that this injury may be related to the peroxidation of cell membrane phospholipids and tested this hypothesis using isolated pancreatic acini. Pancreatic acini were prepared from male Sprague-Dawley rats by collagenase digestion. Linoleic acid was added (0.1-1.0 mM) to the acinar cell suspension to induce cell injury. Acinar cell damage was measured by lactate dehydrogenase release and by trypan blue exclusion. Phosphatidylcholine hydroperoxide and alpha-tocopherol in the acinar cells were measured. Protective effects of alpha-tocopherol (0.5, 5.0 mM) against this type of cell injury were also evaluated. When isolated acinar cells were treated with linoleic acid, a significant decrease in viability was observed in a time- and dose-dependent manner. In addition, the levels of phosphatidylcholine hydroperoxide after treatment of 0.5 mM of linoleic acid were increased and levels of alpha-tocopherol were decreased significantly. alpha-Tocopherol significantly ameliorated both cellular injury (p < 0.01) and increases in phosphatidylcholine hydroperoxide (p < 0.01). These data suggest that lipid peroxidation of the cellular membrane is an important component of the pancreatic cell injury mediated by free fatty acids.
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PMID:Involvement of lipid peroxidation in free fatty acid-induced isolated rat pancreatic acinar cell injury. 982 Nov 80

Chronic pancreatitis is a rare disease in children and is usually secondary to underlying diseases such as hereditary pancreatitis, cystic fibrosis, hyperlipidemia, prolonged malnutrition, gallstones or anomalies of the biliary-pancreatic duct system. Hereditary pancreatitis is a common cause of chronic pancreatitis in children but is often unrecognized until months or years later. We report here a family with hereditary pancreatitis in which four members are affected.
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PMID:Hereditary pancreatitis: report of a family from Turkey. 989 1

Intravascular coagulation of the intraosseous microcirculation (capillaries and venous sinusoids) progressing to generalized venous thrombosis, and less commonly retrograde arterial occlusion, now appears to be the cause of nontraumatic osteonecrosis. However, this coagulopathy is only an intermediary event, which is always activated by some underlying etiologic risk factor(s). Conditions capable of triggering intravascular coagulation include familial thrombophilia (resistance to activated protein C, decreased protein C, protein S, or antithrombin III), hyperlipemia and embolic lipid (alcoholism and hypercortisonism), hypersensitivity reactions (allograft organ rejection, immune complexes, and antiphospholipid antibodies), bacterial endotoxic (Shwartzman) reactions and various viral infections, proteolytic enzymes (pancreatitis), tissue factor release (inflammatory bowel disease, malignancies, neurotrauma, and pregnancy), and other prothrombotic and hypofibrinolytic conditions.
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PMID:Coagulopathies and osteonecrosis. 1008 10


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