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

Patients with chronic renal failure retain Na+ and H2O, and they retain K- and acid. This disordered homeostasis results in hypertension, edema, hyperkalemia and acidosis. Diuretics may be used to favorably modify these disturbances. However, because of the limited filtered load of water and electrolytes, and the low renal blood flow, measures need to be taken to maximize the response to diuretics. These measures include: (a) the use of the most bioavailable drug, torasemide, when using the oral route; (b) the use of the drug with the least hepatic elimination, furosemide, when using the intravenous route; (c) the use of combinations of loop- and distal tubule-acting diuretics; (d) the use of the maximum effective diuretic dose; and (e) the use of repeated doses or constant infusion. In benefiting hypertension, vascular congestion and hyperkalemia diuretics appear to exert their effects not only on the kidneys but also on extrarenal sites, such as the vascular tree and the gastrointestinal tract. The use of diuretics, however, is not without complications, which include: intravascular volume depletion and azotemia, ototoxicity (when using loop-acting diuretics), hyperlipidemia, acute pancreatitis, hyperkalemia (when using K(+)-sparing agents), and acidosis (when using carbonic anhydrase inhibitors).
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PMID:Use of diuretics in chronic renal failure. 918 1

Lipoprotein lipase (LPL) is the rate-limiting enzyme for the hydrolysis of triglyceride-rich lipoproteins. Numerous LPL gene mutations have been described as a cause of familial chylomicronemia in various populations. In general, allelic heterogeneity is observed in LPL deficiency in different populations. However, a founder effect has been reported in certain populations, such as French Canadians. Although familial chylomicronemia is observed in Morocco, the molecular basis for the disease remains unknown. Here, we report two unrelated Moroccan families of Berber ancestry, ascertained independently in Holland and France. In both probands, familial chylomicronemia manifested in infancy and was complicated with acute pancreatitis at age 2 years. Both probands were homozygous for a Ser259Arg mutation, which results in the absence of LPL catalytic activity both in vivo and in vitro. In heterozygous relatives, a partial decrease in plasma LPL activity was observed, sometimes associated with combined hyperlipidemia. This mutation previously unreported in other populations segregated on an identical haplotype, rarely observed in Caucasians, in both families. Therefore, LPL deficiency is a cause of familial chylomicronemia in Morocco and may result from a founder effect in patients of Berber ancestry.
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PMID:A single Ser259Arg mutation in the gene for lipoprotein lipase causes chylomicronemia in Moroccans of Berber ancestry. 929 16

The effect of tamoxifen, an antiestrogenic agent, on lipid metabolism was studied in postmenopausal patients with breast cancer who received the drug for postoperative adjuvant treatment following mastectomy. To measure total cholesterol and triglyceride concentrations, fasting blood samples were collected before and 2 months after the initiation of tamoxifen therapy from 16 patients who satisfied the study criteria. All patients were normolipidemic before tamoxifen was administered. Control samples were obtained from hypertriglyceridemia patients who were free from breast cancer. Marked hypertriglyceridemia was observed in 3 of 16 patients after tamoxifen treatment. The activity of lipoprotein lipase and hepatic triglyceride lipase, the key enzymes of triglyceride metabolism, decreased significantly in all of 16 patients as a result of tamoxifen treatment (P = 0.008 and P = 0.007, respectively). However, the mean mass of lipoprotein lipase significantly increased (P = 0.011) after tamoxifen treatment. We therefore conclude that tamoxifen might increase inactive lipoprotein lipase. Because marked hyperlipidemia is a potent risk factor for life-threatening acute pancreatitis and arteriosclerosis, plasma lipid levels should be tested periodically during tamoxifen treatment, even if the patients are normolipidemic during the pretreatment stage.
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PMID:Effect of tamoxifen on serum lipid metabolism. 958 69

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

A patient who was given tamoxifen as adjuvant treatment for breast cancer developed very severe hypertriglyceridaemia, hypercholesterolaemia and acute pancreatitis after being treated for 4 months. The hyperlipidaemia was corrected after cessation of the tamoxifen and the institution of gemfibrozil treatment. This patient appears to have type IV hyperlipidaemia. It is suggested that, in such patients, tamoxifen should be used with extreme caution because the weakly oestrogenic effect of this agent can cause severe and life threatening hyperlipidaemia.
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PMID:Severe hypertriglyceridaemia and hypercholesterolaemia associated with tamoxifen use. 976 83

Primary Hyperchylomicronemia is known as a syndrome in which the accumulation of chylomicron occurs in the circulation. The main clinical symptoms of this disorder are the huge increase in plasma trigriceride and cholesterol, and the presence of xanthomatous eruption, lipemia retinalis, hepatosplenomegaly, and the complication of acute pancreatitis. With gene analysis, a deficiency of lipopreteinlipase (LPL) or apolipoprotein C-II is revealed as a main cause of primary chylomicronemia. Furthermore, in some cases, abnormalities of remnant receptors, the presence of antibody against LDL, apolipoprotein C-II, and LDL receptor are reported as causes of chylomicronemia syndrome. In the present paper, we summarized the major gene polymorphism and characteristics of clinical symptom of these disease.
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PMID:[Primary hyperchylomicronemia and gene defects]. 1063 9

Induction of acute pancreatitis follows a uniform mechanism independent of the different etiologic factors such as gallstones, alcohol, ischemia, hyperlipidemia, hypercalcemia, hereditary and others. Each cause seems to affect primarily the acinar cell, resulting in premature intracellular activation of trypsinogen and other digestive enzymes. Activated enzymes and oxygen free radicals injure the acinar cell and cause a release of cytokines and vasoactive mediators, attract inflammatory cells and activate the vascular endothelium as well as the expression of adhesion molecules. The disturbance of the pancreatic microcirculation induces a progression from edematous to necrotizing pancreatitis independent of the early intracellular events, including protease activation. Specific therapy must be directed towards microperfusion failure as a secondary pathogenetic step, since the initial enzyme activation and cytokine release is irreversible by the time of clinical presentation. In experimental designs comparable to the clinical situation the following therapeutic principles have proven beneficial: increase of blood fluidity by dextran, inhibition of leukocyte-endothelium interaction by ICAM-1 antibodies, and blockade of local vasoconstriction by endothelin-receptor antagonists.
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PMID:[New pathophysiologic knowledge about acute pancreatitis]. 1078 41

Acute pancreatitis and eruptive xanthomata are the only recognised direct complications of severe hypertriglyceridaemia, although peripheral neuropathy has been described in patients with hyperlipidaemia. We describe a patient with mixed hyperlipidaemia presenting with severe scalp pain and eruptive xanthomata. Both resolved with treatment. We suspect that high triglyceride concentration can affect the function of sensory nerve fibres.
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PMID:Scalp pain and hyperlipidaemia. 1107 May 77

With the exception of cystic fibrosis and hereditary pancreatitis, case reports about pancreatitis in children have rarely been mentioned. We report here an 11-year-old boy with type V hyperlipidemia, who suffered from two episodes of acute pancreatitis. Sudden onset of severe upper abdominal pain, fever, and hypertriglyceridemia were the common presentations. Initial treatments including analgesics, fasting, parenteral nutrition support and following diet control with medium-chain triglycerides seem to be successful in our case.
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PMID:Recurrent pancreatitis secondary to type V hyperlipidemia: report of one case. 1110 May 29


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