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

Lipid analysis should be tailored to the likelihood of hyperlipidemia and atherosclerosis. In healthy individuals without a family history of hyperlipidemia, it is sufficient to obtain readings of total cholesterol and high-density lipoprotein (HDL) cholesterol. In patients with a family history of hyperlipidemia, in addition, triglycerides should be measured. In patients with manifest atherosclerotic disease, the lipid profile should always include plasma cholesterol and triglycerides as well as HDL cholesterol; if these do not explain presence or extent of atherosclerosis, apolipoprotein (a) should be measured. Patients with diabetes mellitus should undergo the same diagnostic work-up as those with atherosclerotic disease. An apolipoprotein B reading (together with triglyceride levels) is sometimes helpful in patients with diabetes mellitus, allowing to estimate the size of triglyceride-rich lipoproteins. In patients with pancreatitis, longitudinal assessment of plasma triglycerides and, if available, measurement of HDL triglyceride are useful to unmask underlying hyperlipidemia.
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PMID:[Lipid status in the physician's laboratory]. 777 Aug 20

Infected pancreatic necrosis is the most lethal form of pancreatic infections. We have compared our results of open packing and closed catheter drainage after surgical debridement in 20 patients between 1978 and 1993. There were 18 men and 2 women, ages 18 to 72 (mean 54 years). Pancreatitis was attributed to alcohol in eight patients, gallstones in four, surgery in four, hyperlipidemia in one, and was unknown in one. The most common infectious organisms were Strep. viridans, E. coli, Staph aureus, and Candida albicans. Surgical debridement and closed catheter drainage without lavage was the initial treatment in nine patients. Seven of 9 (78%) required reoperation for recurrent abscess and necrosis. Procedure related morbidity was 70 per cent and overall mortality was 44 per cent. Sepsis was the cause of death in three patients and multi-system organ failure in one patient. Surgical debridement and open packing was performed in 11 patients. Each patient had scheduled reoperations for repeat debridement and packing an average of 10 times over 21 days. Procedure-related morbidity was 73 per cent and overall mortality was 18 per cent. One patient died of cardiac failure and one of multisystem organ failure. Retroperitoneal hemorrhage and recurrent abscesses were more frequent after closed drainage, whereas gastric fistula and incisional hernia were more frequent after open packing. Ventilator dependence, pancreatic and intestinal fistula, and organ failure occurred at the same rate. In conclusion, surgical debridement and open packing, with planned redebridement and packing, is more effective in controlling the septic process than is closed catheter drainage of infected pancreatic necrosis.
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PMID:Closed drainage versus open packing of infected pancreatic necrosis. 779 43

Apo C-II has a central role in triglyceride metabolism as a cofactor for lipoprotein lipase (LPL), the enzyme that catalyzes the hydrolysis of triglycerides on plasma lipoproteins. Apo C-II deficiency is a rare genetic disorder that is inherited as an autosomal recessive trait. Patients with this syndrome have marked alterations of triglyceride metabolism which include elevated fasting triglycerides, chylomicrons, and VLDL. Clinical features also include lipemia retinalis, eruptive xanthomas, and an increased incidence of pancreatitis. The initial description of the first patient with apo C-II deficiency by Breckenridge et al. established the important role of apo C-II as a cofactor for LPL. Since then, many kindreds with apo C-II deficiency have been described and the underlying molecular defect characterized.
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PMID:[Apolipoprotein C-II deficiency]. 785 17

We analyzed the molecular defects in the lipoprotein lipase gene of a patient with type I hyperlipidemia suffering from recurrent pancreatitis, indicative for lipoprotein lipase deficiency. Postheparin lipoprotein lipase activity in the patient was decreased by 70%. Direct genomic sequencing revealed compound heterozygosity for two mutation: the well-known Gly188-->Glu and a new Val69-->Leu substitution. Val69 is situated in a conserved hydrophobic region of the lipoprotein lipase protein, and the substitution with leucine gives rise to a 80% decrease in specific catalytic activity, as supported by site-directed mutagenesis experiments, followed by expression in COS-cells. The combination of both defects in the lipoprotein lipase gene was incidentally associated with severe clinical expression of disease, and triglyceride levels of more than 30 mmol/l were measured. In our patient, triglyceride levels wer usually below 10 mmol/l. We, therefore, postulate that the residual LPL activity in our patient is usually sufficient to keep the triglyceride level within bounds and expression of disease occurred only when conditions such as alcohol abuse or poor compliance to diet were present.
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PMID:A compound heterozygote for lipoprotein lipase deficiency, Val69-->Leu and Gly188-->Glu: correlation between in vitro LPL activity and clinical expression. 791 54

Aetiologic factors (gallstones, hyperlipidemia I-IV, hypertriglyceridaemia) make their occurrence, mainly, in the third trimester of gestation. Two cases of acute pancreatitis in pregnancy are described; in both cases patients referred healthy diet, no habit to smoke and no previous episode of pancreatitis. An obstructive pathology of biliary tract was the aetiologic factor. Vomiting, upper abdominal pain are aspecific symptoms that impose a differential diagnosis with acute appendicitis, cholecystitis and obstructive intestinal pathology. Laboratory data (elevated serum amylase and lipase levels) and ultrasonography carry out an accurate diagnosis. The management of acute pancreatitis is based on the use of symptomatic drugs, a low fat diet alternated to the parenteral nutrition when triglycerides levels are more than 28 mmol/L. Surgical therapy, used only in case of obstructive pathology of biliary tract, is optimally collected in the third trimester or immediately after postpartum. Our patients, treated only medically, delivered respectively at 38th and 40th week of gestation. Tempestivity of diagnosis and appropriate therapy permit to improve prognosis of a pathology that, although really associated with pregnancy, presents high maternal mortality (37%) cause of complications (shock, coagulopathy, acute respiratory insufficiency) and fetal (37.9%) by occurrence of preterm delivery.
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PMID:[Acute pancreatitis and pregnancy]. 813 93

Dieticians computed the fat and cholesterol contents of 11 foods that were commercially produced as ready-to-eat food from food component lists and obtained the P/S ratio (polysaturated/saturated fatty acids) from the fatty acid component list. Meanwhile the same foods were diluted and homogenized. The internal standard was combined with hepatadecanoic acid and tricaprin. The samples that had been extracted by the Folch method were analyzed for their lipid content (GC analysis using a HS-SS-10 columns for fatty acids and an OV-1 column for lipid and cholesterol). A significant positive correlation was noted between the results of dieticians' analysis and those obtained from a gas chromatographic analysis of lipid and cholesterol contents and the P/S ratio, proving that lipid analysis of food by dieticians is highly reliable. Therefore for diseases (such as hyperlipemia, arteriosclerosis, obesity, diabetes mellitus, fatty liver, and pancreatitis) in which dietary factors have a significant effect on their clinical course, dietary instructions on dietary fats based on an analysis by dieticians are considered to be effective.
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PMID:A study on the values computed by dieticians and chemical analysis of fats, cholesterol, and P/S ratio in food. 818 6

"Hyperlipidemic crisis" is a term used to describe episodic abdominal pain in patients with hyperlipidemia. The morphologic correlates of this phenomenon have not been investigated and the etiology of the disorder is uncertain. We report a unique histologic finding in the pancreas of a 34-year-old woman with a 17-year history of episodic abdominal pain, sometimes accompanied by hyperamylasemia. At the age of 18 years, grossly elevated cholesterol and triglyceride levels were documented and type V hyperlipidemia was diagnosed. At the age of 34 years, subtotal pancreatectomy was performed for intractable abdominal pain. Histologic examination identified an increased number of enlarged pancreatic nerves that were infiltrated by foamy macrophages and encircled by fibrous tissue; endoneurial infiltration with macrophages occasionally split nerves into individual fascicles. Otherwise, the pancreas had only minimal fibrosis, nesidioblastosis, mucinous metaplasia of some pancreatic ducts, and scattered small collections of chronic inflammatory cells, subtle features suggesting very mild chronic pancreatitis. We propose that this novel xanthomatous neuropathy mimicked pancreatitis and was one of the underlying pathophysiologic mechanisms of abdominal pain in this patient. Further studies are necessary to document the prevalence of this new entity in patients with hyperlipidemia and to correlate its occurrence with "hyperlipidemic crisis" in those individuals.
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PMID:Pancreatic xanthomatous neuropathy associated with hyperlipidemia: a cause of abdominal pain mimicking chronic pancreatitis. 811 25

Secondary causes of hyperlipidemia are important to recognize. In fact, hyperlipidemia may be a clue to the presence of an underlying systemic disorder. It may greatly heighten the risk of atherosclerosis with a raised LDL-c, triglyceride-rich lipoprotein excess, and increased lipoprotein(a) as well as lowered HDL-c. The search for secondary causes may provide a clue as to why patients with primary lipid disorders suddenly develop worsening lipid profiles. The point is a crucial one because some acquired causes of hyperlipidemia, such as alcohol, estrogens, steroids, or pregnancy, when superimposed on a primary familial form of hypertriglyceridemia can result in a saturated removal system and a buildup of chylomicrons, which can lead to life-threatening pancreatitis. A convenient way to remember secondary causes is to think of the four D's of diet, drugs, disorders of metabolism, and diseases. Although diets rich in saturated fats and cholesterol are a common cause of the mild hypercholesterolemia seen in our society, alcohol excess and weight gain can explain much of the tendency toward hypertriglyceridemia. Interestingly anorexia nervosa has long been associated with severe but reversible hypercholesterolemia. Several classes of drugs need to be considered as common causes of altered lipid profiles. Glucocorticoids and estrogens elevate triglycerides and raise levels of HDL-c. Anabolic steroids taken orally markedly reduce levels of HDL-c in contrast to injectable testosterone, which does not adversely affect the LDL-to-HDL ratio. Oral contraceptives affect atherosclerotic risk depending on the kind and doses of progestin/estrogen. In those with an underlying primary hypertriglyceridemia and associated obesity, estrogenic medications can depress triglyceride removal mechanisms, leading to the chylomicronemia syndrome and pancreatitis. Antihypertensives have variable effects on lipids and lipoproteins. Although short-term thiazide usage raises cholesterol, triglycerides, and LDL-c, long-term usage is not necessarily associated with significant alterations in lipid levels. Alpha blockers may cause an increase in HDL-c, whereas beta blockers raise triglycerides and lower HDL-c. Sympatholytics, angiotensin converting enzyme inhibitors, and calcium channel blockers are essentially lipid neutral. Retinoids can be associated with increased LDL-to-HDL ratios and occasionally striking elevations in triglycerides. Cyclosporine raises LDL-c and lipoprotein(a). Classes of drugs that may raise HDL-c include cimetidine, antiepileptic drugs, and tamoxifen, but the effect may be seen primarily in women. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered. A thyroxine and TSH level should be obtained on all new cases of clinically important hyperlipidemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Secondary causes of hyperlipidemia. 828 27

This article has focused on the appropriate indications for lipid-lowering drugs in adult patients with different lipoprotein disorders, which we have divided into primary hypercholesterolemia, combined hyperlipidemia,and hypertriglyceridemia. The mechanism of action, efficacy, and safety profile of the major drugs have been reviewed, and based on this information, we have presented our views on the appropriate drugs of first choice and appropriate second-choice agents for treatment of adult patients with different dyslipidemias. The rationale for the use of hypolipidemic drugs is strongest in patients with hyperlipidemia who concurrently have evidence for coronary or peripheral vascular disease, in whom the goal of secondary prevention is to retard further progression of atherosclerosis and potentially induce some regression, whereas in selected high-risk patients without evidence of atherosclerosis, the goals of therapy are to prevent the premature development of CAD or, in patients with severe hypertriglyceridemia, prevent the adverse sequelae of hepatomegaly, splenomegaly, and potentially pancreatitis. We have focused on the use of hypolipidemic drugs in adult patients, and the guidelines discussed are not appropriate for use in children with hyperlipidemia, in whom drug therapy should be undertaken selectively and in consultation with a lipid specialist. Many areas of controversy in the use of lipid-lowering drugs remain to be addressed by future studies; these include the use of lipid-lowering drugs in patients with secondary causes of hyperlipidemia (e.g., the nephrotic syndrome), the use of lipid-lowering drugs in women, and recommendations for drug therapy in older patients.
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PMID:Drug treatment of dyslipoproteinemia. 828 33

In a population of 716 patients with end-stage renal disease (ESRD), 46 patients (6.4%) were identified as having pancreatitis. Pancreatitis was significantly more common in those with alcohol abuse, systemic lupus erythematosus (SLE), and polycystic kidney disease. It was not significantly associated with hyperlipidemia, biliary tract disease, or hypercalcemia. Acute pancreatitis occurring before the patient developed ESRD was mainly alcohol-related and did not appear to be a significant risk factor for future episodes of pancreatitis during dialysis. Chronic calcific pancreatitis diagnosed before ESRD was almost invariably due to alcohol abuse, and tended to be a marker for recurrent acute exacerbation after development of ESRD, whether alcohol consumption continued or not. Pancreatitis occurring for the first time after ESRD in patients on dialysis was generally benign, and was usually accompanied by an uneventful recovery and few recurrent episodes. However, a significant elevation of the calcium x phosphate product was observed in these patients, occurring in about half the patients without any known precipitating factor. After kidney transplantation, the development of pancreatitis was associated with higher morbidity and mortality. Chronic calcific pancreatitis diagnosed after ESRD occurred only in patients with SLE; reported here for the first time, it may be a manifestation of long-standing disease, chronic steroid therapy, or both.
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PMID:Pancreatitis in patients with end-stage renal disease. 830 63


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