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Query: UMLS:C0030305 (pancreatitis)
 16,014 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

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

Marked elevation of triglyceride levels appears to be causally linked to acute pancreatitis and is found in 12% to 38% of patients presenting with acute pancreatitis. Elevated cholesterol levels are not associated with pancreatitis. The pathogenesis of pancreatitis associated with hypertriglyceridemia is not clear. Clinical recognition of this association is extremely important, because therapy with diet and lipid-lowering agents may prevent development of pancreatitis.
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PMID:Hyperlipidemic pancreatitis. 226 17

The long term use of lipid-lowering drugs in the treatment of patients with hyperlipoproteinaemia is aimed at reducing plasma concentrations of known atherogenic lipoproteins with a favourable effect on lipid deposition in the arterial wall. A less common aim is to prevent the adverse sequelae of hyperchylomicronaemia in patients with severe hypertriglyceridaemia. The decision to begin drug therapy should be made only after the exclusion of secondary factors and after an adequate trial of diet has failed to produce acceptable concentrations of plasma lipids and lipoproteins. The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate and inhibitors of hydroxymethylglutaryl coenzyme A (HMG CoA) reductase (e.g. lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolaemia; these agents reduce plasma concentrations of total and LDL-cholesterol by 15 to 45%. For those patients with concurrent hypertriglyceridaemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use; bile acid sequestrants frequently exacerbate hypertriglyceridaemia in these patients. Fibric acid derivatives (e.g. clofibrate, gemfibrozil, bezafibrate or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinaemia, as is nicotinic acid and I have found lovastatin to be effective also. Gemfibrozil or nicotinic acid are the most effective agents to use in the treatment of patients with severe hypertriglyceridaemia who are at increased risk of abdominal pain and pancreatitis. Combined therapy with drugs which have different mechanisms of action can be effectively used in the treatment of patients with severe hypercholesterolaemia or combined hyperlipidaemia; for the former group, combinations which use bile acid sequestrants, HMG CoA reductase inhibitors and nicotinic acid are the most effective.
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PMID:An overview of lipid-lowering drugs. 307 24

Drug treatment of patients with hyperlipoproteinaemia is indicated to reduce the risk of atherosclerosis in patients with increased concentrations of atherogenic lipoproteins, and to lower the plasma concentrations of triglyceride-rich lipoproteins in patients with severe hypertriglyceridaemia who are at risk of abdominal pain and pancreatitis. Such therapy should be initiated only after satisfactory exclusion of secondary causes of hyperlipoproteinaemia, and should be regarded as an adjunct to rather than a substitute for appropriate dietary therapy. Drug therapy should be strongly considered in those patients with concentrations of atherogenic lipoproteins which exceed the 90th to 95th percentile for age. In patients with increased plasma concentrations of low density lipoproteins (LDL), agents which enhance the rate of LDL catabolism (cholestyramine and colestipol) or reduce the rate of LDL synthesis [e.g. nicotinic acid (niacin)] are the 'drugs of choice'. For those patients with concurrent hypertriglyceridaemia, nicotinic acid is the preferred initial drug, and in both patient groups combined drug therapy is often necessary to attain optimal reductions in LDL cholesterol concentrations. Clofibrate remains the 'drug of choice' for the rare patient with type III hyperlipoproteinaemia, whereas the newer agent gemfibrozil should be used in patients with plasma triglyceride concentrations above 1000 mg/dl who are at increased risk of abdominal pain and pancreatitis. Although currently limited to investigational use, mevinolin and related compounds, which are specific inhibitors of the rate-limiting enzyme in cholesterol biosynthesis (HMG Co-A reductase), offer considerable promise in the therapy of patients with primary hypercholesterolaemia due to elevated levels of LDL cholesterol.
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PMID:Lipid-lowering drugs. An overview of indications and optimum therapeutic use. 355 97

Effects of acute pancreatitis on circulating lipids in dogs were evaluated by comparing the serum cholesterol and triglyceride concentrations and plasma lipoprotein electrophoretic patterns of 4 dogs with experimentally induced pancreatitis (EIP), 2 (healthy) sham-operated control (SOC) dogs, and 4 dogs with naturally acquired pancreatitis (NAP) with the concentrations and patterns of 23 healthy, nonoperated control (HNC) dogs. Blood samples were collected once from HNC dogs, 1 to 3 times during the course of the disease in dogs with NAP, and prior to and at 6, 12, 24, 48, 72, and 96 hours after induction of pancreatitis in dogs with EIP or after the sham operation in the SOC dogs. The dogs with EIP did not have turbid serum and did not develop hypercholesterolemia or hypertriglyceridemia. Three of the dogs with NAP had turbid serum and hypertriglyceridemia, and 3 had hypercholesterolemia. The electrophoretic tracings of HNC dogs had predominant alpha-1 peaks and small beta peaks; 2 of the HNC dogs also had small alpha-2 peaks. The tracings of dogs with EIP were similar to those of HNC dogs until 48 to 72 hours after induction of pancreatitis, when dogs with EIP developed increased beta lipoproteins, decreased alpha-1 lipoproteins, and movement of lipoproteins into the alpha-2 zone. The tracings of SOC dogs were similar to those of HNC dogs at all times. Compared with HNC dogs, dogs with NAP all had increased beta lipoproteins, and 2 had decreased alpha-2 lipoproteins. Two dogs with NAP had additional lipoprotein alterations, unlike any seen in dogs with EIP.
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PMID:Effects of acute pancreatitis on circulating lipids in dogs. 367 59

Endogenous sex hormone activity results in higher levels of VLDL, LDL, and apo B in males than in females, while HDL and particularly HDL2, and apo A1 levels are lower, apo A2 being reduced to a lesser degree. This sex-related difference appears progressively during puberty. There is increasing elevation of LDL cholesterol, apo B, and VLDL TG in women at the menopause, HDL cholesterol levels either diminishing or remaining constant. These differences in lipoprotein and apoprotein concentrations probably play a major role in protecting women against atherosclerosis development during the period of gonadal activity. Similar differences are provoked by exogenous hormone activity: the androgens increase LDL cholesterol and reduce HDL cholesterol, and total cholesterol is therefore only slightly altered. Estrogens provoke elevation of VLDL TG only at supraphysiological doses of the order of 30-50 mcg ethinyl estradiol. In contrast, reductions in LDL cholesterol and increases in HDL cholesterol occur even after low physiological doses of estrogens. This latter increase is dose-related and can be as high as 20%. The action of progestogens is less clearly defined and depends on the molecule administered, the dosage, and its possible androgenic action. When the latter activity is marked, lipoprotein and apoprotein variations are similar to those resulting from testosterone effects. The influence of sex hormones on the course of idiopathic hyperlipidemias varies. They may have a beneficial effect, but this is a fairly rare event and occurs only in very precise situations: improvement of type 3 hyperlipidemia by low dose estrogen therapy; improvement of moderate isolated hypercholesterolemia in menopausal women with low doses of estrogens, and improvement of type 5 mixed hypertriglyceridemia by certain progestogens such as oxandrolone. They usually produce the opposite effect, however, with marked increases of type 1, 4, and 5 hyperlipidemia under estrogens, sometimes leading to attacks of pancreatitis and elevation of preexisting hypercholesterolemias or mixed hyperlipidemias resulting in vascular accidents due to thrombosis. (author's modified)
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PMID:[Sex hormones and metabolism of lipoproteins]. 634 27

Excretion of adrenaline was increased in patients with chronic recurrent pancreatitis, excretion of noradrenaline tended to decrease although the content of this amine exceeded 1.5-2-fold its normal concentration in individual patients; excretion of DOPA was unaltered. Hyperlipoproteinemia was found in the majority of the patients. Maximal level of the adrenaline excretion was mainly observed in the patients with high activity of the trypsin inhibitor in blood serum as well as with the high ratio trypsin inhibitor/trypsin. An increase in the adrenaline excretion correlated with hypercholesterolemia and to a lesser extent--with hypertriglyceridemia. The most pronounced hypertriglyceridemia was typical for the patients with alcoholic abuse. Relationship between catecholamines and extrasecretory functions of pancreatic gland as well as with hyperlipoproteinemia in pancreatitis is discussed. An increase in the total antitryptic activity might be caused by activation of the sympathoadrenal system or by hyperproduction of adrenaline.
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PMID:[Excretion of catecholamines and lipid composition of blood in patients with chronic pancreatitis]. 640

Hypertriglyceridaemia is an inappropriate elevation in plasma of chylomicrons, very low density lipoprotein, or both, functioning in the transport of exogenous and endogenous neutral fat respectively (lewis, 1976; Miller, 1979). The elevation may be due to rare genetically-determined defects or to a specific imbalance between triglyceride production and utilization, either secondary to or accentuated by other metabolic disturbances such as obesity or diabetes mellitus. Various surveys indicate that some degree of hypertriglyceridaemia affects more than 10 per cent of the adult population, with a male preponderance and a reduced expression during childhood (Lewis, 1976). Ophthalmological complications of hypertriglyceridaemia include eruptive and other forms of xanthomata including xanthelasmata, corneal arcus, lipaemia retinalis, effects on retinal blood flow, and lipid emboli affecting vision. The clinical features overlap those of hypercholesterolaemia and these features may lead to initial presentation and diagnosis of either disorder. Recognition of the underlying disorder is important since with treatment the incidence of major cardiovascular and other problems such as pancreatitis may be reduced, and with familial disorders other affected members may then be sought.
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PMID:Ophthalmological complications of the hypertriglyceridaemias. 694 19

Treating hyperlipidemia in diabetics requires distinguishing between hypercholesterolemia, with its high risk of cardiovascular disease, and hypertriglyceridemia, which, if severe, may cause pancreatitis. Hypercholesterolemia is best managed with diet and, if necessary, colestipol and niacin. Hypertriglyceridemia with chylomicrons responds best to diabetic control, weight loss, and low-fat diet.
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PMID:Hyperlipidemia - a diabetic emergency. 705 73


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