Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

Screening for dyslipoproteinemias should be undertaken in all individuals older than 20 years of age at least once every 5 years. The initial screening, as recommended by the Adult Treatment Guidelines Panel of the National Cholesterol Education Program, is to determine the concentration of total blood cholesterol. This initial determination can be made on blood obtained in the nonfasting state. Further evaluation of the patient's lipoprotein concentrations is dependent upon the presence of other cardiovascular risk factors. in the absence of definite coronary heart disease, hypertension, diabetes mellitus, a family history of coronary artery disease, cigarette smoking, or severe obesity, the patient with a total blood cholesterol concentration less than 200 mg/dL requires no specific instruction and should have a repeated screening performed within 5 years. Patients with blood cholesterol concentrations greater than 200 mg/dL should have their lipoprotein profiles determined if they have atherosclerotic cardiovascular disease or two other cardiovascular disease risk factors. The lipoprotein profile includes the determination of fasting cholesterol and triglyceride and HDL cholesterol concentrations. From these values, the LDL cholesterol concentration can be calculated. This LDL cholesterol concentration is central in selecting the appropriate therapy. HDL cholesterol concentrations may be useful in evaluating patients with ischemic heart disease. Concentrations of HDL cholesterol less than 35 mg/dL are associated with increased risk for coronary artery disease. Although there is currently no convincing evidence that support the specific treatment of depressed HDL cholesterol concentrations, therapy directed to modulating lipoprotein metabolism in patients with heart disease and low HDL concentrations may be of benefit. Patients with recurrent abdominal pain, pancreatitis, and eruptive xanthomatosis frequently have fasting hypertriglyceridemia concentrations exceeding 1000 mg/dL. These patients should be identified in order to effectively reduce their triglyceride concentrations, which can prevent these complications.
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PMID:Detection and evaluation of dyslipoproteinemia. 219 76

Cholesterol crystallization in a necessary step in the formation of cholesterol gallstones. Our purpose was to study the relationship between the presence of biliary cholesterol crystals and radiolucent gallstones. Bile was obtained by duodenal intubation from 60 subjects free of hepatic disease: 40 patients had radiolucent gallstones and in the remaining 20 subjects no gallstones could be found either by oral cholecystography or by ultrasound examination. In each patient a bile sample was used to search for cholesterol crystals; in another sample, biliary cholesterol, phospholipids and bile acids were measured to calculate the lithogenic index. Among the 44 subjects with lithogenic bile, 34 had radiolucent gallstones. Twenty-two out of the 60 patients had both cholesterol crystals and radiolucent gallstones; 21 subjects out of the 22 had lithogenic bile. In patients with frequent biliary colic or subacute pancreatitis without visible gallstones, finding cholesterol crystals in bile might suggest medical or surgical specific treatment.
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PMID:[Cholesterol crystals and biliary lithiasis. Importance of the study of bile collected by duodenal intubation]. 673 59

No systematic study of the composition of common duct stones has been carried out to date. In this study, we assessed the chemical composition and morphologic characteristics of common duct stones from 115 patients, and compared them with gallbladder stones in 67 patients who had both. Visually and chemically, common duct stones could be divided into two groups: cholesterol stones and pigment stones. Cholesterol common duct stones contained 83 +/- 1 percent cholesterol, 2.3 +/- 0.4 percent bilirubin, and 5.5 +/- 1 percent insoluble pigment residue. Pigment common duct stones contained 7 +/- 1 percent cholesterol, 24 +/- 2 percent bilirubin, and 38 +/- 3 percent pigment residue. There were two subgroups of pigment stones: one with large amounts of bilirubin and one with large amounts of pigment residue. A high proportion (46 percent) of common duct stones were composed of pigment. Patients with pigment common duct stones were more likely to have cholangitis and pancreatitis than were patients with cholesterol stones. It was not possible to distinguish primary from secondary stones on morphologic grounds. In 65 of 67 patients (97 percent), gallbladder stones and common duct stones were of the same chemical type. Morphologically, cholesterol common duct stones were very similar (3.6+ on a scale of 0 to 4+) to their counterparts. Pigment common duct stones and gallbladder stones were less similar (2.4+). Chemically, cholesterol common duct stones were identical to their gallbladder counterparts. Pigment common duct stones regularly contained a greater fraction of bilirubin and less pigment residue than associated gallbladder stones (p less than 0.05). Earthy common duct stones were associated with earthy gallbladder stones, and were chemically indistinguishable from other pigment stones. These data suggest that all cholesterol common duct stones, and when the gallbladder is present, most pigment common duct stones, are secondary. The latter stones, however, probably grow after entering the duct, adding pigment with a high proportion of bilirubin relative to pigment residue.
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PMID:Composition and morphologic and clinical features of common duct stones. 674 33

A 47-year-old woman with stones in the gall-bladder suddenly developed severe upper abdominal pain. Cholesterol concentration was elevated, as were amylase (555 U/l) and lipase (408 U/l) concentrations, suggesting biliary pancreatitis. Endoscopic retrograde cholangiography demonstrated a cyst, about 10 cm in diameter, in the left lobe of the liver, connected to the biliary tract system. Ultrasonography and computed tomography additionally showed a smaller cyst in the right lobe. Infection with Echinococcus granulosus was proven microbiologically on bile (demonstration of hooklets and protoscolices) as well as serologically. Transpapillary cholangioscopy demonstrated daughter cysts within the echinococcal cyst. The main cyst was rinsed with 20% NaCl for 10 days via a nasocystic catheter. In addition, mebendazole (three times daily 1000 mg) was administered for 13 months. The signs if inflammation receded and the cyst shrank to a small residual volume. Surgical intervention became unnecessary.
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PMID:[Acute pancreatitis due to the rupture of an echinococcal cyst into the bile duct system]. 751 77

The authors report two cases of cholesterol embolism and review the literature on this subject. Cholesterol crystal emboli are very serious complication of atheroma, generally situated in the aorta and usually in patients in their sixties. The frequency of cholesterol embolism is 20% in autopsy studies in this population. The embolic process accounts for the polymorphic clinical feature. Clinical signs are always delayed in relation to triggering factors. The symptoms can sometimes simulate a systemic disease. Cutaneous signs are present in 40 to 75% of cases. Acute renal failure is present in 30% of cases. Other signs may also be observed: alteration of the general state, fever, neurological disorders, pain of the lower limbs, myalgia, gastrointestinal haemorrhage or perforation, ischaemic colitis, pancreatitis, mesenteric or coronary angina. A triggering factor is revealed in 80% of cases: aortic surgery, retrograde aortic catheterization, fibrinolysis or oral anticoagulant treatment. The prognosis is poor due to the clinical context, the patient's age and the absence of any specific treatment. The short-term mortality is 60 to 80% according to various series. The best treatment is prevention: carefully assess the indication for an endovascular procedure in an atheromatous patient; if necessary, perform transoesophageal ultrasonography to evaluate the risk; whenever possible change the incision in vascular investigations or operative procedures in high-risk patients.
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PMID:[Systemic cholesterol embolism]. 866 92

To further elucidate the incidence and potential mechanism of asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia (ALL), we serially obtained fasting lipid and lipoprotein studies on 38 of the 43 consecutively diagnosed children with ALL before, during, and after asparaginase therapy. We also evaluated a second population of 30 long-term survivors of childhood ALL; a fasting lipid and lipoprotein profile was obtained once at study entry. The mean peak triglyceride level during asparaginase of 465 mg/dL (standard deviation [SD] 492) was significantly higher (P = .003) than the level of 108 mg/dL (SD 46) before the initiation of asparaginase therapy. Sixty-seven percent of the newly diagnosed patients had fasting triglyceride levels greater than 200 mg/dL during asparaginase therapy; 15 patients (42%) had levels greater than 400 mg/ dL, 7 with levels greater than 1,000 mg/dL. The incidence of hypertriglyceridemia did not vary by type of asparaginase or risk status of ALL (defined by white blood cell count and age). None of the 7 patients with triglyceride levels greater than 1,000 mg/dL developed pancreatitis. In contrast, 4 of the 13 patients without triglyceride elevation developed pancreatitis; 3 of the 4 patients had fasting studies at the height of their abdominal pain. Nuclear magnetic resonance analysis of lipid subclasses showed a significant increase in the smaller, denser forms of very low density lipoprotein (VLDL) and negligible chylomicron fraction in a subset of patients with marked triglyceride elevation. Lipoprotein lipase activity was consistently above normative values for all levels of triglyceride and could not be explained by obesity or hyperglycemia. Apolipoprotein B(100) levels increased during asparaginase therapy, although the mechanism of this remains unclear. LDL reciprocally decreased with increased VLDL during asparaginase therapy. After asparaginase therapy, triglyceride levels (mean, 73 mg/dL [SD 33]) were significantly lower than levels obtained during asparaginase therapy. Triglyceride levels for survivors did not differ from the normal range or postasparaginase levels in the newly diagnosed patients. These data show a striking temporal association between asparaginase therapy and hypertriglyceridemia. Changes in cholesterol, in contrast, were not temporally related to asparaginase treatment. Cholesterol levels were elevated (>200 mg/dL) in 20% of the patients after asparaginase, which may be due to continued treatment with corticosteroids. The mean cholesterol level of long-term survivors of 177 mg/dL was significantly higher than the norm (P = .045). High-density lipoprotein (HDL) levels were significantly lower than normal at all time periods and for both populations; 25% of survivors had HDL levels less than 35 mg/dL. We conclude that modifications in asparaginase therapy are not necessary. In cases of triglyceride elevation greater than 2,000 mg/dL when the risk of pancreatitis is increased, close clinical monitoring is imperative. Larger studies are needed to determine the incidence of dyslipidemia in long-term survivors of ALL as well as the relationship between lipid abnormalities and other late effects of treatment, notably obesity and cardiomyopathies.
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PMID:Asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia. 905 8

Abnormal lipid and lipoprotein cholesterol values have been defined as a low-density lipoprotein (LDL) cholesterol (C) value of 160 mg/dL (4.1 mmol/L) or greater, a high-density lipoprotein (HDL) C value less than 40 mg/dL (1.0 mmol/L), triglycerides (TG) 150 mg/dL (1.7 mmol/L) or greater, and a lipoprotein (a) (Lp(a)) of 30 mg/dl or greater. Such values all increase coronary heart disease (CHD) risk. The National Cholesterol Education Program Adult Treatment Panel III guidelines continue to focus on optimizing LDL-C values (established as < 100 mg/dL or 2.6 mmol/L), especially in those with established CHD, diabetes, or a 10-year CHD risk over 20%. Dietary saturated fat (< 7% of calories) and cholesterol (< 200 mg/day) restriction, and the use of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are the mainstays of treatment in this regard. Such treatment substantially reduces CHD risk. Severe hypertriglyceridemia (> 1000 mg/dL or 11.0 mmol/L) is associated with pancreatitis, and fat restriction, control of glucose, and fibrate therapy are indicated in such patients. Niacin is currently the most effective agent for lowering Lp(a) and raising HDL-C. Current recommendations for treatment by diet and drugs are outlined.
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PMID:Diagnosis and management of lipoprotein abnormalities. 1213 66

HIV protease inhibitors decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with serum lipid elevations, which may pose an increased risk of cardiovascular disease and pancreatitis. Treatment of protease inhibitor-related hyperlipidaemia (PIH) is complicated by drug interactions, which significantly increase concentrations of most 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Although pravastatin and atorvastatin effectively lower cholesterol and triglyceride concentrations in HIV-infected patients, a significant number of patients did not achieve their National Cholesterol Education Program low density lipoprotein concentration goals. Nonetheless, due to the increased risk of rhabdomyolysis with elevated statin concentrations, atorvastatin should be considered a second-line agent. The limited available PIH data supports the fact that pravastatin and atorvastatin are well-tolerated in HIV-infected individuals. More data are needed on the appropriate starting doses, maximum safe doses, role of combination statin-fibrate therapy, documentation of coronary heart disease benefit and incidence of myotoxicity and hepatotoxicity. Pravastatin has an acceptable risk-benefit ratio in PIH, while theoretical toxicity concerns exist with atorvastatin.
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PMID:Risk-benefit of HMG-CoA reductase inhibitors in the treatment of HIV protease inhibitor-related hyperlipidaemia. 1290 55

Dyslipidemia, characterized by elevated serum levels of triglycerides and reduced levels of total cholesterol, low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol, has been recognized in patients with human immunodeficiency virus (HIV) infection. It is thought that elevated levels of circulating cytokines, such as tumor necrosis factor-alpha and interferon-alpha, may alter lipid metabolism in patients with HIV infection. Protease inhibitors, such as saquinavir, indinavir and ritonavir, have been found to decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with a syndrome of fat redistribution, insulin resistance, and hyperlipidemia. Elevations in serum total cholesterol and triglyceride levels, along with dyslipidemia that typically occurs in patients with HIV infection, may predispose patients to complications such as premature atherosclerosis and pancreatitis. It has been estimated that hypercholesterolemia and hypertriglyceridemia occur in greater than 50% of protease inhibitor recipients after 2 years of therapy, and that the risk of developing hyperlipidemia increases with the duration of treatment with protease inhibitors. In general, treatment of hyperlipidemia should follow National Cholesterol Education Program guidelines; efforts should be made to modify/control coronary heart disease risk factors (i.e. smoking; hypertension; diabetes mellitus) and maximize lifestyle modifications, primarily dietary intervention and exercise, in these patients. Where indicated, treatment usually consists of either pravastatin or atorvastatin for patients with elevated serum levels of LDL-C and/or total cholesterol. Atorvastatin is more potent in lowering serum total cholesterol and triglycerides compared with other hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, but it is also associated with more drug interactions compared with pravastatin. Simvastatin and lovastatin are significantly metabolized by cytochrome P450 enzymes (CYP3A4) and are therefore not recommended for coadministration with protease inhibitors. A fibric acid derivative (gemfibrozil or fenofibrate) should be used in patients with primary hypertriglyceridemia. However, it must be kept in mind that protease inhibitors, such as nelfinavir and ritonavir, induce enzymes involved in the metabolism of the fibric acid derivatives and may, therefore, reduce the lipid-lowering activity of coadministered gemfibrozil or fenofibrate. In certain patients HMG-CoA reductase inhibitors may be used in combination with fibric acid derivatives but patients should be carefully monitored for liver and skeletal muscle toxicity. Select patients may experience improvements in serum lipid levels when their offending protease inhibitor(s) is/are exchanged for efavirenz, nevirapine, or abacavir; however each patient's virologic and immunologic status must be taken closely into consideration.
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PMID:Management of protease inhibitor-associated hyperlipidemia. 1472 85


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