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)

We report two cases of severe hypertriglyceridaemia associated with human immunodeficiency virus infection and highly active antiretroviral therapy (HAART). The first patient, a 39-year-old man, developed moderate hypertriglyceridaemia (5.88 mmol/L) and hypercholesterolaemia (7.0 mmol/L) after 8 months of HAART. When his therapy was altered, triglyceride and cholesterol concentrations increased further to 15.9 and 10.9 mmol/L, respectively, after 6 weeks. The second patient, a 31-year-old man, presented with triglyceride and cholesterol concentrations of 16.2 and 5.7 mmol/L, respectively, following an 8-year history of HAART. Therapy was changed, but 1 month later the triglyceride concentration had increased to 39.4 mmol/L and the cholesterol concentration to 12.1 mmol/L. Both patients were managed by a change in HAART and the introduction of a fibric acid derivative. Although neither patient displayed any clinical symptoms associated with hypertriglyceridaemia, it is important to recognize such cases because of the associated risk of pancreatitis and coronary disease.
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PMID:Severe hypertriglyceridaemia associated with human immunodeficiency virus and highly active antiretroviral therapy. 1211 47

A 36-year-old male patient, after 3 months' treatment with fluvastatin 40 mg/d for hypercholesterolemia, presented with acute pancreatitis. The pancreatitis was mild, and the patient settled on medical treatment. Other causes of the disease were ruled out. Some months later, the patient reintroduced fluvastatin on his own initiative, which caused a recurrence of pancreatitis within a few days. Previous reports are reviewed, showing that statin-induced acute pancreatitis may occur within the first day of therapy or after several months. It is generally mild and runs a benign course, and no mortality has been reported. The frequency of this side effect is unknown, but it is most likely rare.
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PMID:Acute pancreatitis induced by fluvastatin therapy. 1239 30

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

Xanthoma and xanthelasma are typical symptoms of lipid and lipoprotein metabolism impairment. On the basis of their incidence and morphology, it is even possible to specify the impairment type. Hypercholesterolemia or certain liver dysfunctions are characterized by slow development of surface xanthelasmas usually located on mechanically stressed regions (e.g. eyelids). Tuberous and tendinous xanthomas are typical for familiar hypercholesterolemia and are common symptoms of homozygous familiar hypercholesterolemia. Small and quickly developing eruptive xanthomas are typical for mixed hyperlipoproteinemia (secondary hyperlipoproteinemia is typical for diabetes). Mechanism of accumulation of lipids in skin morphs is similar to the development of atheroma, especially when talking about the role of modified LDL and the way of accumulation of lipids in macrophages. The following factors are very important for etiopathogenesis of skin xanthomas development: mechanical stress of tissues, increased permeability of skin capillaries and reaction of proteoglycans in sparse connective tissue. Xanthomas and xanthelasmas are typical indicators of other complicating diseases as e.g. development of acute pancreatitis during hyperlipoproteinemic crisis, aggravation of insulin resistance, and decompensation of type 2 diabetes mellitus. The therapy focuses on adjustment of dietary regime (elimination of dietary fat and concentrated saccharides); no food and sufficient hydration via infusion of crystalloid solutions is indicated in cases of serious hyperlipoproteinemic crisis. In vital indication, it is possible to perform repeated plasmapheresis (or better continual plasmapheresis) that can correct even serious hyperlipoproteinemic crises within several hours. And what is more, continual plasmapheresis can significantly reduce the period when hyperlipoproteinemic crisis might induce acute necrotizing pancreatitis. In the long run, we require that patients strictly observe their dietary regime based on the type of hyperlipoproteinemia. As for medicamentous therapy, fibrates and atorvastatin (from statin family) are the preparations of choice. It is very important not to focus on symptoms, i.e. xanthoma or xanthelasma, but fully compensate lipid metabolism impairment or the disease that underlies hyperlipoproteinemia (e.g. type 2 diabetes mellitus or metabolic syndrome). Unfortunately, it still can be seen that dermatologists, ophthalmologists or plastic surgeons remove extensive xanthelasmas, while the underlying cause is not approached diagnostically and therapeutically at all.
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PMID:[Internist's view on skin manifestations of hyperlipidemia in diabetic patients]. 1677 Oct 91

The aim of the overview is to show the distribution of common apolipoprotein E (APOE) genotypes in the Croatian population, and to test whether it could serve as a new molecular biomarker in some clinical entities. The study included the following groups: patients with angiographically confirmed coronary artery disease, myocardial infarction, Alzheimer's dementia, vascular dementia, hyperlipidemias, diabetes mellitus, pancreatitis, and healthy subjects. Group comparisons of different clinical entities and control group were performed using Pearson's Chi2-test. There was no difference in APOE genotype frequencies between coronary artery disease neither myocardial infarction and control group. The ApoE genotype frequencies in patients with Alzheimer's disease were significantly different from those in the control group. APOE-4 allele tends to be a risk factor for the development of Alzheimer's disease. The frequencies were only marginally different in vascular dementia. Patients with hypercholesterolemia, those with inherited familial hypercholesterolemia, children with diabetes mellitus, and patients with pancreatitis of different etiology showed distributions of APOE genotypes that differed from the control group. It is concluded that the frequencies of APOE genotypes yielded no statistically significant result to confirm the association between APOE genotypes and any specific disease with the exception of Alzheimer's disease; APO-epsilon4 allell has become one of the important biomarkers in diagnosis of Alzheimer's dementia.
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PMID:[The frequencies of apolipoprotein E genotypes in health and disease in the Croatian population--an overview of expectations and real results]. 1721 95

With current dietary therapy, life expectancy in glycogen storage disease (GSD) has improved considerably and more children reach adulthood. Notwithstanding intensive dietary therapy, moderate to severe hyperlipidaemia is still observed frequently. There is limited information about the type and extent of hyperlipidaemia. We studied the lipid profile in 20 patients, aged 8-54 years, of the three (types I, III and IX) most common forms of adult GSD. Hyperlipidaemia was shown to be type-specific, affecting predominantly patients with GSD type Ia, who showed marked combined hypercholesterolaemia and hypertriglyceridaemia. By contrast, a heterogeneous distribution of HDL was found in patients with GSD I and III. There was no significant difference in Apo Al and Apo B concentrations between groups. In addition, mass measurements of the fractions of VLDL1, VLDL2 and IDL were raised in all patients with GSD Ia by comparison with all other patients with GSD. Patients with GSD type Ia have lipid concentrations and individual mass measurements that are consistent with ranges found in patients who have a significant risk of atherosclerosis. Accumulated evidence, however, suggest GSD type Ia patients do not have an increased risk of atherosclerotic cardiovascular disease (CVD) but the reason remains unknown. Intervention to reduce their lipid levels could therefore be on the basis of seeking to prevent the risk of pancreatitis rather than that of CVD.
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PMID:Serum lipid and lipoprotein profile of patients with glycogen storage disease types I, III and IX. 1740 2

Ezetimibe is a lipid-lowering agent that inhibits the intestinal absorption of cholesterol and other related phytosterols. It is used alone or in combination with other lipid-lowering agents in the treatment of various forms of hypercholesterolemia. Since its FDA approval in 2002, there are no known citations of ezetimibe-induced pancreatitis.
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PMID:Ezetimibe-induced acute pancreatitis. 1745 5

Although turmeric (Curcuma longa; an Indian spice) has been described in Ayurveda, as a treatment for inflammatory diseases and is referred by different names in different cultures, the active principle called curcumin or diferuloylmethane, a yellow pigment present in turmeric (curry powder) has been shown to exhibit numerous activities. Extensive research over the last half century has revealed several important functions of curcumin. It binds to a variety of proteins and inhibits the activity of various kinases. By modulating the activation of various transcription factors, curcumin regulates the expression of inflammatory enzymes, cytokines, adhesion molecules, and cell survival proteins. Curcumin also downregulates cyclin D1, cyclin E and MDM2; and upregulates p21, p27, and p53. Various preclinical cell culture and animal studies suggest that curcumin has potential as an antiproliferative, anti-invasive, and antiangiogenic agent; as a mediator of chemoresistance and radioresistance; as a chemopreventive agent; and as a therapeutic agent in wound healing, diabetes, Alzheimer disease, Parkinson disease, cardiovascular disease, pulmonary disease, and arthritis. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. Other clinical trials suggest a potential therapeutic role for curcumin in diseases such as familial adenomatous polyposis, inflammatory bowel disease, ulcerative colitis, colon cancer, pancreatic cancer, hypercholesteremia, atherosclerosis, pancreatitis, psoriasis, chronic anterior uveitis and arthritis. Thus, curcumin, a spice once relegated to the kitchen shelf, has moved into the clinic and may prove to be "Curecumin".
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PMID:Curcumin as "Curecumin": from kitchen to clinic. 1790 May 36

Statins have revolutionized the treatment of hypercholesterolemia and radically reduced the mortality from disease. If the triglyceride level is notably high and causes the risk of pancreatitis, immediate drug therapy is advantageous. A secondary cause that should be treated, such as overweight, diabetes, use of alcohol, hypothyroidism or medication may underlie a moderately elevated triglyceride level. A moderately elevated triglyceride level occurs commonly as part of type 2 diabetes or metabolic syndrome, whereby elucidation of arterial disease risk is most important alongside a modification of living habits. Strong end-point evidence favours statins as the first-line therapy in hypertriglyceridemia.
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PMID:[Elevated triglyceride level]. 1935 17

During pregnancy of healthy women, it is usual for blood lipids to increase significantly. Total cholesterol, HDL- and LDL-cholesterol increase 25-50%, while triglycerides increase twice to four times, and there is also an increase ofapolipoproteins B. However, this lipid expansion in blood does not lead to endothelial disfunction. Clinical problem are therapy dilemas about the women who were treated with antihyperlipemics during preconception period, possibility of diagnosing hyperlipidemia in pregnancy and their treatment during the pregnancy, then lactacy. It is generally accepted that neither of antihyperlipemic groups is completely harmless to be applied in preconception period, pregnancy and lactacy period. Those patients who had low to medium increased values of triglycerides prior to pregnancy may develop severe hypertriglyceridemia, especially in the third trimester. They must be educared about dietetic measures and body mass reduction even in preconcepticon period, while during pregnancy they must be supervised and in case of triglycerides increase above 11.5 mmol/l and the resulting risk of pancreatitis, other therapy options must be taken into consideration. In women who had hypercholesterolemia before pregnancy as well as those who developed it only during pregnancy, there is a risk of atherosclerosis development in fetus at the birth itself. Besides, children born by mothers with hypercholesterolemia have a risk of faster progression of these fatty streak during the first living year. Although statins do not represent major teratogenic substances in human pathology, it is advised to stop their application either before conception in planned pregnancy, or at the very moment when pregnany is confirmed (abortions are not encouraged).
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PMID:[Hyperlipidemia and pregnancy]. 1970 22


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