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)

Tamoxifen exhibits favorable effects on the lipid and lipoprotein profile since it decreases the total and LDL cholesterol levels as well as the Lp(a) levels. Additionally, a small increase in serum triglycerides is commonly found after tamoxifen administration. However, severe hypertriglyceridemia which can sometimes be associated with life-threatening complications is occasionally noticed. Herein, we describe a patient who developed tamoxifen-induced severe hypertriglyceridemia and pancreatitis. An analysis of the underlying pathogenetic mechanisms as well as a review of the relevant literature is also provided.
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PMID:Tamoxifen-induced severe hypertriglyceridemia and pancreatitis. 1103 48

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

The paper presents the data available in the literature on mutations in known genes in pancreatitis, such as cationic trypsinogen (PRSS1), pancreatic secretory trypsin inhibitor (PSTI/SPINK1), cystic fibrosis (CFTR), and apolipoprotein E (APOE) genes, as well as the new candidate gene--chymotrypsinogen (CTRC). It also gives the results of the authors studies estimating the spread of the mutations in the PRSS1 (2.5%), PSTI/SPINK1 (3.3%), and CFTR (0.8%) genes, as well as APOE polymorphism in patients with pancreatitis. It is shown that the E4 allele of the APOE gene was more frequently identified in patients with acute pancreatitis than in those with chronic pancreatitis (0.143 +/- 0.05 and 0.026 +/- 0.02, respectively; p < 0.05). An overview is given of 7 major classes of candidate genes implicated in the pathogenesis of cholesterol cholelithiasis (CL): hepatic enzymes regulating blood lipid composition; receptors of lipoproteins, hepatic and intestinal membrane and intracellular transport proteins; factors regulating the transcription of lipids and bile salts, cholecystokinin and its receptors, and mucin. In the authors' epidemiological study, the spread of APOE alleles and genotypes did not differ in women with and without CL; low molecular-weight apolipoprotein(a) isoforms (B, S2) were significantly found in patients with CL than in those without CL; the spread of the CG genotype in the TRPM8 gene was significantly lower in women with cholesterol CL than that in the Novosibirsk population. These polymorphisms have been proved to be associated with bile cholesterol concentrations in women with cholesterol CL. The opposite effect of the APOE4 allele on gallbladder stone formation processes is demonstrated, by using the APOE polymorphism as an example, which shows it necessary to examine each specific population to elicit a possible association between the polymorphism of different genes and gastrointestinal tract diseases.
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PMID:[Genetic aspects of digestive diseases. Part 1]. 2038 81

During pregnancy physiological changes occur in the lipid metabolism due to changing hormonal conditions: the LDL cholesterol (LDL-C), triglycerides (TG) and lipoprotein(a) [Lp(a)] increase throughout pregnancy. Common lipoprotein disorders are associated in pregnancy with two major clinical disorders: severe hypertriglyceridemia (SHTG) is a potent risk factor for development of acute pancreatitis and elevated cholesterol due to greater concentrations of LDL and remnant lipoproteins and reduced levels of HDL promote atherosclerosis. The combination of homozygous Familial Hypercholesterolemia (HoFH) and pregnancy can be a fatal condition. Therapeutic plasma exchange (TPE) may be used for an urgent need of a fast and effective lowering of TG levels in order to prevent a severe pancreatitis episode or hypertriglyceridemia-induced complications during pregnancy. LDL apheresis can decrease LDL-C and prevent complications and can be considered in the treatment of pregnancies complicated by high LDL-C. These conditions are configured in patients with HeFH who were taking statins before pregnancy (selected cases), patients already receiving apheresis before pregnancy suffering from HoFH, patients suffering from hypertriglyceridemia due to familial hyperlipoproteinemia types I and V, and cases of hypertriglyceridemia secondary to diabetes.
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PMID:Severe dyslipidemia in pregnancy: The role of therapeutic apheresis. 2662 68

The prevalence of lipid disorders is alarmingly increasing in the Western world. They are the result of either primary causes, such as unhealthy lifestyle choices or inherited risk factors, or secondary causes like other diseases or medication. Atypical changes in the synthesis, processing and catabolism of lipoprotein particles may lead to severe hypercholesterolemia, hypertriglyceridemia or elevated Lp(a). Although cholesterol-lowering drugs are the most prescribed medications, not all patients achieve guideline recommended cholesterol levels with the current treatment options, emphasising the need for new therapies. Also, some lipid disorders do not have any treatment options but rely only on stringent dietary restriction. Patients with untreated lipid disorders carry a severe risk of cardiovascular disease, diabetes, non-alcoholic fatty liver disease and pancreatitis among others. To achieve better treatment outcome, novel selective gene expression and epigenetic targeting therapies are constantly being developed. Therapeutic innovations employing targeted RNA technology utilise small interfering RNAs, antisense oligonucleotides, long non-coding RNAs and microRNAs to regulate target protein production whereas viral gene therapy provides functional therapeutic genes and CRISPR/Cas technology relies on gene editing and transcriptional regulation. In this review, we will discuss the latest advances in clinical trials for novel lipid-lowering therapies and potential new targets in pre-clinical phase.
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PMID:Recent advances in novel therapies for lipid disorders. 3122 25