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)

Hypertrophic obstructive cardiomyopathy with significant hypertrophy of the basal septum is the most frequently reported cause of left ventricular outflow tract (LVOT) obstruction. Additionally, other conditions such as dehydration, sepsis, vasodilatation, or mitral valve repair have been associated with LVOT obstruction. In this report, we present a case of a patient without hypertrophy who developed severe dynamic left ventricular outflow tract obstruction during catecholamine stimulation for shock that complicated severe pancreatitis. The present case serves as a reminder that hypovolemia together with a hyperdynamic state resulting from catecholamine administration may result in the development of dynamic LVOT obstruction even if baseline cardiac evaluation is unremarkable. Early detection and intensive efforts to reverse the underlying conditions, including cessation of catecholamine therapy and correction of hypovolemia are essential.
Int J Cardiol 2005 May 25
PMID:Catecholamine therapy inducing dynamic left ventricular outflow tract obstruction. 1588 88

The use of fibrates in the management of lipoprotein disorders has a history dating back to the mid-1960s. This group of drugs has now been tested in several large long-term trials with cardiovascular end points. Overall, there is good evidence for the reduction of cardiovascular disease in primary prevention studies and in those of subjects with manifest disease. More recent trials have suffered from high interference due to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) introduction, particularly in their placebo control groups. However, there is very good evidence for overall safety from a combined study of >20,000 patients in these controlled clinical trials lasting approximately 5 years. Abdominal pain has been observed more frequently in the statin vs placebo group. Myopathy, liver enzyme elevations, and cholecystitis have been potential adverse reactions of interest. However, these have occurred at a very low rate and are rarely found to be statistically more frequent in the active-treatment group compared with the subjects taking placebo. The recent Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study found a slightly higher incidence of pancreatitis, deep venous thrombosis, and pulmonary embolism. Small creatinine and homocysteine elevations are observed in many patients taking fibrates, and the effect of this on long-term outcomes is under study. The FIELD study also described a significant reduction in the rates of progression of proteinuria and vascular retinopathy with fibrate therapy. To date, there has been no study exclusive to patients with elevated triglycerides, raising the question of the potential benefit of these drugs in patients with the lipid abnormalities most effectively treated with fibrates.
Am J Cardiol 2007 Mar 19
PMID:Expert commentary: the safety of fibrates in lipid-lowering therapy. 1736 73

In an attempt to improve quality of care for patients admitted to our medical service we have implemented the use of pathways. These are printed standards of care and a mechanism for daily multidisciplinary documentation. The goals of our pathways are to: improve quality using printed standards of care; improve documentation of the care delivered; improve communication about daily goals between all team members, patients and families; standardize our in-patient chart format throughout the hospital; and increase efficiency of care. Pathways were designed to provide physicians and nurses with the standards for care and provide a mechanism for multidisciplinary documentation on our in-patient charts. We now have 2 pathways in use on our medical service. One is a clinical care plan (CCP) and the other is a Pancreatitis Pathway (PP) for patients admitted with acute pancreatitis and the other a guideline for care for all patients. The pathways were developed by teams including attending physicians (General Internists and Gastroenterologists), medicine house officers, nurses, and care coordinators. The pathways are used for all patients admitted to our medical service if they are admitted to one of 2 floors. This paper includes a comparison of outcomes for our first 9 patients who were managed using the pancreatitis pathway versus 7 patients cared for without the pathway. Significant differences in the pancreatitis pathway treated patients included: 1) less intense pain on day 2, (P = 0.04); 2) less pain on day of refeeding (P = 0.004); and 3) less IV fluids administered (P = 0.05). We also describe several lessons we have learned about using pathways for in-patients on a medical service in an academic medical center. We have learned the following lessons. Nursing documentation is improved. Physicians need ongoing encouragement and education about the value of pathways. There is considerable work involved for unit coordinators, care coordinators, and nursing in using pathways on a medical-surgical floor. There must be physician and nurse champions. There must be ongoing feedback to users. There must be input from users and edits. We believe the use of pathways as a process to remind clinicians of quality standards will improve the care of our patients by decreasing variation, improving team communication, and enhancing patient and family education.
Crit Pathw Cardiol 2004 Mar
PMID:Implementing clinical pathways for patients admitted to a medical service: lessons learned. 1834 Jan 38

Combinations of statins and fibrates may be increasingly prescribed to achieve lipid goals in high-risk patients and those with other cardiovascular risk factors, such as mixed dyslipidemia. The purpose of this retrospective cohort study was to compare rates of hospitalization for specific diagnoses in a cohort of new users of statins or fibrates, using claims data from a large United States health insurer. New users of statin, fibrate, or statin-fibrate therapy from 2004 to 2007 were identified; followed for hospitalization with rhabdomyolysis, renal impairment, hepatic injury, or pancreatitis; and confirmed by medical record review. Incidence rates (IRs) were compared across categories of fibrate or statin use, with adjusted IR ratios estimated using Poisson regression. A total of 584,784 patients initiated statins or fibrates. The IR of rhabdomyolysis in statins was 3.30 per 100,000 patient-years; the adjusted IR ratio for statin-fenofibrate combinations compared to statins alone was 3.75 (95% confidence interval 1.23 to 11.40). The IRs of renal impairment and pancreatitis in statins were 108.87 per 100,000 patient-years and 45.76 per 100,000 patient-years, respectively; the adjusted IR ratios for statin-fenofibrate combinations compared to statins alone were 1.47 (95% confidence interval 1.12 to 1.93) and 2.87 (95% confidence interval 2.05 to 4.02), respectively. The IR of hepatic injury with statins was 8.57 per 100,000 patient-years, with no risk difference between exposure groups. In conclusion, the risk for rhabdomyolysis was low, although higher in patients newly treated with statin-fibrate concurrent therapy than those treated with either as monotherapy. The risk for pancreatitis was higher in patients treated with fenofibrate, whether in combination with statins or alone.
Am J Cardiol 2010 Dec 01
PMID:Pharmacoepidemiology safety study of fibrate and statin concomitant therapy. 2109 60

No previous reports are available about the potential dramatic effects resulting from the combination of acquired long QT interval not associated to bradycardia and myocardial ischemia. We report the case of a man that during acute necrotic pancreatitis presented QT interval prolongation without bradycardia, TdP, and two episodes of cardiac arrest. A coronary angiogram revealed a subocclusive stenosis of left anterior descending coronary artery, treated with a percutaneous coronary intervention. After myocardial revascularization, even in presence of long QT interval, no arrhythmic events occurred suggesting the key role of myocardial ischemia in triggering TdP in acquired long QT even without bradycardia. ECG performed six months later, after complete recovery from pancreatitis, showed a normal QT interval.
Cardiol Res Pract 2011 Mar 03
PMID:Partners in crime in the setting of recurring cardiac arrest. 2140 70

Alcohol has been consumed by most societies over the last 7000 years. Abraham Lincoln said "It has long been recognized that the problems with alcohol relate not to the use of a bad thing, but to the abuse of a good thing." Light to moderate alcohol consumption reduces the incidence of coronary heart disease (CHD), ischemic stroke, peripheral arterial disease, CHD mortality, and all-cause mortality, especially in the western populations. However, heavy alcohol consumption is detrimental causing cardiomyopathy, cardiac arrhythmias, hepatic cirrhosis, pancreatitis, and hemorrhagic stroke. In this article, we review the effects of alcohol on CHD, individual cardiovascular risk factors, cardiomyopathy, and cardiac arrhythmias, including the most recent evidence of the effects of alcohol on CHD.
Int J Cardiol 2013 Apr 15
PMID:Alcohol and the heart: to abstain or not to abstain? 2445 87

Hypertriglyceridemia is associated with a number of severe diseases such as acute pancreatitis and coronary artery disease. In severe hypertriglyceridemia (SHTG, triglycerides > 1,000 mg/dL), rapid lowering of plasma triglycerides (TG) has to be achieved. Treatment regimes include nutritional intervention, the use of antihyperlipidemic drugs, and therapeutic apheresis. Apheretic treatment is indicated in medical emergencies such as hypertriglyceridemic pancreatitis. Reviewing the current literature, plasmapheresis appears to be a safe and useful therapeutic tool in patients suffering from SHTG. Apheretic treatment is able to remove the causative agent for pancreatic inflammation. Data suggests that the use of apheresis should be performed as early as possible in order to achieve best results. The use of plasmapheresis, however, is limited due to the rather high costs and the limited availability of the procedure.
Clin Res Cardiol Suppl 2012 Jun
PMID:Treatment options for severe hypertriglyceridemia (SHTG): the role of apheresis. 2252 30

The three major pathways of lipoprotein metabolism provide a superb paradigm to delineate systematically the familial dyslipoproteinemias. Such understanding leads to improved diagnosis and treatment of patients. In the exogenous (intestinal) pathway, defects in LPL, apoC-II, APOA-V, and GPIHBP1 disrupt the catabolism of chylomicrons and hepatic uptake of their remnants, producing very high TG. In the endogenous (hepatic) pathway, six disorders affect the activity of the LDLR and markedly increase LDL. These include FH, FDB, ARH, PCSK9 gain-of-function mutations, sitosterolemia and loss of 7 alpha hydroxylase. Hepatic overproduction of VLDL occurs in FCHL, hyperapoB, LDL subclass pattern B, FDH and syndrome X, often due to insulin resistance and resulting in high TG, elevated small LDL particles and low HDL-C. Defects in APOB-100 and loss-of-function mutations in PCSK9 are associated with low LDL-C, decreased CVD and longevity. An absence of MTP leads to marked reduction in chylomicrons and VLDL, causing abetalipoproteinemia. In the reverse cholesterol pathway, deletions or nonsense mutations in apoA-I or ABCA1 transporter disrupt the formation of the nascent HDL particle. Mutations in LCAT disrupt esterification of cholesterol in nascent HDL by LCAT and apoA-1, and formation of spherical HDL. Mutations in either CETP or SR-B1 and familial high HDL lead to increased large HDL particles, the effect of which on CVD is not resolved. The major goal is to prevent or ameliorate the major complications of many familial dyslipoproteinemias, namely, premature CVD or pancreatitis. Dietary and drug treatment specific for each inherited disorder is reviewed.
Curr Cardiol Rep 2013 Jun
PMID:Diagnosis and management of familial dyslipoproteinemias. 2366 84

Hypertriglyceridaemia (typical triglyceride level 1.7-5.0 mmol/l) is caused by interactions between many genetic and nongenetic factors, and is a common risk factor for atherosclerotic cardiovascular disease (CVD). Patients with hypertriglyceridaemia usually present with obesity, insulin resistance, hepatic steatosis, ectopic fat deposition, and diabetes mellitus. Hypertriglyceridaemia reflects the accumulation in plasma of proatherogenic lipoproteins, triglyceride-rich lipoprotein (TRL) remnants, and small, dense LDL particles. Mendelian randomization studies and research on inherited dyslipidaemias, such as type III dysbetalipoproteinaemia, testify that TRLs are causally related to atherosclerotic CVD. Extreme hypertriglyceridaemia (a triglyceride level >20 mmol/l) is rare, often monogenic in aetiology, and frequently causes pancreatitis. Treatment of hypertriglyceridaemia relies on correcting secondary factors and unhealthy lifestyle habits, particularly poor diet and lack of exercise. Pharmacotherapy is indicated for patients with established CVD or individuals at moderate-to-high risk of CVD, primarily those with metabolic syndrome or diabetes. Statins are the cornerstone of treatment, followed by fibrates and n-3 fatty acids, to achieve recommended therapeutic levels of plasma LDL cholesterol, non-HDL cholesterol, and apolipoprotein (apo) B-100. The case for using niacin has been weakened by the results of clinical trials, but needs further investigation. Extreme hypertriglyceridaemia requires strict dietary measures, and patients with a diagnosis of genetic lipoprotein lipase deficiency might benefit from LPL gene replacement therapy. Several therapies for regulating TRL metabolism, including inhibitors of diacylglycerol O-acyltransferase and microsomal triglyceride transfer protein, and apoC-III antisense oligonucleotides, merit further investigation in patients with hypertriglyceridaemia.
Nat Rev Cardiol 2013 Nov
PMID:Demystifying the management of hypertriglyceridaemia. 2439 48

Coronary heart disease remains the leading cause of death of men and women in the United States. Angiography and percutaneous coronary interventions (PCI) are an integral part in management of acute coronary syndromes. Well-defined complications of coronary angiography include allergic and anaphylactic reactions, vascular access complications, stroke, and contrast-induced kidney injury. Radiographic contrast agents (RCAs) are known to cause acute kidney injury. RCAs are also postulated to induce pancreatitis in experimental animal models. We present a patient with acute pancreatitis immediately following coronary angiography. Recent studies have described that the use of RCA is associated with worse prognosis in patients with ongoing pancreatitis. The pathophysiology of RCA-induced pancreatitis is poorly understood. Although extremely rare, RCA-induced pancreatitis should be considered in the appropriate clinical setting.
J Invasive Cardiol 2013 Oct
PMID:A case of contrast-induced pancreatitis following cardiac catheterization. 2408 37


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