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)

A patient with a history of diabetes, coronary artery disease, stroke, previous renal transplantation, and multiple hospital admissions for recurrent pancreatitis was transferred to the hospital from a chronic care facility because of fever and severe epigastric discomfort. At the time of admission, she was receiving hyperalimentation through a central venous TPN catheter. Multiple blood cultures obtained on the first and second hospital days yielded pure cultures of the yeast, Pichia ohmeri. The patient developed acute renal failure, and despite high-dose amphotericin B therapy, ultimately expired.
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PMID:Pichia ohmeri fungemia. 957 30

Atherogenic risk is accurately defined by the turnover of the lipoprotein classes that transport cholesterol and triglycerides, and by the apolipoproteins that determine the fate of these particles. Post-prandial triglyceride levels have also been shown to be an accurate predictor of atherogenic risk. The post-prandial triglyceride levels and conversion of very low density lipoprotein (VLDL) to intermediate density lipoprotein (IDL) are controlled by a dynamic metabolic process involving lipoprotein lipase (LPL) and hepatic lipase. The interaction between the two enzymes modulates triglyceride transport through the plasma and influences the structure and serum concentrations of the denser cholesterol-rich low density lipoproteins (LDL) and high density lipoproteins (HDL). Inadequate LPL function, a consequence either of impaired enzyme function or simply post-prandial overloading, can have profound pathophysiological consequences. High levels of large HDL2 reflect effective catabolism of triglyceride-rich lipoproteins by LPL whereas low levels of this lipoprotein reflect inadequate LPL activity or elevated hepatic lipase activity. Individuals with low levels of HDL2 are prone to coronary artery disease. Overloading of LPL can occur in insulin resistance due to the absence of normal insulin-mediated suppression of VLDL secretion and the consequence is hypertriglyceridaemia. In addition, a deficiency in LPL can arise from a genetic defect which, in the homozygous state, results in pronounced hypertriglyceridaemia and pancreatitis. The correct management for patients with inadequate LPL activity is to optimize triglyceride metabolism, particularly in the post-prandial state.
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PMID:Influence of lipolysis on chylomicron clearance and HDL cholesterol levels. 971 57

Hyperlipidemia is recognized as one of the major risk factors for the development of coronary artery disease and progression of atherosclerotic lesions. Dietary therapy together with hypolipidemic drugs are central to the management of hyperlipidemia, which aims to prevent atherosclerotic plaque progression, induce regression, and so decrease the risk of acute coronary events in patients with pre-existing coronary or peripheral vascular disease. In patients at high risk of coronary artery disease but without evidence of atherosclerosis, treatment is designed to prevent the premature development of coronary artery disease, whereas in those with hypertriglyceridemia, treatment aims to prevent the development of hepatomegaly, splenomegaly, and pancreatitis. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are the most potent lipid-lowering agents currently available, and their use in the treatment of hyperlipidemia provides the focus for this review. Particular emphasis is given to cerivastatin, a new HMG-CoA reductase inhibitor that combines potent cholesterol-lowering properties with significant triglyceride-reducing effects. Recently completed primary and secondary intervention trials have shown that the significant reductions in low-density lipoprotein (LDL) cholesterol achieved with statins result in significant reductions in morbidity and mortality associated with coronary artery disease as well as reductions in the incidence of stroke and total mortality. Such benefits occur early in the course of statin therapy and have led to suggestions that these drugs may possess antiatherogenic effects over and above their capacity to lower atherogenic lipids and lipoproteins. Experimental studies have also shown statin-induced improvements in endothelial function, decreased platelet thrombus formation, improvements in fibrinolytic activity, and reductions in the frequency of transient myocardial ischemia.
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PMID:Current and future treatment of hyperlipidemia: the role of statins. 973 40

The importance of plasma triglycerides as a risk factor for the development of coronary artery disease (CAD) has been controversial for many years. In univariate analysis plasma triglycerides predict CAD in several studies, but this effect is attenuated when high-density lipoprotein (HDL) cholesterol is included in the analysis. The controversy can be explained by the complexity of lipoprotein metabolism. Plasma triglycerides serve as markers for metabolic and clinical conditions associated with increased CAD risk. Several recent studies shed new light on the significance of triglycerides for the development of CAD, depending on their level in plasma: there appears to be an optimal concentration < 1.1 mmol/l, an intermediate range with increased risk at values 1.1-4 mmol/l, above which level the risk decreases. Very high levels of triglycerides confer increased risk of pancreatitis.
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PMID:[Serum triglycerides as a risk factor for atherosclerosis]. 1022 Oct 81

We describe the case of a young HIV-positive patient undergoing three-drug antiretroviral therapy that included a protease inhibitor for 9 months, who was admitted to the hospital with an acute myocardial infarction. A coronary angiogram revealed occlusion caused by a thrombus in the proximal third of the anterior descending artery. Complete recanalization was obtained after an angioplasty was performed. At the time of the infarction, only the triglyceride levels were found to be high. Metabolic alterations associated with the prolonged use of protease inhibitors have been described such as an increase in the triglyceride and cholesterol serum levels, diabetes, resistance to insulin, lipodystrophy, and pancreatitis. The consequences of chronic hyperlipidemia are well known in the medical literature, especially premature coronary artery disease. No family history of coronary artery disease was identified in this patient. Whether the genesis of this localized coronary thrombosis was due to a change in the metabolism of the vascular endothelium caused by the protease inhibitors, or by related dyslipidemia, is still to be determined. In this case, the data suggest a strong link between coronary insufficiency and prolonged use of the protease inhibitor.
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PMID:Acute Myocardial Infarction in a 34-Year-Old HIV-Positive Female Patient While Undergoing Active Antiretroviral Therapy Containing a Protease Inhibitor. 1108 68

Because hyperlipidemia may present as xanthomas, a dermatologist may be the first to diagnose these skin lesions and associated lipid abnormalities. Xanthomas are of concern because of their association with coronary artery disease and pancreatitis. We describe the case of a 40-year-old white male with chest pain and eruptive xanthomas. Laboratory tests revealed severe hypercholesterolemia, hypertriglyceridemia, and diabetes mellitus, and the histopathology of the skin lesions was consistent with eruptive xanthomas. Surprisingly, even with overwhelming risk factors for both atherosclerosis and pancreatitis, this patient did not show evidence of either disease process. After initiating therapy for the diabetes and hyperlipidemia, the patient has had no recurrence of chest pain, and the skin lesions have gradually resolved. The most likely explanation for this patient's pattern of symptoms and laboratory results is the chylomicronemia syndrome, which can be seen in patients with type I or type V hyperlipoproteinemia.
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PMID:Eruptive xanthomas and chest pain in the absence of coronary artery disease. 1132 91

Transient electrocardiographic changes in patients with acute pancreatitis are well known in the literature. Mostly these changes are in the form of T-wave inversion, ST-segment depression, and rarely ST-segment elevation without the presence of coronary artery disease. We report a patient, in whom electrocardiographic changes mimicked acute inferior myocardial infarction with subsequent evolution of Q-waves in the inferior leads and ischaemia in the anterior wall. To the authors' knowledge, this is the first report documenting the evolution of Q-waves on surface ECG in the absence of myocardial necrosis verified by postmortem examination in the patient, who died of cardiorespiratory failure and massive haemoperitoneum as a complication of ongoing acute necrotizing haemorrhagic pancreatitis. The authors also discuss diagnostic and therapeutic options in patients with acute pancreatitis and ECG pattern of acute myocardial infarction. Acute pancreatitis may mimic acute myocardial ischaemia (or infarction) or these two diseases may be present at the same time. In differential diagnosis, selective coronarography might be helpful and it allows also immediate revascularisation. Administration of thrombolytic therapy in such patients is not safe and might end up with fatal consequences.
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PMID:[Electrocardiographic changes in patients with acute pancreatitis. Case report and review of the literature]. 1149 89

A 56-year-old male with apolipoprotein C-II deficiency experienced a myocardial infarction without pancreatitis. A coronary angiogram showed complete occlusions of both the right and circumflex coronary arteries. His serum lipid levels were as follows: fasting total cholesterol 3.15 mmol/l; postprandial total cholesterol 3.62 mmol/l; fasting triglycerides 1.46 mmol/A; postprandial triglycerides 6.14 mmol/l; fasting high-density lipoprotein-cholesterol 0.47 mmol/l; and postprandial high-density lipoprotein cholesterol 0.36 mmol/l. His fasting level of plasma apolipoprotein C-II was 0.005 g/l, but his plasma levels of other apolipoproteins were within normal ranges. A DNA sequence analysis of the apolipoprotein C-II gene showed no mutations in exon 1, 2, 3, or 4, where most gene mutations related to apolipoprotein C-II deficiency occur. We report this patient's very rare heterozygous apolipoprotein C-II deficiency with coronary artery disease. Although this patient had some risk factors for coronary artery disease, coronary atherosclerosis in this patient might have occurred as a result of lipoprotein abnormalities caused by at least one mutation in the apolipoprotein C-II gene.
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PMID:A case of apolipoprotein C-II deficiency with coronary artery disease. 1204 86

To understand recent temporal trends in acquired immunodeficiency syndrome (AIDS) mortality in the era of highly active antiretroviral therapy (HAART), trends in causes of death among persons with AIDS in San Francisco who died between 1994 and 1998 were analyzed. Among 5234 deaths, the mortality rate for human immunodeficiency virus (HIV)-related or AIDS-related deaths declined after 1995 (P<.01), whereas the mortality rate for non-HIV- or non-AIDS-related deaths remained stable. The proportion of deaths of persons with AIDS associated with septicemia, non-AIDS-defining malignancy, chronic liver disease, viral hepatitis, overdose, obstructive lung disease, coronary artery disease, and pancreatitis increased (P<.05). The standardized mortality ratio was high for these causes in both pre- and post-HAART periods, except for pancreatitis, a possible complication of HAART, which demonstrated an increasing standardized mortality ratio trend after 1996. With increasing AIDS survival, prevention of chronic diseases, assessment of long-term toxicity from HAART, and surveillance for additional causes of mortality will become increasingly important.
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PMID:Trends in causes of death among persons with acquired immunodeficiency syndrome in the era of highly active antiretroviral therapy, San Francisco, 1994-1998. 1223 45

A 71-year-old man presented with left upper quadrant abdominal pain. Serial electrocardiograms (ECGs) demonstrated an evolving left bundle branch block, a sign of acute myocardial infarction (AMI). However, a coronary angiogram demonstrated minimal coronary artery disease, and serum troponin T was undetectable in serial serum measurements. Later, serum pancreatic enzyme levels were elevated and a computed tomography scan of the abdomen was consistent with pancreatitis. In patients presenting with acute pancreatitis and ECG changes suggesting AMI, measurement of serum troponin T concentrations can aid in differentiating ECG changes driven by acute pancreatitis from those of true myocardial ischemia or infarction.
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PMID:A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. 1473 Jan 76


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