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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipidemia is a rare cause of pancreatitis. It has been believed that free fatty acids released from hydrolyzed serum chylomicrons or triglycerides and chylomicrons induce hyperlipidemic pancreatitis by damaging acinar cells and capillaries. Type I, IV or V hyperlipidemic (Fredrickson's classification) pancreatitides have distinctive features of increased and heightened serum chylomicron and triglyceride levels. In contrast, type IIb hyperlipidemia usually doesn't have increased chylomicrons. It is a dominant inherited genetic disorder and doesn't manifest the subjective symptom before combining vascular complications such as coronary artery disease. Only a few cases of type IIb hyperlipidemic pancreatitis have been reported. We experienced a male patient with recurrent hyperlipidemic pancreatitis combined with type IIb hyperlipidemia. We present the case report and a review of the literature of hyperlipidemic pancreatitis, especially cases in Korea.
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PMID:Recurrent acute pancreatitis in a patient with type IIb hyperlipoproteinemia: a case report and review of the literature in Korea. 1650 98

Hypertriglyceridemia is a commonly encountered lipid abnormality frequently associated with other lipid and metabolic derangements. The National Cholesterol Education Program recommends obtaining a fasting lipid panel in adults over the age of 20. The discovery of hypertriglyceridemia should prompt an investigation for secondary causes such as high fat diet, excessive alcohol intake, certain medications, and medical conditions (eg, diabetes mellitus, hypothyroidism). In addition, patients should be evaluated for other components of the metabolic syndrome. These include abdominal obesity, insulin resistance, low high-density lipoprotein (HDL), high triglyceride, and hypertension. Hypertriglyceridemia is classified as primary hypertriglyceridemia when there are no secondary causes identified. Primary hypertriglyceridemia is the result of various genetic defects leading to disordered triglyceride metabolism. It is important to treat hypertriglyceridemia to prevent pancreatitis by reducing triglyceride levels to <500 mg/dL. Furthermore, lowering triglycerides while treating other dyslipidemias and components of the metabolic syndrome will reduce coronary events. However, it is controversial how much isolated hypertriglyceridemia correlates directly with coronary artery disease and further studies are needed to clarify whether treatment for this condition leads to meaningful clinical outcomes. Therapeutic lifestyle changes (TLC) are the first line of treatment for hypertriglyceridemia. These changes include a low saturated fat, carbohydrate-controlled diet, combined with alcohol reduction, smoking cessation, and regular aerobic exercise. High doses of omega-3 fatty acids from fish and fish oil supplements will lower triglyceride levels significantly. When patients do not reach their goals by TLC, drug therapy should be started. In cases of isolated hypertriglyceridemia, fibrates are initially considered. When elevated low-density lipoprotein levels accompany hypertriglyceridemia, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors are preferred. In patients with low HDL levels and hypertriglyceridemia, extended release niacin can be considered. A combination of the medicines may be necessary in recalcitrant cases.
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PMID:Hypertriglyceridemia. 1667 84

The aim of this study was to prospectively analyze the possible association of delayed gastric emptying and postoperative pancreatic complications after pancreaticoduodenectomy. Although hospital mortality after pancreaticoduodenectomy is minimal, morbidity is still high; delayed gastric emptying is one of the most frequent complications. Thirty-nine consecutive patients undergoing pancreaticoduodenectomy were included in this study: 14 females and 25 males (median age 65 years; range, 7-82). Delayed gastric emptying was defined as the need for a nasogastric tube or recurrent vomiting that prevented normal feeding on the 10th postoperative day. Blood analysis was performed on postoperative days 4, 6, and 10; Gastrografin examination on day 6; CT scan on days 2 and 5; and drain amylases were measured on day 5. Pancreatitis was defined as pancreatitis changes in CT scan interpreted by an experienced radiologist without knowing other data. Pancreatic fistula was defined according to the recent international recommendations. We had no mortality. Twelve patients (31%) developed delayed gastric emptying. Surgical (9/12 vs. 5/27; P = 0.001) but not medical complications occurred more often in the delayed gastric emptying group. Of the single complications, postoperative CT-detected pancreatitis (6/12 vs. 4/27; P = 0.03) and postoperative pancreatic fistula (5/12 vs. 1/27; P = 0.0007) were significantly associated with delayed gastric emptying compared with the patients without delayed gastric emptying. This pancreatitis was already detected in CT scan on day 2 in most patients (6/10, 60%). In delayed gastric emptying patients, the only parameters in blood analysis that differed significantly from patients without this complication were serum amylase activity (mean +/- SEM, 715 +/- 205 vs. 152 +/- 70 IU/L; P = 0.02), blood leukocyte count (16 +/- 2 vs. 9 +/- 0.6 x 10(9)/L; P = 0.007) and serum C-reactive protein (CRP) concentration (144 +/- 28 vs. 51 +/- 14 mg/L, P = 0.01). Postoperative pancreatic (subclinical) fistula was also associated with postoperative pancreatitis (6/10 vs. 0/29; P = 0.003). Preoperative coronary artery disease (OR = 16; 95% CI, 1.0-241; P = 0.05) and soft pancreatic texture at operation (OR = 9; 95% CI, 1.4-52; P = 0.02) were significant risk factors for the development of postoperative pancreatitis. The diagnosis of delayed gastric emptying after pancreaticoduodenectomy often follows postoperative pancreatitis. Delayed gastric emptying is also associated with postoperative pancreatic fistula, for which this pancreatitis seems to be a risk factor. Preoperative coronary artery disease and soft texture of the pancreas are significant risk factors for postoperative CT-detected pancreatitis.
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PMID:Postoperative acute pancreatitis as a major determinant of postoperative delayed gastric emptying after pancreaticoduodenectomy. 1696 32

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

In continuous ambulatory peritoneal dialysis (CAPD)-related cases of fungal peritonitis, Candida parapsilosis (C. parapsilosis) has become as common as Candida albicans (C. albicans) in fungal isolates. This report describes a 74-year-old male CAPD patient who received bypass surgery for coronary artery disease, followed by an episode of bacterial peritonitis. The peritonitis was successfully treated with intraperitoneal antibiotics. However, C. parapsilosis peritonitis with concomitant pancreatitis and infected pseudocysts occurred one month later. Despite surgical drainage and intravenous administration of fluconazole, fungal peritonitis persisted. Finally, he died of nosocomial pneumonia. This case demonstrates the poor outcome of C. parapsilosis peritonitis, suggesting a more aggressive treatment in peritoneal dialysis patients.
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PMID:Candida parapsilosis peritonitis complicated with infected pancreatic pseudocysts in a peritoneal dialysis patient: a challenge for nephrologists. 1853 25

A 55-year-old man presented to the emergency department with a 12-hour history of severe crampy abdominal pain, nausea, vomiting and obstipation. The patient had a complex medical history, including coronary artery disease, lupus, hypothyroidism, epilepsy, pancreatitis and renal calculi. However, the patient had no history of a hernia or abdominal surgery. Physical examination revealed a temperature of 38.5 degrees C and a soft distended abdomen that was diffusely tender without signs of peritonitis. The rest of the physical examination was unremarkable. Routine laboratory investigations including a complete blood cell count, electrolytes, liver enzymes and amylase were normal, with the exception of a decreased hemoglobin level of 116 g/L. We ordered a plain abdominal radiograph (Fig. 1) and a contrast-enhanced computed tomography (CT) scan of his abdomen. What is your diagnosis?
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PMID:Soft tissue case 61. 1968 May 23

Acute pancreatitis is a disease initially located into the pancreas that may become a systemic disease involving organs distant from the pancreas. All organs may be involved during an acute attack of pancreatitis: lungs, kidney, heart, liver, brain. The differential is sometime difficult because acute pancreatitis may sometimes mimic an acute coronary syndrome. We report a case of a 36-year-old man who was admitted to Emergency Room for persistent epigastric pain. Serial electrocardiograms (ECG) showed signs of acute myocardial infarction. However, a coronary angiogram demonstrated no coronary artery disease, and serum troponin was undetectable. Later, serum pancreatic enzyme levels were elevated and an ultrasonography scan of the abdomen was consistent with pancreatitis. Physicians should keep in mind the possibility of an attack of pancreatitis in a patient with abdominal pain and ECG modifications who is a heavy drinker.
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PMID:Abdominal pain and ECG alteration: a simple diagnosis? 2049 72

Hypertriglyceridemia, characterized by the accumulation of triglyceride-rich lipoproteins in the blood, affects 10-20% of the population in western countries and increases the risk of atherosclerosis, coronary artery disease, and pancreatitis. The etiology of hypertriglyceridemia is complex, and much interest exists in identifying and characterizing the biological and environmental factors that affect the synthesis and turnover of plasma triglycerides. Genetic studies in mice have recently identified that heparan sulfate proteoglycans are a class of receptors that mediate the clearance of triglyceride-rich lipoproteins in the liver. Heparan sulfate proteoglycans are expressed by endothelial cells that line the hepatic sinusoids and the underlying hepatocytes, and are present in the perisinusoidal space (space of Disse). This chapter discusses the dependence of lipoprotein binding on heparan sulfate structure and the identification of hepatocyte syndecan-1 as the primary proteoglycan that mediates triglyceride-rich lipoprotein clearance.
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PMID:Hepatic heparan sulfate proteoglycans and endocytic clearance of triglyceride-rich lipoproteins. 2080 47

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.
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PMID:Treatment options for severe hypertriglyceridemia (SHTG): the role of apheresis. 2252 30

Type III hyperlipoproteinemia (type III HLP) rarely manifests in childhood. Long-term follow-up (37 years) of the first patient revealed hypothyroidism at diagnosis requiring thyroxine replacement, palmar xanthomas requiring surgical removal, splenomegaly requiring splenectomy, 18 episodes of pancreatitis and premature coronary artery disease. Investigation revealed an apolipoprotein E phenotype of E2/E2 and partial lipoprotein lipase deficiency. Investigation of the second patient revealed a combination of apoE2/E2 phenotype and heterozygous familial hypercholesterolaemia. The third patient had a complete deficiency of lipoprotein lipase activity, an abnormal thyroid stimulating hormone on diagnosis (with subsequent normalisation without treatment), and apoE2/E2 phenotype. Type III HLP is a serious disorder with lifelong consequences of premature vascular disease and recurrent pancreatitis. Early presentation of disease in our patients was associated with additional precipitating factors. Drug treatment of paediatric type III HLP is indicated if dietary modifications alone are insufficient in managing the dyslipidaemia.
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PMID:Case series of type III hyperlipoproteinemia in children. 2269 86


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