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

We conducted a retrospective analysis of 37 children with Escherichia coli O157:H7-associated hemolytic-uremic syndrome. The infection was traced to contaminated hamburgers at a fast-food restaurant chain. Within 5 days of the first confirmed case, the Washington State Department of Health identified the source and interrupted transmission of infection. Ninety-five percent of the children initially had severe hemorrhagic colitis. Nineteen patients (51%) had significant extrarenal abnormalities, including pancreatitis, colonic necrosis, glucose intolerance, coma, stroke, seizures, myocardial dysfunction, pericardial effusions, adult respiratory disease syndrome, and pleural effusions. Three deaths occurred, each in children with severe multisystem disease. At follow-up two children have significant impairment of renal function (glomerular filtration rate < 80 ml/min/per 1.73 Hm2); both of these children have a normal serum creatinine concentration. Hemolytic-uremic syndrome is the most common cause of acute renal failure in children, and this experience emphasizes the systemic nature of this disease. Clinicians should anticipate that multisystem involvement may occur in these patients, necessitating acute intervention or chronic follow-up. This outbreak of Hemolytic-uremic syndrome also highlights the microbiologic hazards of inadequately prepared food and emphasizes the importance of public health intervention in controlling Hemolytic-uremic syndrome.
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PMID:Escherichia coli O 157:H7-associated hemolytic-uremic syndrome after ingestion of contaminated hamburgers. 793 69

Hyperglycemia may occur as a complication in patients with leukemia during induction therapy with L-asparaginase and steroids. The reported incidence is about 10%. The present report concerns three patients with acute lymphoblastic leukemia (ALL), complicated by hyperglycemia. Their ages were 10, 12, and 9 years, respectively. Past histories were normal, with no diabetes mellitus or other endocrine disorders in their families. Case 1 was an obese boy who developed pancreatitis and diabetic ketoacidosis (DKA) in his remission induction therapy which had included both L-asparaginase and steroids. Cases 2 and 3 both presented with polyuria and elevated postprandial blood sugar. For all patients, insulin was administered to control their blood sugars; the maximal daily dosage of insulin dispensed was 2.1 U/kg, 0.5 U/kg, and 0.7 U/kg, respectively. Increased plasma insulin and C-peptide levels suggestive of insulin resistance were observed in Case 3. The outcome of hyperglycemia in these three patients was good. The symptoms of this complication may vary from mild glucose intolerance to severe, or even fatal, DKA. Thus, periodic determinations of urine glucose and postprandial blood sugar are important for early recognition to prevent further life-threatening consequences.
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PMID:Hyperglycemia induced by chemotherapeutic agents used in acute lymphoblastic leukemia: report of three cases. 828 94

A 65-yr-old woman presented for evaluation of a pancreatic mass. She had been suffering from severe constitutional symptoms for 18 months; those symptoms included weight loss, increasing fatigue, night sweats, and recurrent fever attacks up to 40 degrees C. Later, bluish subcutaneous nodules developed on her lower limbs. Laboratory tests yielded signs of chronic inflammation and impaired glucose tolerance with elevated serum insulin and glucagon concentrations. Skin biopsy revealed lobular panniculitis. Ultrasonography and a CT scan demonstrated enlargement of the pancreas, and endoscopic retrograde pancreaticography disclosed displacement and stenosis of the main pancreatic duct. The patient was referred for explorative laparotomy, which was highly suggestive of a malignant pancreatic tumor. However, histological examination of the resected pancreatic and peripancreatic mass revealed tuberculous pancreatitis. This form of isolated tuberculous pancreatitis, associated with lobular panniculitis and laboratory features consistent with a tumor of the endocrine pancreas, has not been reported previously. Active tuberculosis should be a leading differential diagnosis in a patient with an enlarged pancreas when the usual diagnostic reasoning does not yield conclusive results.
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PMID:Isolated tuberculosis of the pancreas masquerading as a pancreatic mass. 854 May 23

An A3243G point mutation of the mitochondrial tRNA(Leu(UUR)) gene was detected in a Caucasian family with maternal diabetes mellitus and signs of mitochondrial dysfunction such as muscular hypotonia, encephalopathy, lactic acidosis, stroke-like episodes (MELAS), neurosensory hearing loss, cardial pre-excitation, and short stature. Low levels (10 JDF) of islet cell antibodies (ICA) in insulin-treated diabetes of the mother and impaired glucose tolerance with high levels of ICA (80 JDF) in her older son indicated that mitochondrial diabetes mellitus may involve beta cell damage. Furthermore, exocrine pancreas cell damage may also occur since the stroke-like episodes of this son were combined with pancreatitis. In all family members HLA types and plasma antioxidants were determined. Normal concentrations of hydro- and lipophilic antioxidants (including ubiquinol-10) were found.
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PMID:Islet cell antibodies in diabetes mellitus associated with a mitochondrial tRNA(Leu(UUR)) gene mutation. 881 38

Tropical calcific pancreatitis (TCP) is a variant of chronic pancreatitis, occurring only in developing countries. It frequently leads to diabetes at a young age. To determine the pathogenesis of glucose intolerance, beta-cell function and insulin sensitivity were measured in 11 TCP patients with normal glucose tolerance (TCP-NGT), six TCP patients with mild hyperglycemia [TCP-DM] median fasting plasma glucose, 6.1 mmol/L), and 16 healthy control subjects. The technique of continuous infusion of glucose with model assessment (CIGMA) was used to calculate beta-cell function (%B) and insulin sensitivity (%S), based on plasma glucose and insulin levels achieved after an intravenous infusion of glucose. %S was similar in both groups of TCP patients and controls. In contrast, %B was significantly lower in TCP-DM patients (median, 53; interquartile range, 41 to 62) compared with controls (90; 65 to 143; P < .01) and with TCP-NGT patients (119; 91 to 159; P < .01). TCP-NGT and control subjects had similar beta-cell function. Among patients with TCP, %B negatively correlated with the duration of pancreatitis (r = -.63, P < .05). Our results suggest that patients with TCP develop diabetes due to a diminution in beta-cell function, and that insulin resistance does not play a significant role in its pathogenesis.
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PMID:Beta-cell function and insulin sensitivity in tropical calcific pancreatitis from north India. 910 51

Sequelae of Escherichia coli O157:H7-associated hemolytic uremic syndrome (HUS) 2-3 years following an outbreak in Washington State have been prospectively studied to identify predictors of adverse sequelae. Logistic regression analysis was used to examine associations between findings in the acute course and long-term renal and gastrointestinal outcomes. Twenty-one percent of patients had gastrointestinal sequelae, which included cholelithiasis resulting in cholecystectomy (3/29), persistent pancreatitis (2/29), late colon stricture (1/29), and/or glucose intolerance (1/29). Logistic regression analysis found long-term gastrointestinal sequelae were higher in patients who, during HUS, had hypertension [odds ratio (OR) = 21.2, 95% confidence interval (CI) = 1.9-164.4, P = 0.01] or gastrointestinal complications (OR = 21.2, 95% CI = 1.9-164.4, P = 0.01). Renal sequelae were seen in 35% of patients. One patient (4%) had persistent hypertension and 9 (31%) had minor urinary findings (hematuria or proteinuria). Thrombocytopenia lasting longer than 10 days during the acute illness was associated with a risk for subsequent renal sequelae (OR = 15.0, 95% CI = 1.98-1,703.0, P = 0.009). We conclude a high incidence of gastrointestinal sequelae, especially cholelithiasis presenting long after the acute illness, may be seen with HUS. The short follow-up period may underestimate the extent and severity of eventual renal sequelae.
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PMID:Cholelithiasis following Escherichia coli O157:H7-associated hemolytic uremic syndrome. 963 42

Mutations in presenilin 1 and 2 are causative factors for early onset familial Alzheimer's disease and possible roles for presenilins include protein trafficking, regulation of apoptosis and/or calcium homeostasis. Presenilin 2 mRNA is expressed in brain, muscle and pancreas but the role of pancreatic presenilin 2 and its relationship to diabetes are unknown. Presenilin 2 immunoreactivity was localised in human and rodent pancreas to islet cells and found in granules of beta-cells. Presenilin 2 was identified in primitive islet and duct cells of human foetal pancreas and in proliferating exocrine duct cells in human pancreatitis but not found in islet amyloid deposits in Type 2 diabetic subjects. Full length, approximately 50 kDa, and the approximately 30 kDa N-terminal fragment of presenilin 2 were identified by western blotting in extracted rodent pancreas but only the 30 kDa fragment was detected in mouse islets and human insulinoma. Post-mortem pancreatic morphology was normal in a subject with the presenilin 2 Met239Val variant and early onset familial Alzheimer's disease. Oral glucose tolerance tests on subjects with the presenilin 2 Met239Val mutation unaffected by early onset familial Alzheimer's disease (mean age 35 years) and on their first-degree relatives without the mutation demonstrated no evidence of glucose intolerance or increased proinsulin secretion. PS2 is a novel &bgr;-cell protein with potential roles in development or protein processing but pancreatic islet structure and function appear to be unaffected by the Met239Val mutation.
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PMID:Localisation of presenilin 2 in human and rodent pancreatic islet beta-cells; Met239Val presenilin 2 variant is not associated with diabetes in man. 1036 43

Acute pancreatitis is a hypermetabolic state characterized by increased protein catabolism, lipolysis, and glucose intolerance. Most patients presenting with acute pancreatitis are better within 5 to 7 days and can be resume a regular diet. Patients with severe pancreatitis and who are unable to eat within 7 to 10 days should receive nutritional support. The decision to use parenteral or enteral nutrition is controversial. More recent data suggest that jejunal feedings are just as beneficial, if not better, than parenteral nutrition. Marked weight loss and abdominal pain are the features of chronic pancreatitis. Steatorrhea develops when greater than 90% of pancreatic exocrine dysfunction occurs. Treatment focuses on pain control and pancreatic enzyme replacement. Pancreatic enzymes should be given with meals. Patients with refractory steatorrhea may benefit from the addition of an H2 antagonist or proton-pump inhibitor with pancreatic enzyme replacement. Micronutrients, including antioxidants, should be replaced if serum levels suggest a deficiency.
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PMID:Nutrition supplementation in patients with acute and chronic pancreatitis. 1050 45

The incidence of invasive ductal carcinoma of the pancreas was 3.1% (6 cases) in 196 patients with definite chronic pancreatitis. Five patients (3 men and 2 women) had calcific pancreatitis and 1 patient (man) had non-calcific pancreatitis. Large pancreatic stones were recognized in 2 women. Most of the patients complained of continuous intractable abdominal pain and/or back pain together with weight loss and appetite loss. Serum CA19-9 levels and exacerbation of glucose intolerance were retrospectively noted to have been elevated in 1 patient. However, it was difficult to obtain a definitive diagnosis by imaging examinations earlier, due to the presence of chronic pancreatitis. Median survival of the 6 patients was 6.5 months from admission.
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PMID:Pancreatic carcinoma associated with chronic pancreatitis. 1062 33

The metabolism of acute pancreatitis is characterized by hypermetabolism and catabolism. Evidence for glucose intolerance occurs in anywhere from 40 to 90% of cases and urine urea nitrogen may increase up to 40 g/day. The most important aspect when considering nutritional therapy is determining the severity of the pancreatitis. The APACHE-II-scoring-system and the time honored Ranson criteria are useful for differentiating severe from mild pancreatitis. Despite some limitations in sensitivity and specificity, studies have suggested that patients with 2 or less Ranson criteria and an APACHE-II-score of 9 or less have mild pancreatitis, while patients with 3 or more Ranson criteria and an APACHE-II-score of 10 or more have severe pancreatitis. Evidence of organ failure on clinical presentation and pancreatic necrosis on dynamic CT scan are also important factors in determining severity of pancreatitis and are probably the two major indicators of patient outcome. Only 3 prospective randomized controlled trials have compared enteral to parenteral nutrition for pancreatitis. All studies described successful use of enteral feeding without exacerbating the disease process although a mild stimulation of exocrine pancreatic secretion could not be prevented, even when the tube was placed below the ligament of Treitz. Kalfarentzos [11] and McClave [14] could show that hyperglycemia was worse in the parenteral feeding patients compared to the enteral feeding group and Windsor [24] concluded with respect to the results of his study, that enteral feeding modulates the inflammatory response in acute pancreatitis. Conclusions regarding the use of enteral or parenteral nutrition in acute pancreatitis are difficult to form, as there is a need of more prospective studies. As ileus may be a problem in patients with greater severity of pancreatitis, limiting the application of early enteral feeding, the route of nutritional support should be determined by the clinical course and the severity of the disease.
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PMID:[Enteral nutrition in acute pancreatitis]. 1122 88


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