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

Coxsackie B viruses are known etiological agents of pancreatic diseases, including diabetes. The pathogenesis of these infections is influenced by both host and viral factors. In this report, we examined whether the outcome of Coxsackie B4 virus infection is dependent on the genes within the major histocompatibility complex (MHC). We generated a pancreatic variant, CB4-V and established an animal model system of pancreatitis with concurrent hypoglycemia in mice. Infection of various B10 H-2 congenic strains of mice revealed that the development of hypoglycemia with accompanying pancreatitis was independent of the MHC haplotype. However, the severity of the disease as monitored by the extent and duration of hypoglycemia and by mortality rate was found to be associated with the H-2 haplotype, specifically the H-2Kq locus. Pancreatic damage induced by CB4-V appeared to be both immune-mediated and viral-mediated. Histological examination of pancreatic tissue from infected B10 H-2 congenic mice revealed an association between acute destruction of the exocrine pancreas and lymphocytic infiltration. This infiltration may correlate with immune-mediated destruction of the infected pancreatic tissue. Since preferential replication of CB4-V was not observed in the most susceptible B10 mouse strain, direct viral destruction may not be the major mechanism of pancreatic injury.
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PMID:Severity of disease induced by a pancreatropic Coxsackie B4 virus correlates with the H-2Kq locus of the major histocompatibility complex. 256 Feb 95

Infection with 100 Opisthorchis viverrini (OP) metacercariae prior to two injections of dihydroxy-di-n-propyl nitrosamine (DHPN) (1000 mg/kg body weight) brought about significant enhancement of resultant preneoplastic lesion development in Syrian hamster liver and pancreas tissue. Thus combined treatment with carcinogen and parasite was associated with pancreatic atypical (dysplastic) foci, hepatocellular nodules, cholangiofibrosis and cholangiocarcinomas. No such lesions were observed in carcinogen alone, parasite alone or untreated control groups. In addition, parasite induced hyperplastic gall bladder epithelium was found to include areas of putative preneoplastic cells only in the DHPN-OP combined group. The results strongly suggest that pancreatitis and biliary cirrhosis associated with liver fluke infestation are responsible for the observed enhancement of carcinogenesis, and that the resultant increased proliferation plays a major role in tumorigenesis.
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PMID:Enhancement of DHPN induced hepatocellular, cholangiocellular and pancreatic carcinogenesis by Opisthorchis viverrini infestation in Syrian golden hamsters. 283 5

Thirty-seven clinical isolates of coxsackievirus (CV) serotypes B-1, B-3, B-4, and B-5 were inoculated into male SJL mice. Twelve strains resulted in minor abnormalities of glucose metabolism in one or more of six infected mice (Tables 1 and 2). Sequential infection of male SJL mice with CVB-3, CVB-4, and CVB-5 resulted in abnormal glucose metabolism in 25 percent of the mice (Fig. 1). The glucose index of the abnormal animals was similar to that produced by sequential infection with reovirus and cytomegalovirus but less than that seen with more severe beta cell tropic agents such as streptozotocin or encephalomyocarditis virus. Infection of autoimmune New Zealand (NZB X NZW) F1 male mice with CBV-3, CVB-4, and CVB-5 resulted in transient elevation of the blood glucose concentration associated with acute acinar pancreatitis (Fig. 2). In spite of recent evidence that infection with the coxsackie B viruses can result in human diabetes mellitus, the diabetogenic potential of CVB field strains appears to be limited. Diabetes mellitus may occur as a rare event, limited to genetically susceptible hosts. Autoimmune mechanisms or repeated infection with other CVB serotypes may convert minimal beta-cell destruction into clinically overt disease.
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PMID:Diabetogenic potential of coxsackie B viruses in nature. 299

The significance of megamitochondria in the alcoholic liver injury of humans was investigated as part of a large Veterans Administration cooperative study of the natural history of alcoholic hepatitis. Two hundred twenty patients were clinically stratified into the following three groups according to disease severity using serum bilirubin and prothrombin time as indicators: Group 1 (mild disease), serum bilirubin levels less than 5 mg/dl and prothrombin time prolonged for less than 4 s; group 2 (moderate disease), serum bilirubin levels greater than 5 mg/dl but prothrombin time prolonged for less than 4 s; and group 3 (severe disease), serum bilirubin levels greater than 5 mg/dl and prothrombin time prolonged for greater than 4 s. Megamitochondria were observed in 20% of the patients (45 of 220). Of these, 43 patients were in groups 1 and 2 of severity and only 1 patient belonged in group 3. The association of megamitochondria with cirrhosis was infrequent (33%, 15 of 45 patients). The differences in severity correlated with the differences in mortality: in patients with megamitochondria, only 1 had died at 6 mo compared with 40 deaths in patients without megamitochondria. By 12 mo, there were two deaths in patients with megamitochondria versus 51 deaths in those patients without. No complications were present in 72% of patients with megamitochondria versus 39% for those without. Infection, gastrointestinal bleeding, pancreatitis, hyperglycemia, azotemia, delirium tremens, seizures, and hepatic encephalopathy were all more common in patients without megamitochondria. The patients with megamitochondria appear to represent a subcategory of alcoholic hepatitis with a milder degree of clinical severity, lower incidence of cirrhosis, fewer complications, and good long-term survival.
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PMID:Significance of megamitochondria in alcoholic liver disease. 369 4

Patients undergoing elective intraabdominal operations received a three-dose prophylactic regimen of either moxalactam (83 patients) or cefazolin (98 patients) in a blinded, randomized fashion. There was a 9% overall infection rate with 6% for those in the cefazolin group (6/98), and 12% for those treated with moxalactam (10/83) (p = 0.26). Infection rates stratified by types of surgery were similar for both regimens. The drugs were well tolerated, with minimal side effects. Patients at highest risk of infection were those with obstruction of upper gastrointestinal tract and those with pancreatitis. We concluded that moxalactam was no more effective than cefazolin in preventing postoperative infections in this study population.
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PMID:Comparison of the effectiveness of moxalactam and cefazolin in the prevention of infection in patients undergoing abdominal operations. 388 Dec 11

Infection of ABAF hybride mice with MengoM viruses prepared as a suspension of mouse brain tissue (0.1 ml 10 LD50) after a series of more than 90 animal passages produced a severe panencephalitis and pancreatitis 60 h after inoculation. Histological examinations of the brain, pancreas, and heart revealed damage to the central nervous system and the acinar cells of the pancreas, consisting of a degeneration of the specific cells and their organelles, with little involvement of the heart muscle cells detectable with the electron microscope. This was consistent with high virus titers in the tissues in the period immediately following infection. The acute damage of exocrine tissues was without evidence of diabetes-like changes in the islets of Langerhans.
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PMID:[Light and electron microscopic studies of the brain, heart and pancreas in mice infected with MengoM virus]. 609 76

Infection of guinea pigs with an attenuated strain of Junin virus (JV) produced 16% mortality between days 17 and 27 postinfection (p.i.). The morphological study showed a marked pancreatitis between days 6 and 23 p.i. and meningoencephalitis between days 17 and 20 p.i. in a large proportion of the animals. These lesions were coincident with the presence of JV antigenic determinants in the pancreatic acinar cells, neurons and blood vessels of the brain. Infectious virus could be isolated from lymph nodes, spleen, bone marrow, lungs, adrenal glands, and brain. The lesions appeared to be reversible, as they were absent in animals studied after day 64 p.i. Meningoencephalitis, present in all animals dying spontaneously, appeared to be the most important cause of death. Our observations indicate that more accurate markers of virulence must be investigated in the search for attenuated strains of JV as potential vaccine candidates for Argentine hemorrhagic fever.
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PMID:Pathogenicity of an attenuated strain (XJCl3) of Junin virus. Morphological and virological studies in experimentally infected guinea pigs. 631 4

Computed tomography (CT) gives unique information about the margins of the intra-abdominal organs and the intervening fat and fascial planes. Not infrequently, these planes appear abnormal without any visible underlying cause. We present 85 patients in whom such an abnormality was shown. Although the appearances are non-specific, tumour infiltration was the most common cause (57 (70%) out of 82 where the cause is known). Infection, secondary effects of pancreatitis, granulomatous disease, haemorrhage, early ascites or oedema and the effects of radiotherapy should all be considered in the differential diagnosis.
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PMID:Abnormal fat: a useful marker of intra-abdominal disease at computed tomography. 649 86

Thirty-two patients died of pancreatitis and its complications over a 10-year period. Infection (bacteremia, fungemia, or pancreatic abscess) was the major cause of death in 80%. In the remaining 20%, refractory hypotension or respiratory failure were the lethal mechanisms. In only 78% of patients was the correct diagnosis made before death. Ninety-four percent of those who died did so during their first clinical episode of pancreatitis. Prophylactic antibiotics did not prevent the development of pancreatic abscesses and organisms resistant to the antibiotics used often became the primary pathogens. Certain prognostic factors reliably separated those who died from those who lived. Peritoneal lavage and dialysis may be helpful in both the early diagnosis and therapy of severe acute pancreatitis.
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PMID:Lethal pancreatitis. 665 Apr 70

A 47-year-old woman with stones in the gall-bladder suddenly developed severe upper abdominal pain. Cholesterol concentration was elevated, as were amylase (555 U/l) and lipase (408 U/l) concentrations, suggesting biliary pancreatitis. Endoscopic retrograde cholangiography demonstrated a cyst, about 10 cm in diameter, in the left lobe of the liver, connected to the biliary tract system. Ultrasonography and computed tomography additionally showed a smaller cyst in the right lobe. Infection with Echinococcus granulosus was proven microbiologically on bile (demonstration of hooklets and protoscolices) as well as serologically. Transpapillary cholangioscopy demonstrated daughter cysts within the echinococcal cyst. The main cyst was rinsed with 20% NaCl for 10 days via a nasocystic catheter. In addition, mebendazole (three times daily 1000 mg) was administered for 13 months. The signs if inflammation receded and the cyst shrank to a small residual volume. Surgical intervention became unnecessary.
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PMID:[Acute pancreatitis due to the rupture of an echinococcal cyst into the bile duct system]. 751 77


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