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

Mengo virus has been described to cause, in dependence on the virus dose, lethal panencephalomyelitis and exocrine pancreatitis in mice after i.p. inoculation. Two immunosuppressive agents, cyclophosphamide and 1,3-bis(piperidinomethyl)-5-ethyl-5-phenyl-barbituric acid (ZIMET 176/68), were shown to potentiate Mengo virus infection as demonstrated by histopathology and enhanced mortality. Organotropism of Mengo virus did not change under the drug treatment. However, the histological lesions in brain, spinal cord and pancreas failed to exhibit any inflammatory reaction in case of cyclophosphamide, due to its antiphlogistic properties. Considering the mode of action of the drugs employed and the pathogenesis of Mengo virus infection in mice, it is concluded that in the system used both cyclophosphamide and ZIMET 176/68 exert their potentiating effects by interfering with primary virus-macrophage interaction.
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PMID:Pathogenicity of Mengo virus to mice. III. Potentiation of infection by immunosuppressants. 22 63

A prospective study of 116 patients with acute pancreatitis included routine screening for evidence of viral infection. Five patients (all female) exhibited significant rising antibody titres to Coxsackie B or mumpsvirus, while none of the remaining 111 patients did. Diarrhoea was a prodromal feature of the pancreatitis in those patients with evidence of viral disease. Screening patients with acute pancreatitis for Coxsackie B and mumpsvirus infections is worthwhile in the identification of aetiological factors and may minimise protracted biliary investigations. The incidence of "idiopathic" acute pancreatitis in this study was 5-2% (six patients).
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PMID:Coxsackie and mumpsvirus infection in a prospective study of acute pancreatitis. 83 3

Four renal allograft recipients with evidence of ischemic damage to the colon are presented and compared with 11 cases from 5 major series. Similarities in the patients included: deterioration of renal function, multiple immunosuppressive and antibiotic regimens, the use of cadaver renal allografts, and diagnostic and therapeutic measures requiring frequent enemas with barium and ion-exchange resins. Two of our patients underwent surgery for the removal of segments of necrotic colon after several weeks of fever and abdominal pain initially attributed to either acute rejection, viral infection, or pancreatitis. One patient had three days of melena and responded to non-operative therapy. The fourth patient developed ischemic colonic changes 10 weeks after allograft nephrectomy and was receiving no immunosuppression at the time. Broad spectrum antibiotics were used at various times in all patients. Early aggressive evaluation of gastrointestinal complaints--including barium enema, upper gastrointestinal series with small bowel follow-through, proctosigmoidoscopy or colonoscopy, and arteriography--is indicated, in view of the lethality of the complication of colonic ulceration. The clinical pictures presented emphasize the fact that recipients of renal allografts are commonly heir to many complications which may be considered rare in the normal population.
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PMID:Acute colitis in the renal allograft recipient. 110 14

Viral studies were performed on sera from 54 patients with recent acute pancreatitis, 10 with recurrent acute pancreatitis, seven with chronic pancreatitis, and 10 with pancreatic carcinoma, and on sera from 81 age- and sex-matched controls. In 29 of the acute pancreatitis patients from whom paired sera were obtained no convincing evidence of recent viral infection was found. A higher incidence of raised antibody titres against Coxsackie B3 and B4 was observed in the group of acute pancreatitis patients compared with their controls. The possible signficance of these observations and their relationship to the aetiology of the pancreatitis and to other immunological findings are discussed.
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PMID:Viral antibody studies in pancreatic disease. 119 16

A male infant and a three year old girl, both with acute febrile illness, were admitted to our hospital for suspected meningitis/sepsis and gastroenteritis/severe viral infection, respectively. Both showed all six principal features of Kawasaki syndrome and revealed several other symptoms and laboratory findings commonly associated with the disease. The infant had multiple coronary aneurysms. The girl developed ascites, pancreatitis and iritis, all of which are seldomly recognized symptoms of the Kawasaki syndrome. The prompt and satisfactory therapeutic responses of both patients to the combined therapy consisting of oral acetylsalicylic acid (50-100 mg/kg b.w./d) and intravenous gamma-globuline (400 mg/kg b.w./d) at the eight and even eleventh day of illness support the use of gamma-globuline therapy beyond the first week of the disease. Prior to their illnesses both children had been exposed to carpet shampoo, an agent which has been repeatedly associated with an increased risk of Kawasaki syndrome.
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PMID:[Kawasaki syndrome. Association with exposure to carpet shampoo and successful therapy with immunoglobulins in the second week of the illness]. 161 54

We report here three recipients of allogeneic bone marrow transplantation in whom visceral varicella-zoster virus infection preceded cutaneous dissemination producing life-threatening complications including hepatitis, pancreatitis and haemorrhage.
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PMID:Abdominal presentation of varicella-zoster infection in recipients of allogeneic bone marrow transplantation. 151 Dec 59

A 33-year-old man, vaccinated against hepatitis B virus, working in an hemodialysis unit, pricked himself with a needle used in a patient. Four weeks later he developed acute hepatitis along with acute pancreatitis. The pancreatitis resolved, but the liver disease ran a chronic course. The diagnosis of hepatitis non-A-non-B (NANB) was made on the following criteria: (a) epidemiologic circumstances, (b) exclusion of other causes of acute and/or chronic liver disease, (c) chronic indolent course, and (d) compatible histological features. The diagnosis of acute pancreatitis was made with clinical, biological, and radiological data. We believe that the pancreatitis was related to the NANB viral infection, as they began simultaneously and other causes of pancreatitis were eliminated. Such an association has been reported mainly with hepatitis B and exceptionally with hepatitis A. It has also been observed in the course of fulminant NANB viral hepatitis, but we believe this to be the first case associated with a benign form of NANB.
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PMID:Acute pancreatitis associated with non-A-non-B hepatitis. Report of a case. 210 6

Since 1981, when the liver transplantation program was initiated at the University of Pittsburgh, we have been impressed with the prevalence of pancreatitis occurring following liver transplantation in patients transplanted for hepatitis B-related liver disease. To either confirm this clinical impression or refute it, the records of the 27 HbsAg+ patients and those of an additional 24 HbsAg- but HbcAb and/or HbsAb+ patients who underwent orthotopic liver transplantation were reviewed to determine the prevalence of clinical pancreatitis and hyperamylasemia (biochemical pancreatitis) following liver transplantation (OLTx). Post-OLTx hyperamylasemia occurred significantly more frequently in HbsAg+ patients (6/27) than it did in the HbsAg- patients (0/24) (P less than 0.05). More importantly, clinical pancreatitis occurred in 14% (4/27) of the HbsAg+ patients and 0% (0/24) of the HbsAg- patients. Interestingly, in each case, the pancreatitis was associated with the occurrence of acute hepatitis B infection of the allograft. Based upon these data, we conclude that pancreatitis occurring after liver transplantation is more common in patients transplanted for active viral liver disease caused by hepatitis B than in those with inactive viral liver disease. These observations suggest that pancreatitis occurring in, at least some cases following liver transplantation for viral liver disease, may result from hepatitis B virus infection of the pancreas.
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PMID:Pancreatitis following liver transplantation. 245 20

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

Of 37 pancreases removed at necropsy from patients with type 1 diabetes 34 had residual beta cells. In 33 of the 34 the beta cells were positive for immunoreactive alpha-interferon, and this finding in islets was related to hyperexpression of class I major histocompatibility complex (MHC) antigens. Of islets showing class I hyperexpression 93% contained alpha-interferon compared with 0.4% of those showing no hyperexpression. Among 80 control pancreases significant numbers of beta cells containing alpha-interferon were present only in 4 cases of acute infantile viral pancreatitis, known to be caused by Coxsackie-B viral infection in 3 cases. Chronic viral infection of beta cells may underlie the pathogenesis of some cases of type 1 diabetes.
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PMID:Immunoreactive alpha-interferon in insulin-secreting beta cells in type 1 diabetes mellitus. 289 93


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