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)

Lesions of the pancreas induced by viral infection have drawn relatively little attention because of their low incidence, and the histopathologic features of viral pancreatitis have not been fully elucidated. We report the autopsy findings of 2 patients, a 59-year-old woman with allergic granulomatous angiitis and a 73-year-old man with invasive pulmonary aspergillosis who had a disseminated visceral herpes simplex virus (HSV) infection. In both cases, the liver was the organ most severely affected by the viral infection. The pancreas showed multiple small foci of hemorrhagic necrosis, which were not accompanied by fat necrosis of the surrounding adipose tissue. Histopathologically, Cowdry type A intranuclear inclusions and a ground-glass appearance of the nuclei were found in many degenerated acinar cells around the necrotic foci. The gross appearance and histopathologic features of HSV pancreatitis were characteristic and, in particular, distinct from those of the more common acute hemorrhagic pancreatitis. Immunohistochemistry using an anti-HSV antibody revealed immunoreactivity in the intranuclear inclusions and ground-glass nuclei, and polymerase chain reaction analysis disclosed that the causative virus in these 2 cases was HSV-1. Herpes simplex virus pancreatitis constitutes a rare, but distinct pathologic entity among a group of acute pancreatitis diseases with diverse etiopathogenesis.
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PMID:Herpes simplex pancreatitis. 1256 43

Acute pancreatitis following renal transplantation is an unusual complication that carries a high mortality. Over the last 10 yr, five of 185 patients at our center developed acute pancreatitis. All had live related donors and were on conventional triple drug immunosuppression. Pancreatitis was classified according to the computed tomography scan based on Atlanta Classification. All five patients who developed acute pancreatitis had evidence of symptomatic or serologically active viral infection (chicken pox in two, cytomegalovirus infection in two, hepatitis E virus in one) and no patient without viral infection developed pancreatitis. Overall, 45 patients developed symptomatic or serologically active viral infection. There was a significant association between viral infection and pancreatitis (chi-square test, p < 0.001). Three patients with severe acute pancreatitis died while both patients with mild pancreatitis survived. An active search for viral infections should be made in all patients with acute pancreatitis. Specific antiviral measures may help reduce the mortality of acute pancreatitis in these patients. Consideration must be given to varicella immunization in patients with renal failure.
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PMID:Acute pancreatitis following kidney transplantation - role of viral infections. 1258 19

Association of drug-induced hypersensitivity syndrome with viral infection is debated. Human herpesvirus 6 (HHV-6) reactivation has been the most frequently reported infection associated with this syndrome. However, a case of cytomegalovirus (CMV) infection was recently described associated with anticonvulsant-induced hypersensitivity syndrome. We report a case of severe allopurinol-induced hypersensitivity syndrome with pancreatitis associated with Epstein-Barr virus (EBV) infection. Active EBV infection was demonstrated in two consecutive serum samples by the presence of anti-EBV early antigen (EA) IgM antibodies and an increase in anti-EBV EA IgG antibodies, whereas no anti-EBV nuclear antigen IgG antibodies were detected. EBV DNA was detected by polymerase chain reaction (PCR) in peripheral blood mononuclear cells. Reactivation of HHV-6 was suggested only by the presence of anti-HHV-6 IgM antibodies, but HHV-6 DNA was not detected by PCR in the serum. Other viral investigations showed previous infection (CMV, rubella, measles, parvovirus B19), immunization after vaccination (hepatitis B virus), or absence of previous infection (hepatitis C virus, human immunodeficiency virus). We suggest that EBV infection may participate in some cases, as do the other herpesviruses HHV-6 or CMV, in the development of drug-induced hypersensitivity syndrome.
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PMID:Drug-induced hypersensitivity syndrome associated with Epstein-Barr virus infection. 1278 38

Pancreatitis is clearly associated with alcohol abuse, but only a relatively small percentage of people who abuse alcohol develops obvious pancreatitis. These observations have led to the concept that the development of alcoholic pancreatitis requires cofactors. Although diet and smoking have been studied, a clear cofactor has not been identified. The study results presented in this paper were obtained to determine whether viral infection of the pancreas would be a cofactor for alcoholic pancreatitis similar to the role of hepatitis virus infections in the development of alcoholic liver disease. To test this hypothesis, mice were fed ethanol with a liquid diet protocol and infected with coxsackievirus B3 (CVB3). It was found that consumption of alcohol alone did not result in pancreatitis as determined by serum levels of amylase or histologic changes in the pancreas. Two strains of CVB3 that are tropic for the pancreas were used; a virulent and an avirulent strain. Infection of alcohol-fed animals with the virulent CVB3 strain 28 resulted in a more severe pancreatitis than the pancreatitis noted in control animals. Alcohol-fed mice infected with the avirulent strain (GA) showed severe pancreatitis, whereas the infection of control mice did not result in obvious pathologic effects in the pancreas. This model allows mechanistic studies to define the role of viral infection as a cofactor for alcoholic pancreatitis.
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PMID:Animal model of alcoholic pancreatitis: role of viral infections. 1457 91

Dengue fever is an acute febrile viral disease, which frequently presents with high fever, headache, bone pain and skin rash. Acute pancreatitis and seizure are rare manifestations of dengue virus infection. A 66-year-old woman with diabetes mellitus presented with epigastralgia, nausea, vomiting, diarrhea and fever. Acute pancreatitis, abnormal liver function and thrombocytopenia were diagnosed at a local hospital. After persistent fever, thrombocytopenia and seizure developed she was transferred to our medical center. Dengue virus infection was confirmed by serology study and dengue hemorrhagic fever grade II was diagnosed. No further neurological symptoms occurred and pancreatitis improved gradually after supportive care. She recovered and had no sequelae at 1 year follow-up. Acute pancreatitis and seizure may be manifestations of dengue virus infection, especially in patients with delayed diagnosis, prolonged fever and thrombocytopenia.
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PMID:Dengue hemorrhagic fever complicated with acute pancreatitis and seizure. 1554 56

The 8th Meeting of the Alcohol and Immunology Research Interest Group (AIRIG) was held at Loyola University Medical Center, Maywood, Illinois, USA, on November 21, 2003. Reports from multiple laboratories reveal that the functional integrity of the immune system is of paramount importance to the survival of the individual after infection or injury. Evidence supports the idea that exposure to alcohol causes dysregulation of both the innate and the adaptive arms of the immune system. Gaining a better understanding of how alcohol interferes with normal inflammatory and immunoregulatory processes will aid researchers in the design of therapeutic interventions that can be used to improve these responses to better fight infection and maintain the health of the individual. At this meeting, nine speakers presented a summary of their recent work on the combined effects of ethanol and injury, infection, or inflammatory challenge. Topics were (1) T-cell activation after chronic ethanol ingestion in mice, (2) effect of ethanol consumption on the severity of acute viral-mediated pancreatitis, (3) ethanol and alveolar macrophage dysfunction, (4) impaired intestinal immunity and barrier function: a cause for enhanced bacterial translocation in alcohol intoxication and burn injury, (5) immune consequences of the combined insult of acute ethanol exposure and burn injury, (6) consequences of alcohol-induced dysregulation of immediate hemodynamic and inflammatory responses to trauma/hemorrhage, (7) regulation of tumor necrosis factor-alpha production by Kupffer cells after chronic exposure to ethanol, (8) acute exposure to ethanol and suppression of cytokine responses induced through Toll-like receptors, and (9) inhibition of antigen-presenting cell functions by alcohol: implications for hepatitis C virus infection. We anticipate that the work presented at the 8th Meeting of AIRIG, summarized in this article, and presented in the nine articles to follow in this Special Issue of Alcohol will stimulate ideas that will develop into research projects in these topical areas.
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PMID:Alcohol and immunology: introduction to and summary of the 2003 Alcohol and Immunology Research Interest Group (AIRIG) meeting. 1559 84

Alcohol abuse is often associated with acute pancreatitis. The pathogenesis of alcoholic pancreatitis remains poorly understood, in part because of the lack of a suitable animal model to study the mechanism or mechanisms of this disease. It has been proposed that ethanol predisposes or sensitizes the pancreas to the effects of co-factors, and the combination of the effects of ethanol on the pancreas and the actions of these co-factors results in alcoholic pancreatitis. A number of viruses are known to infect the pancreas, and we have suggested that one co-factor that could be involved in the development of alcoholic pancreatitis is a viral infection. One of the most-studied groups of viruses that infect the pancreas and cause pancreatitis in human beings is the coxsackieviruses. We have shown that short-term (5-14 days) and subchronic (>28 days) administration of ethanol to mice increases the severity of coxsackie B3-induced pancreas damage. We hypothesize that consumption of ethanol would result in an impairment of pancreas regeneration after injury, similar to the effect of ethanol on liver regeneration. With the use of the murine model of coxsackie B3-mediated alcoholic pancreatitis we have obtained preliminary data to support the hypothesis. Specifically, consumption of ethanol by mice is associated with changes in the replication of acinar cells and their organization into acini after viral-mediated injury. We believe that this model will be a valuable tool to study the biochemical and molecular mechanisms involved in alcoholic pancreatitis.
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PMID:Ethanol consumption potentiates viral pancreatitis and may inhibit pancreas regeneration: preliminary findings. 1559 86

We previously reported that soluble decay-accelerating factor (DAF) and coxsackievirus-adenovirus receptor (CAR) blocked coxsackievirus B3 (CVB3) myocarditis in mice, but only soluble CAR blocked CVB3-mediated pancreatitis. Here, we report that the in vitro mechanisms of viral inhibition by these soluble receptors also differ. Soluble DAF inhibited virus infection through the formation of reversible complexes with CVB3, while binding of soluble CAR to CVB induced the formation of altered (A) particles with a resultant irreversible loss of infectivity. A-particle formation was characterized by loss of VP4 from the virions and required incubation of CVB3-CAR complexes at 37 degrees C. Dimeric soluble DAF (DAF-Fc) was found to be 125-fold-more effective at inhibiting CVB3 than monomeric DAF, which corresponded to a 100-fold increase in binding affinity as determined by surface plasmon resonance analysis. Soluble CAR and soluble dimeric CAR (CAR-Fc) bound to CVB3 with 5,000- and 10,000-fold-higher affinities than the equivalent forms of DAF. While DAF-Fc was 125-fold-more effective at inhibiting virus than monomeric DAF, complement regulation by DAF-Fc was decreased 4 fold. Therefore, while the virus binding was a cooperative event, complement regulation was hindered by the molecular orientation of DAF-Fc, indicating that the regions responsible for complement regulation and virus binding do not completely overlap. Relative contributions of CVB binding affinity, receptor binding footprint on the virus capsid, and induction of capsid conformation alterations for the ability of cellular DAF and CAR to act as receptors are discussed.
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PMID:Inhibition of coxsackie B virus infection by soluble forms of its receptors: binding affinities, altered particle formation, and competition with cellular receptors. 1614 Jul 77

Highly pathogenic avian influenza (HPAI) is an extremely infectious, systemic viral disease of birds that produces high mortality and morbidity. HPAI was diagnosed in the three dead magpies (Pica pica sericea) submitted to the National Veterinary Research and Quarantine Service. At necropsy, the prominent lesions were multifocal or coalescing necrosis of the pancreas with enlargement of the livers and spleens. Microscopically, there were severely necrotizing pancreatitis and lymphocytic meningoencephalitis. Influenza viral antigen was also detected in areas closely associated with histologic lesions. Avian influenza virus was isolated from cecal tonsils and feces of the magpies. The isolated virus was identified as a highly pathogenic H5N1, with hemagglutinin proteolytic cleavage site deduced amino acid sequence of QREKRKKR/GLFGAIAG. To determine the pathogenicity of the isolate, eight 6-wk-old specific-pathogen-free chickens were inoculated intravenously with the virus, and all birds died within 24 hr after inoculation. This is the first report of HPAI in magpies.
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PMID:Highly pathogenic avian influenza in magpies (Pica pica sericea) in South Korea. 1624 75

In this case report, a young woman with gallbladder sludge and acute pancreatitis due to acute hepatitis A (HAV) is presented. She was admitted to our hospital with abnormal hepatic enzymes. Five days prior to her admission, an initial abdominal ultrasound was performed at another hospital and revealed no abnormality, while her serum aspartate aminotransferase (AST) level was at the upper limit of normal (ULN) x 8. A second ultrasound was performed at our hospital and revealed a gallbladder wall thickness (9.3 mm), gallbladder sludge in the gallbladder lumen, pancreatic edema, ascites, and hepatomegaly while AST was at the ULN x 50. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed imaging features of an acute stage of pancreatitis and gallbladder wall thickness with coexisting sludge in the gallbladder lumen. HAV infection was diagnosed by the detection of immunoglobulin M against HAV in the serum. The patient underwent two repeated abdominal ultrasound examinations on the 5th (AST was at the ULN x 3) and the 20th days (AST was at the normal) after her discharge, and both revealed normal findings. In our case, we observed reversible changes in the hepatobiliary and pancreatic system which was related to the severity of hepatic necro-inflammation. HAV-associated pancreatitis may be due to the formation of biliary sludge during the acute phase of the viral illness, but this association needs further investigation.
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PMID:Gallbladder sludge and acute pancreatitis induced by acute hepatitis A. 1790 17


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