Acute pancreatitis in coxsackie B infection.

Ursing, Bo

doi:10.1136/bmj.3.5879.524

Cited by 61 publications

(19 citation statements)

References 7 publications

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“…The viruses most frequently thought to be responsible are mumps virus (Feldstein et al, 1974;Naficy et al, 1973), Coxsackie B virus (Capner et al, 1975;Ursing, 1973;Tsui et al, 1972), Epstein-Barr virus (Wislocki, 1968), and measles virus (Bunnel & Monif, 1972). An association between viral hepatitis and acute pancreatitis has also been observed, although most of the patients concerned had fulminating hepatitis and the causal agent has been identified in only a very few patients (Archod, 1968;Parbhoo et al, 1973;Wands et al, 1973).…”

Section: Introductionmentioning

confidence: 99%

Acute pancreatitis in hepatitis A infection

Morante

Lope

Miguel

et al. 1986

Postgraduate Medical Journal

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Section: Introductionmentioning

confidence: 99%

Acute pancreatitis in hepatitis A infection

Morante

Lope

Miguel

et al. 1986

Postgraduate Medical Journal

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“…Coxsackie B viruses have been reported to cause acute pancreatitis (Kibrick and Benirschke, 1958;Fechner et al, 1963;Murphy and Simmul, 1964;Ursing, 1973) and, in an outbreak of Coxsackie B5 induced aseptic meningitis in children, a positive result was obtained in 31 % of those screened for raised amylase in blood and/or urine (Nakao et al, 1964). In addition, it has clearly been shown that Coxsackie B virus infections in animals cause acute pancreatitis (Pappenheimer et al, 1951;Burch et al, 1971;Tsui et al, 1972;Ross et al, 1974).…”

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Coxsackie and mumpsvirus infection in a prospective study of acute pancreatitis.

Imrie¹,

Ferguson²,

Sommerville³

1977

Gut

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SUMMARY 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).Recent prospective studies of acute pancreatitis (Ranson et al., 1974;Imrie and Whyte, 1975) have indicated that the group of patients considered to have 'idiopathic' acute pancreatitis represent no more than 12% of the total cases. The two common aetiological factors associated with acute pancreatitis in over 75 % of patients are biliary disease and excess alcohol ingestion (Ranson et al., 1974;Howes et al., 1975;Imrie and Whyte, 1975). Hyperlipoproteinaemia, hyperparathyroidism, steroids, hypothermia, and pancreatic neoplasm are aetiological factors in a small percentage of cases.

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“…The CVB have been associated with diverse human diseases, among the more serious of which are myocarditis, pancreatitis, and aseptic meningitis. The CVB have been soundly implicated as causes of human myocarditis (1, 26, 42, 60-62, 73, 74, 108, 109) and pancreatitis (2,41,54,58,66,107) and, furthermore, cause these diseases readily in mice (9,40,43,85,86,105). Although CVB have been suggested as infectious triggers of human insulin-dependent (type 1) diabetes mellitus (T1D) (7,22,34,53,116), there is no consensus as to the etiologic role for CVB in T1D development (25,32,33,47,52,63,64,110).…”

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Toward Testing the Hypothesis that Group B Coxsackieviruses (CVB) Trigger Insulin-Dependent Diabetes: Inoculating Nonobese Diabetic Mice with CVB Markedly Lowers Diabetes Incidence

Tracy

Drescher

Chapman

et al. 2002

J Virol

147

164

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Insulin-dependent (type 1) diabetes mellitus (T1D) onset is mediated by individual human genetics as well as undefined environmental influences such as viral infections. The group B coxsackieviruses (CVB) are commonly named as putative T1D-inducing agents. We studied CVB replication in nonobese diabetic (NOD) mice to assess how infection by diverse CVB strains affected T1D incidence in a model of human T1D. Inoculation of 4-or 8-week-old NOD mice with any of nine different CVB strains significantly reduced the incidence of T1D by 2-to 10-fold over a 10-month period relative to T1D incidences in mock-infected control mice. Greater protection was conferred by more-pathogenic CVB strains relative to less-virulent or avirulent strains. Two CVB3 strains were employed to further explore the relationship of CVB virulence phenotypes to T1D onset and incidence: a pathogenic strain (CVB3/M) and a nonvirulent strain (CVB3/GA). CVB3/M replicated to four-to fivefold-higher titers than CVB3/GA in the pancreas and induced widespread pancreatitis, whereas CVB3/GA induced no pancreatitis. Apoptotic nuclei were detected by TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay in CVB3/M-infected pancreata but not in CVB3/GA-infected pancreata. In situ hybridization detected CVB3 RNA in acinar tissue but not in pancreatic islets. Although islets demonstrated inflammatory infiltrates in CVB3-protected mice, insulin remained detectable by immunohistochemistry in these islets but not in those from diabetic mice. Enzyme-linked immunosorbent assay-based examination of murine sera for immunoglobulin G1 (IgG1) and IgG2a immunoreactivity against diabetic autoantigens insulin and HSP60 revealed no statistically significant relationship between CVB3-protected mice or diabetic mice and specific autoimmunity. However, when pooled sera from CVB3/M-protected mice were used to probe a Western blot of pancreatic proteins, numerous proteins were detected, whereas only one band was detected by sera from CVB3/GA-protected mice. No proteins were detected by sera from diabetic or normal mice. Cumulatively, these data do not support the hypothesis that CVB are causative agents of T1D. To the contrary, CVB infections provide significant protection from T1D onset in NOD mice. Possible mechanisms by which this virus-induced protection may occur are discussed.The group B coxsackieviruses (CVB; family Picornaviridae, genus Enterovirus, species group B coxsackievirus; six serotypes, CVB1 to -6) are among the best studied of human enteroviruses (102). The CVB genome is a single strand of positive sense RNA 7,400 nucleotides in length that encodes 11 proteins in a single open reading frame (89). The CVB have been associated with diverse human diseases, among the more serious of which are myocarditis, pancreatitis, and aseptic meningitis. The CVB have been soundly implicated as causes of human myocarditis (1, 26, 42, 60-62, 73, 74, 108, 109) and pancreatitis (2,41,54,58,66,107) and, furthermore, cause these diseases readily i...

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Acute pancreatitis in coxsackie B infection.

Cited by 61 publications

References 7 publications

Acute pancreatitis in hepatitis A infection

Acute pancreatitis in hepatitis A infection

Coxsackie and mumpsvirus infection in a prospective study of acute pancreatitis.

Toward Testing the Hypothesis that Group B Coxsackieviruses (CVB) Trigger Insulin-Dependent Diabetes: Inoculating Nonobese Diabetic Mice with CVB Markedly Lowers Diabetes Incidence

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