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

Among the rarer causes of acute pancreatitis listed in surgical texts is hypothermia. To assess the evidence for cause and effect, we questioned selected consultants about their experience and examined the case-notes of patients admitted with hypothermia. The 31 consultants who returned our questionnaire (69% response rate; 317 consultant-years' experience) could recall only 5 cases of pancreatitis associated with hypothermia, in 2 of which other aetiological factors were judged primary. In case-notes for 100 months of emergency admissions at a single hospital we identified 310 patients with hypothermia and 1153 with acute pancreatitis; none had the dual diagnosis. Of the hypothermic patients, none had abdominal pain typical of acute pancreatitis. In 43 serum amylase was measured because the patient was unable to give a full history and in 2 of these the enzyme was slightly raised; both had experienced a cerebrovascular accident, which is a known cause of hyperamylasaemia. Considered alongside the weak evidence from previous studies, these findings offer negligible support for the idea that hypothermia is a clinically relevant risk factor for acute pancreatitis.
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PMID:Hypothermia and acute pancreatitis: myth or reality? 1272 32

The aim of this study was to evaluate whether corticosteroid use is the etiological agent in acute pancreatitis in patients with systemic lupus erythematosus, or whether it is related to the underlying connective tissue disorder. Hospital admissions at Thomas Jefferson University Hospital between 1982 and 2002 that carried the dual diagnosis of systemic lupus erythematosus and pancreatitis were identified, and demographic data, clinical interventions and parameters of clinical progression of their disease were identified. From 2947 admissions with systemic lupus erythematosus 25 (0.85%) were diagnosed as having acute pancreatitis; 76% of cases had active systemic lupus erythematosus on presentation, with an average of 4.4 organ involvement, and a clustering of renal disease (56%), pleural effusion (48%) and arthritis (44%) in these patients. Fifteen patients with active disease and three whose disease was inactive received increased doses of corticosteroids, and four active cases and one inactive one stayed on the same doses. Two inactive patients received no corticosteroids before or after the diagnosis of pancreatitis. Eighty-two percent of patients had clinical and laboratory improvement on the higher or maintenance dose of corticosteroids. We therefore concluded that acute pancreatitis is a rare manifestation of systemic lupus erythematosus, and corticosteroids do not appear to be the etiological agent.
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PMID:Systemic lupus erythematosus and acute pancreatitis: a case series. 1504 30

Coxsackieviruses (CV) are important human pathogens that have been implicated in the pathogenesis of several diseases, including myocarditis and pancreatitis. How the human immune system recognizes and controls CV infections is not well understood. Studies in mice suggest that natural killer (NK) cells play a critical role in viral clearance and host survival, but the mechanism(s) by which human NK cells may contribute to the host anti-CV defence has not been investigated. Here we show that CVB3 infection markedly reduces HLA class I cell surface expression but does not increase the expression of the activating NK cell receptor ligands MICA/B and ULBP1-3 on human cells. We also demonstrate that the lowered target cell HLA class I surface expression does not correlate with an increased susceptibility to NK cell-mediated killing. However, NK cells responded with a robust production of interferon gamma (IFN-gamma) when peripheral blood mononuclear cells were cocultured with infected cells. In summary, this study shows that CVB3 interferes with the expression of NK cell receptor ligands on infected cells and indicates that IFN-gamma production, rather than cytotoxicity, marks the early human NK cell response to CVB3 infection.
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PMID:IFN-gamma production dominates the early human natural killer cell response to Coxsackievirus infection. 1796 Nov 84