Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review of the gastrointestinal (GI) and hepatic manifestations of systemic lupus erythematosus (SLE), 180 articles from the English literature, found using a medline search from January 1965 to December 2010, were examined. Vasculitis may cause ulcerations, bleeding, stricture formation, and perforation from ischemia and infarction. Otherwise, GI symptoms, occurring in about 50% of patients, are usually mild. Esophageal dysmotility may result in heartburn, regurgitation, and dysphagia. Occasionally, pneumatosis cystoides intestinalis may develop, sometimes associated with benign pneumoperitoneum. Patients are prone to salmonella bacteremia, presenting more commonly with fever and abdominal pain than with diarrhea. Intestinal pseudoobstruction usually is found with active lupus serology, preferentially involving small rather than the large bowel. Protein-losing enteropathy, characterized by diarrhea, edema, and hypoalbuminemia, can be the initial presentation of SLE. Malabsorption with a prevalence of 9.5% is occasionally associated with celiac disease. Pancreatitis, with an annual incidence of 0.4 to 1/1000, has an overall mortality of 27% that is decreased with corticosteroid therapy. Acute and chronic ascites may be due to lupus peritonitis or to associated diseases, such as pancreatitis, nephrotic syndrome, heart failure, or infections. Abnormal liver function tests may be due to steatosis from lupus or from corticosteroid therapy. Only about 10% of patients with autoimmune hepatitis have lupus. Up to 4.7% of patients with SLE have chronic active hepatitis correlating strongly with the presence of antibody to ribosomal P protein. SLE can involve the entire GI tract and the liver. Treatment with corticosteroids, cytotoxic agents, and/or immunosuppressants is often successful.
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PMID:Gastrointestinal and hepatic manifestations of systemic lupus erythematosus. 2142 47

During the past norovirus (NoV) epidemic season, a new GII.17 variant emerged as a predominant NoV strain, surpassed the GII.4 NoVs, causing outbreaks of acute gastroenteritis (AGE) in China. Here we report a study of an AGE outbreak in an elementary school in December 2014 caused by the new GII.17 NoV to explore the potential mechanism behind the sudden epidemics of the GII.17 NoV. A total of 276 individuals were sick with typical NoV infection symptoms of vomiting (93.4%), abdominal pain (90.4%), nausea (60.0%), and diarrhea (10.4%) at an attack rate of 5.7-16.9%. Genotyping of the symptomatic patients showed that individuals with a secretor positive status, including those with A, B, and O secretors and Lewis positive blood types, were sensitive to the virus, while the non-secretors and the Lewis negative individual were not. Accordingly, the recombinant capsid P protein of the GII.17 isolate showed a wide binding spectrum to saliva samples of all A, B, and O secretors. Thus, the broad binding spectrum of the new GII.17 variant could explain its widely spread nature in China and surrounding areas in the past two years.
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PMID:An outbreak caused by GII.17 norovirus with a wide spectrum of HBGA-associated susceptibility. 2663 56