Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tests for both hepatitis B surface antigen (HBsAg) and hepatitis e antigen (HBeAg) were carried out on wild-caught and laboratory-colonized bedbugs (Cimex lectularius L.), the latter after hepatitis B virus (HBV)-positive blood-meals. Positivity for both antigens was interpreted as an indication of HBV infectivity. Of 22 pools in which were tested 211 bugs collected in the northern Transvaal, 18 were HBsAg-positive and 17 HBeAg-positive, with estimated infection rates of 156,7 and 137,7 per 1000 bugs respectively. Passage of HBV in bugs, allowing an extrinsic incubation period of 57-69 days, resulted in 19 out of 25 bugs being positive for HBsAg after the first passage; only a small number of these were positive for HBeAg. After the second passage all bugs tested were HBsAg-negative, showing that the virus had disappeared. Tests on the salivary glands and carcass of each bug at intervals up to 31 days after an infective meal showed a positivity rate of 98% (HBsAg) and 17% (HBeAg) for carcasses and 20% (HBsAg) and 0% (HBeAg) for salivary glands. Attempts to detect HBV particles in the salivary glands by electron microscopy failed. Bugs were shown to continue to excrete HBsAg in their faeces up to the 42nd day, and both HBsAg and HBeAg together up to the 30th day. HBsAg particles were only detected by electron microscopy in faeces harvested on the 10th day. The results as a whole indicate that no biological multiplication of virus occurs in C. lectularius but that mechanical transmission from insects to man could occur by: (i) contamination of a person when crushing infective bugs; (ii) contamination from infected faeces; and (iii) infection by bite due to regurgitation or interrupted feeding.
 ...
PMID:The mechanical transmission of hepatitis B virus by the common bedbug (Cimex lectularius L.) in South Africa. 684 70

Drug-induced cholestasis may be due to impairment of hepatocellular bile secretion (pure cholestasis or cholestatic hepatitis), obstruction of ductules (cholangiolitis) or interlobular ducts (cholangitis), or extrahepatic obstruction (sclerosing cholangitis). Mechanisms of hepatocellular cholestasis are multiple and include inhibition of various transport systems, cytoskeleton poisoning, disturbed intracellular calcium homeostasis and increased permeability with regurgitation of bile constituents into plasma. Pure hepatocellular cholestasis is mostly observed with sex steroid hormones and anabolic steroids. Ductular or ductal cholestasis (drug-induced cholangiopathy) may be acute and self-limited, or prolonged with ductopenia, occasionally leading to biliary cirrhosis. An immune mechanism has been proposed. Sclerosing cholangitis with strictures near the confluent of hepatic ducts is observed after intraarterial administration of floxuridine for chemotherapy of hepatic metastases. Some drugs may induce the formation of cholesterol gallstones, or precipitate in bile and form biliary sludge or stones in the gallbladder or common bile duct.
 ...
PMID:Drug-induced cholestasis. 913 22

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.
 ...
PMID:Gastrointestinal and hepatic manifestations of systemic lupus erythematosus. 2142 47

Introduction. Fluid-attenuated inversion recovery hyperintense vessels (FHVs) can be seen in patients with occlusion or severe stenosis of the cerebral arteries. FHVs are known to reflect stagnant or slow blood flow within the cerebral artery. Case Report. A 75-year-old woman presented with suddenly developed gait disturbance. She had a history of hypertension, heart failure, and dementia. Brain MRI demonstrated FHVs within both middle cerebral arteries (MCAs). However, there was no acute ischemic lesion and severe stenosis or occlusion of the cerebral arteries. In the baseline routine laboratory investigations, the AST, ALT, and B-type natriuretic peptide levels were elevated. Transthoracic echocardiography (TTE) showed mitral valve prolapse with severe regurgitation. Blood pressure control and conservative management for ischemic hepatitis were performed. After 7 days, the transaminase levels were normalized, and the patient was able to walk with normal gait. Conclusions. In this patient, underlying chronic cerebral hypoperfusion and additionally decreased systemic perfusion seemed to provoke ischemic hepatitis and contribute to the development of FHVs.
...
PMID:FLAIR Hyperintense Vessel Sign of Both MCAs with Severe Heart Failure. 2764 20