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

The prognosis of juvenile rheumatoid arthritis (JRA) is generally good, although premature death occurs in a subset of children. Secondary infections, chronic amyloidosis, and heart disease have been reported as common causes. Our experience indicates that JRA can also herald the development of a severe immune enteropathy. In the case presented, typical JRA was followed by fulminant hepatitis; skin rashes; recurrent, severe, watery diarrhea; malabsorption; and ultimately death. Biopsies of the small bowel exposed to the patient's serum revealed deposition of complement and immunoglobulins in the epithelium. Although not widely appreciated, JRA can herald a multisystem syndrome characterized by severe immune enteropathy.
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PMID:Fatal multisystem disease with immune enteropathy heralded by juvenile rheumatoid arthritis. 270 56

Asymmetric affection of the major lower limb joints is a characteristic feature of the joint syndrome in yersiniosis-associated arthritis. The sacroiliac articulations are frequently (47% cases) involved. In addition, yersiniosis-associated arthritis concurs with the signs and symptoms of systemic disease--gastroenterocolitis, myocardiopathy and myocarditis, erythema nodosum, hepatitis, urethritis, conjunctivitis, myositis and myalgia, enteropathy; changes in the CNS typical for the astheno-neurotic syndrome are frequently present. Comparison of the immunological assay data in complicated and uncomplicated yersiniosis shows equally high levels of IgG and CIC. High anti-DNA antibody titres are more frequently found in the serum of uncomplicated yersiniosis patients. ELISA quantitation of specific IgA, IgM, and IgG class antibodies in yersiniosis-associated arthritis patients demonstrated persistence of all the three antibody classes or of IgA-IgG combination in cases with most severe of the joint syndrome. In the presence of cardiac disease, patients were found to have high titres of antibodies reactive with the cardiac interstitial tissue, while in authentically diagnosed myocarditis cases with the sarcolemma. The investigation findings strongly suggest a high degree of involvement of immune and autoimmune processes in the pathogenesis of arthritides secondary to Yersinia infection.
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PMID:[Clinico-immunologic characteristics of complicated and uncomplicated yersiniosis]. 277 63

A case of acute mucosal ulceration of the entire small intestine accompanied by skin rash, hepatitis and marrow suppression is reported. Recovery was complicated by a severe protein losing enteropathy and small intestinal strictures and the patient died post-operatively of a pulmonary embolism. The aetiology remains unknown.
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PMID:Ulceration of the entire small intestine accompanied by rash, hepatitis and pancytopenia. 278 Apr 52

78 previously untreated patients with acute non-lymphoblastic leukemia (ANLL) were assigned to cytosar-anthracyclines therapeutic programs: 29 (group I) received daunorubicin and AraC, 18 (group II) aclacinomycin A and AraC, 12 (group III) the scheme 3 + 7 with 12 mg/m2 novantron instead of daunorubicin, 19 (group IV) the scheme 3 + 7 with 12 mg/m2 idarubicin and cytosar. Groups I-III comprised both prognostically favorable and unfavorable ANLL variants, group 4 patients had for the most part unfavorable prognosis (MO-M3). A mean age of the patients was 41-42. Complete remissions were observed in 17 (58.6%), 9 (50%), 10 (83.3%), 11 (57.9%) patients of groups I, II, III and IV, respectively. An initial course of the treatment produced complete remissions in 65%, 33%, 80% and 90.9% of them, respectively. A mean duration of cytostatic leukothrombocytopenia was the longest in groups III and IV (16-22 days). Nonhematological toxicity occurred in the form of enteropathy and hepatitis. During the remission induction and consolidation 76% of the deaths were caused by infection and hemorrhagic diathesis. The median remission lasted 17.5, 13.5 and 5 months in groups I, II and III, respectively, and was not reached in group IV because of continuing remission in 50% of the patients by the end of the follow-up period (14 months). A 2-year survival rate was observed in 25% (group I), 11% (group II), 30% (group III) and 40% (group IV).
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PMID:[The comparative evaluation of the efficacy of different therapeutic plans in acute nonlymphocytic leukemias]. 821 72

Large bowel disease detected clinically by rectal prolapse was studied in 64 immunodeficient mice (37 athymic NCr-nu/nu, 12 BALB/c AnNCr-nu/nu, 9 C57BL/6NCr-nu/nu, and 6 C.B17/Icr-scid/NCr) naturally infected with Helicobacter hepaticus. Rectal prolapse was found in approximately 5% of immunodeficient mice maintained in a research facility over a period of 3.5 years. All mice had various degrees of chronic proliferative typhlitis, colitis, and proctitis, usually without concomitant hepatitis. Some mice had severe proliferative proctitis with cystic hyperplasia. Histologic study of the large bowel of 48 athymic NCr-nu/nu mice without H. hepaticus infection and housed in another clean facility revealed only 12% of the mice with minimal-to-mild large bowel inflammation. Helicobacter hepaticus infection is associated with large bowel disease in immunodeficient mice but is not seen in H. hepaticus-infected immunocompetent mice. This new pathogenic bacterial infection should be considered as another potential cause or co-factor for rectal prolapse and large bowel disease in mice.
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PMID:Inflammatory large bowel disease in immunodeficient mice naturally infected with Helicobacter hepaticus. 869 13

A 24-year-old male with Crohn's disease who developed three independent episodes of cholestatic liver disease over an eight-year period is described. The first episode was related to an idiosyncratic drug reaction while on sulfasalazine. The second episode, at the time of an exacerbation of his colitis, was characterized by moderate portal inflammation on liver biopsy and resolved quickly while he was on corticosteroid therapy. The most recent episode, occurring when the bowel disease was quiescent, was due to granulomatous hepatitis and resolved clinically with no specific therapy. Because numerous potentially serious hepatobiliary complications have been associated with inflammatory bowel disease, prompt and aggressive investigation in these instances is recommended.
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PMID:Cholestasis in Crohn's disease: a diagnostic challenge. 911 96

We report 81 of 107 cases of hemolytic uremic syndrome (HUS), admitted between July 1994 and February 1996, following an outbreak of Shigella dysenteriae type 1 dysentery in Kwazulu/Natal. All patients, excluding 1, were black with a mean age of 38 months (range 1-121); 50 (61.7%) were males. The mean duration of dysentery was 11.3 days (range 1-41) and HUS 15 days (range 1-91). Most patients had acute oliguric renal failure (90.1%), 42 (51.6%) required peritoneal dialysis. Complications included encephalopathy 30 (37.0%), convulsions 12 (14.8%) and hemiplegia 2 (2.3%), gastrointestinal perforation 8 (9.9%), protein losing enteropathy 26 (32.1%), toxic megacolon 4 (4.9%), rectal prolapse 5 (6.2%), hepatitis 11 (13.6%), myocarditis 5 (6.2%), congestive cardiac failure 3 (3.7%), cardiomyopathy 3 (3.7%), infective endocarditis 1 (1.2%), septicemia 15 (18.5%), disseminated intravascular coagulation 17 (21%). Leukemoid reactions were found in 74 (91.3%) patients, hyponatremia in 56 (69.1%), and hypoalbuminemia in 67 (82.7%). Stool culture for Shigella dysenteriae type I was positive in only 7 (8.6%) patients; Shiga toxin assays were not performed. Outcome was as follows: recovery 32 (39.5%), impaired renal function 8 (9.9%), chronic renal failure 26 (32.1%), end-stage renal disease 1 (1.2%), and death 14 (17.3%) patients.
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PMID:Post-dysenteric hemolytic uremic syndrome in children during an epidemic of Shigella dysentery in Kwazulu/Natal. 932 80

Microsporidia are ubiquitous in nature. Several clinical syndromes have been associated with microsporidiosis, especially in HIV-infected individuals, and include enteropathy, keratoconjunctivitis, sinusitis, tracheobronchitis, encephalitis, interstitial nephritis, hepatitis, cholecystitis, osteomyelitis, and myositis. Diarrhea and malabsorption are the most common clinical problems. Enterocytozoon bieneusi is the most common microsporidial cause of intestinal disease. A second species, Encephalitozoon intestinalis (originally named Septata intestinalis) is associated with disseminated as well as intestinal disease. Microsporidiosis has been seen worldwide, and is recognized as a frequent enteric infection in patients with AIDS. The pathogenesis of intestinal disease is related to excess death of enterocytes as a result of cellular infection. Clinically, microsporidiosis most often presents with diarrhea and weight loss as a result of small intestinal injury and malabsorption. However, microsporidia have been detected in virtually all organs, and may provoke symptoms related to their specific localization. The diagnosis of microsporidiosis is made histologically, either from tissue biopsies or secretions. While transmission electron microscopy was required for diagnosis in the past, special stains and light microscopy, as well as immunohistochemical and molecular techniques are capable of providing a firm diagnosis. Therapeutic options are limited. Enc. intestinalis responds well to albendazole, while no antiparasitic therapy has documented efficacy in Ent. bieneusi infections.
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PMID:Clinical syndromes associated with microsporidiosis. 955 78

Coeliac disease is a gluten-sensitive enteropathy in which, genetic, immunologic and environmental factors are implied. Several extradigestive diseases have been described in association with coeliac disease, which share most of the times an immunologic mechanism. The liver is damaged in coeliac disease, and it has been considered by some authors as an extraintestinal manifestation of the disease. In the present revision we discuss the different hepatic diseases related with the coeliac disease, as well as the best approach to diagnosis and therapy of choice. At diagnosis, it is very frequent to find an asymptomatic hipertransaminasemia, which frequently disappears after gluten suppression; the morphological substratum found in this alteration is a non-specific reactive hepatitis in the majority of cases. Coeliac disease is a demonstrated cause of cryptogenic hipertransaminasemia. In a small percentage of patient with coeliac disease an association has been found with other immunological liver diseases, such as primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis. Few studies exist that include a large number of patient, and the results on occasions are discordant. Nevertheless, the strongest association is with autoimmune hepatitis and with primary biliary cirrhosis. Several communications of isolated cases of rare hepatic diseases, which probably, only reflect a fortuitous association, have been cited in the literature.
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PMID:[Liver involvement in coeliac disease]. 1061 14

Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.
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PMID:Misoprostol therapeutics revisited. 1119 38


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