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)

LIGHT is a member of the TNF superfamily, which is transiently expressed on the surface of activated T lymphocytes and immature dendritic cells. Its known receptors are herpesvirus entry mediator (HVEM) prominently in T lymphocytes, and lymphtoxin beta receptor (LTbetaR) in stromal cells or nonlymphoid hematopoietic cells. Previous studies have shown that overexpression of LIGHT on T cells could lead to autoimmune reaction including lymphocytes activation, inflammation, and tissue destruction. To address the role of LIGHT/HVEM signaling in autoimmune hepatitis, an experimental colitis model induced by intravenous administration of concanavalin A (ConA) was given a soluble LTbetaR-Ig fusion protein as a competitive inhibitor of LIGHT/HVEM pathway. Marked elevation of LIGHT expression was detected in isolate intrahepatic leukocytes (IHLs) of the experimental animal. Treatment with LTbetaR-Ig significantly attenuated the progression and histological manifestations of the hepatic inflammation and reduced the production of inflammatory cytokines including TNF-alpha, IFN-gamma. Moreover, LTbetaR-Ig treatment significantly down-regulated LIGHT expression, leading to reduced lymphocytes (particularly CD4+ T cells), infiltrating into the hepatic inflammation and inhibited NF-kappaB activation and expression. We postulated that blockade of LIGHT/HVEM signaling by LTbetaR-Ig may ameliorate hepatitis by down-regulating LIGHT expression, and therefore we envision that LTbetaR-Ig would prove to a promising strategy for the clinical treatment of human autoimmune hepatitis.
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PMID:Lymphtoxin beta receptor-Ig protects from T-cell-mediated liver injury in mice through blocking LIGHT/HVEM signaling. 1701 45

Invasive adenovirus (AdV) disease is fatal in >50% of allogeneic hematopoietic stem cell transplant (SCT) recipients. Treatment with cidofovir may improve outcomes based on in vitro susceptibility data and case reports. Six consecutive cases of invasive AdV disease treated with cidofovir were reviewed among 84 allogeneic adult SCT recipients (incidence, 7.1%). Cidofovir was administered intravenously at 5 mg/kg per dose (1-7 doses). All patients received intravenous immune globulin. Blood AdV DNA levels (viral loads, VLs) were monitored with a real-time quantitative polymerase chain reaction assay. Published reports of cidofovir treatment of AdV disease in SCT recipients were critically reviewed. The primary manifestations of AdV disease were hepatitis (n = 3), colitis (n = 2), and nephritis (n = 1). All patients had detectable AdV VLs, with peak values from 5 x 10(5) to 2 x 10(8) copies/mL. All patients received CD34+ selected grafts (n = 3) and/or had graft-versus-host disease (n = 4) and had CD4 counts <100 cells/mm3. Only 1 of 5 patients (20%) who received >or=2 doses of cidofovir died with active AdV disease. Four patients exhibited improvement within days of treatment with cidofovir as documented by clinical criteria and declines in AdV VLs (without a change in immunosuppression). In contrast, 1 patient treated late after onset of AdV disease died after 1 dose of cidofovir. In our review of 70 published cases treated with >or=2 doses of cidofovir, 13 (19%) died from AdV disease. In conclusion, early treatment of AdV disease with cidofovir inhibits viral replication in vivo and reduces mortality in allogeneic SCT recipients compared with historical data.
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PMID:Treatment of adenovirus disease in stem cell transplant recipients with cidofovir. 1722 55

Common variable immunodeficiency (CVID) is a primary immunodeficiency disease characterized by hypogammaglobulinemia and recurrent bacterial infections especially in respiratory and gastrointestinal systems. We present here 2 cases of CVID with gastrointestinal complications.Case 1 is a 25-year-old man with a history of chronic diarrhoea from childhood. Ultrasonography revealed ascites, with liver size smaller than normal. Liver biopsy showed non-specific hepatitis. Lymphoid proliferation and Histiocytosis were reported in his ascites cytology. Moreover friability in colonoscopy due to moderate active chronic colitis was detected. Case 2 is a 26-year-old man with chronic diarrhoea since 8 years. Abdominal sonography revealed increased liver echogenicity, increased liver size, and some enlarged lymph nodes beside pancreas. Colonoscopy revealed friability and decreased vascularity while biopsy showed moderate active chronic colitis. Lymph node biopsy showed unusual immunologic reaction. Moreover, small bowel transition test showed nodularity. CVID should be considered in any patient with gastrointestinal manifestations especially chronic diarrhoea in association with recurrent bacterial infections in other organs. Diagnostic delay results in more morbidity and complications in untreated patients..
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PMID:Gastrointestinal complications in two patients with common variable immunodeficiency. 1730 7

We noted naturally occurring infection with Clostridium piliforme (Tyzzer's disease) in 2 captive-reared cotton-top tamarins (Saguinus oedipus). Spontaneous Tyzzer's disease has been reported in multiple species of laboratory, domestic, and wild animals but is extremely rare in humans and nonhuman primates. Distinct from idiopathic colitis, which is common in cotton-top tamarins, these 2 tamarins had severe, transmural, necrotizing typhlocolitis accompanied by myocarditis and hepatitis. Abundant bacteria compatible with C. piliforme, the etiologic agent of Tyzzer's disease, were present adjacent to lesions in the cecum-colon, liver, and heart. Therefore, colitis caused by C. piliforme, although rare, should be included as a differential diagnosis in cotton-top tamarins and as a cause of postnatal mortality in this species.
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PMID:Naturally occurring Tyzzer's disease in cotton-top tamarins (Saguinus oedipus). 1734 1

Aims of treatment for primary sclerosing cholangitis are as follows: prevention of progression of hepatobiliary disease, reduction of symptoms and consequences of cholestasis (pruritus, osteoporosis), and prevention of complications (colorectal cancer, hepatobiliary cancer). Ursodeoxycholic acid (UDCA) improves biliary secretion and laboratory parameters of cholestasis, but its effects on liver histology and survival are not clear. It reduces the incidence of dysplasias and carcinomas of the colon in patients with colitis and possibly has a beneficial effect on the incidence of bile duct carcinomas. At present, UDCA represents the most promising therapeutic option. Immunosuppressive treatment has not been proven to be effective; it appears to be indicated in the overlap syndrome with autoimmune hepatitis but may be harmful in bacterial cholangitis. Bacterial cholangitis is common in patients with dominant stenoses and requires antibiotic treatment. Endoscopic treatment of dominant stenoses improves cholestasis and prolongs survival in comparison to predicted survival. Pruritus represents a problem in some patients, and cholestyramine represents the first-line treatment. If ineffective, opioid antagonists, rifampin, or ondansetron may be tried. For treatment of osteoporosis and osteopenia, calcium and vitamin D supplementation are recommended, and in selected cases, bisphosphonates may be indicated. In patients with severe cholestasis and coagulation defects, parenteral supplementation of vitamin K may be indicated. During treatment, all patients should be regularly screened for colonic and bile duct carcinomas. Patients with cirrhosis of the liver and its complications are treated accordingly, and in end-stage disease, liver transplantation is indicated.
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PMID:Treatment of primary sclerosing cholangitis. 1739 26

To evaluate the response to alpha-interferon (INF) in patients who develop acute hepatitis C virus (HCV) infection during hemodialysis, we studied 17 patients who had infection while on dialysis. We administered three million units of alpha interferon subcutaneously to nine adult patients three times per week for 12 weeks; the rest of the patients served as controls. The patients in both groups were followed for 24 months after the diagnosis of seroconversion to anti-HCV antibody. Serum alanine aminotransferase (ALT) levels, anti-HCV antibody levels and HCV- poly chain reaction (HCV-PCR) were performed at regular intervals during the follow-up. Two patients in the treatment group dropped out; one because of colitis and another because of non-compliance. Of the seven patients who completed the course of therapy, all the patients had normal serum ALT levels in 2-8 weeks of therapy, three (42%) patients converted back to anti-HCV antibodies negative and six (86%) had HCV-PCR negative at 12 weeks of therapy (primary virological response) and remained so till the end of follow-up (sustained virological response). The liver biopsy performed in all the responders to therapy at 4-24 months after completion of treatment showed mild hepatitis. In the control group, all the patients continued to have raised serum ALT levels throughout the study; 12% converted anti-HCV antibodies to negative and HCV-PCR (performed on five patients) remained positive during the whole study period. In conclusion our study suggests the efficacy and safety of alpha interferon in the therapy of acute HCV infection in hemodialysis patients.
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PMID:Treatment of acute hepatitis C virus infection with alpha interferon in patients on hemodialysis. 1764 95

Acute graft-versus-host disease (GVHD) occurs after allogeneic hematopoietic stem cell transplant and is a reaction of donor immune cells against host tissues. Activated donor T cells damage host epithelial cells after an inflammatory cascade that begins with the preparative regimen. About 35%-50% of hematopoietic stem cell transplant (HSCT) recipients will develop acute GVHD. The exact risk is dependent on the stem cell source, age of the patient, conditioning, and GVHD prophylaxis used. Given the number of transplants performed, we can expect about 5500 patients/year to develop acute GVHD. Patients can have involvement of three organs: skin (rash/dermatitis), liver (hepatitis/jaundice), and gastrointestinal tract (abdominal pain/diarrhea). One or more organs may be involved. GVHD is a clinical diagnosis that may be supported with appropriate biopsies. The reason to pursue a tissue biopsy is to help differentiate from other diagnoses which may mimic GVHD, such as viral infection (hepatitis, colitis) or drug reaction (causing skin rash). Acute GVHD is staged and graded (grade 0-IV) by the number and extent of organ involvement. Patients with grade III/IV acute GVHD tend to have a poor outcome. Generally the patient is treated by optimizing their immunosuppression and adding methylprednisolone. About 50% of patients will have a solid response to methylprednisolone. If patients progress after 3 days or are not improved after 7 days, they will get salvage (second-line) immunosuppressive therapy for which there is currently no standard-of-care. Well-organized clinical trials are imperative to better define second-line therapies for this disease. Additional management issues are attention to wound infections in skin GVHD and fluid/nutrition management in gastrointestinal GVHD. About 50% of patients with acute GVHD will eventually have manifestations of chronic GVHD.
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PMID:Acute graft versus host disease. 1778 64

Drug rash with eosinophilia and systemic symptoms (DRESS), also known as hypersensitivity syndrome, is an idiosyncratic drug reaction presenting with fever, diffuse lymphadenopathy, exfoliative dermatitis, and visceral involvement, which may include hepatitis, pneumonitis, pericarditis, myocarditis, nephritis, and colitis. This report describes a 19-year-old, previously healthy man with manifestations of hypersensitivity (DRESS) syndrome after acquiring a titanium bioprosthesis for a spinal fracture. To our knowledge, there have been no prior reports of DRESS syndrome in association with titanium bioprosthetic implants.
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PMID:Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome: suspected association with titanium bioprosthesis. 1787 38

Adenomatous polyposis coli (APC) mutations are linked to human and mouse colorectal cancers. The Apc multiple intestinal neoplasia (Min) mouse mutation causes adenomas to develop throughout the small and large intestines. The BALB-Min (C.B6-Apc(Min/+)) congenic strain was generated by backcrossing into BALB/c the Apc(Min) allele from C57BL/6J-Apc(Min/+) mice. BALB-Min mice have a low tumor multiplicity (27.4 small intestine tumors/mouse) and a relatively long life span (>1 year) that makes them amenable to long-term studies. To investigate the interplay of the adaptive immune system and intestinal tumorigenesis, the immunodeficient compound mutant strain BALB-RagMin (C.Cg-Rag2(-/-) Apc(Min/+)) was generated. BALB-RagMin mice had a significant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts (43.0 versus 24.0 tumors/mouse, respectively). The results suggest that the adaptive immune system plays a role in either the elimination or the equilibrium phase of cancer immunoediting in the small intestine in this model. We investigated the effect of the enterohepatic bacterial pathogen Helicobacter hepaticus on liver and intestine tumorigenesis in BALB-RagMin mice. H. hepaticus-infected BALB-RagMin mice developed moderate hepatitis, moderate typhlitis, and mild colitis. There were no differences in small intestine and cecal tumor multiplicity, regionality, or size relative to that in uninfected mice. However, H. hepaticus-infected BALB-RagMin mice had a significant increase in colon tumor incidence relative to uninfected BALB-RagMin mice (23.5% versus 1.7%, respectively). The data suggest that H. hepaticus, which is present in many research colonies, promotes colon tumorigenesis in the BALB-RagMin mouse and that it has the potential to confound colon tumorigenesis studies.
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PMID:Helicobacter hepaticus infection promotes colon tumorigenesis in the BALB/c-Rag2(-/-) Apc(Min/+) mouse. 1841 Dec 92

Eosinophilic cholangiopathy is a rare cholestatic disorder of unknown etiology. Simultaneous histologic documentation of eosinophilic involvement of the bile ducts and gastrointestinal tract has been reported previously in only a few well-documented cases. We report a 52-year-old man with a history of idiopathic hypereosinophilic syndrome who presented with acute diarrhea and cholestatic hepatitis. Colonoscopy revealed colitis, and a biopsy showed eosinophilic infiltrates in the colonic mucosa. Liver biopsy showed dense eosinophilic inflammation in the portal areas with bile duct damage. This case demonstrates the entity of hepatic involvement in idiopathic hypereosinophilic syndrome and the difficulties related to diagnosis and treatment.
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PMID:Eosinophilic cholangiopathy with concurrent eosinophilic colitis in a patient with idiopathic hypereosinophilic syndrome. 1846 19


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