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)

F(ab')2 fragments of monoclonal antibodies (MAbs) GA 73-3 and CO 29.11, with specific binding reactivity in vitro to human tumors of the gastrointestinal tract, were radioiodinated and injected into nude mice bearing human colon carcinoma xenografts. Fragments of both MAbs preferentially localized in tumor tissue compared with normal mouse tissue, as determined by differential tissue counting of radioactivity. The fragments localized specifically only in those tumors to which they bind in vitro and not in unrelated tumors. Radiolabeled fragments of an anti-hepatitis virus MAb did not localize in the tumors. Whole-body scintigraphy demonstrated tumor localization with 131I-labeled fragments without background subtraction. Best tumor contrast, as quantitated by analyzing digital computer scans, was obtained between Days 2 and 5 after injection. Tumor contrast was significantly enhanced when a mixture of both MAb F(ab')2 fragments was used. The biologic half-life of the MAb mixture in the tumor was significantly greater than that of either MAb alone, suggesting the use of the MAb mixture in radioimmunotherapy.
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PMID:Improved radioimmunoimaging of human tumor xenografts by a mixture of monoclonal antibody F(ab')2 fragments. 377 7

Blood samples of 60 patients and 19 staff members were tested for serological markers of hepatitides B (HBV) and C (HBC) using the Vector-Best JSC enzyme immunoassay kits. HBV and HBC markers were found in 25 in 30% of patients and in 15.8 and 5.3% of staff members, respectively. Part of the sera with HBV and HBC markers were tested for the HBV and HBC RNAs by polymerase chain reaction. The findings confirm that donors should be more thoroughly tested for hepatitis markers, as well as the patients and staff of hematology departments.
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PMID:[Prevalence of serological markers for viral hepatitis B and C in patients and medical personnel in the hematologic ward of Novosibirsk city hospital No. 2]. 910 41

The sequential development of cirrhosis and hepatocellular carcinoma (HCC) in patients with transfusion-associated hepatitis was a clue leading to the identification of hepatitis C virus (HCV) as a risk factor for HCC. The incidence of HCV-related liver cancer is increasing in many developed countries: tumours arise in older patients, are almost invariably associated with cirrhosis and often have a less aggressive course than is seen in HCC related to other aetiological factors. Most HCCs grow as a single hepatic nodule for several years before generating satellite or distant tumour nodules. Tumour progression and hepatic failure are the leading causes of death. HCV might promote cancer through cirrhosis, which is per se an important risk factor for this tumour. HCV might also have oncogenic properties by interacting with cellular genes that regulate cell growth and differentiation. The primary prevention of HCC through vaccination against HCV is not yet available. The treatment of patients with chronic hepatitis C with interferon might attenuate the risk of HCC.
Baillieres Best Pract Res Clin Gastroenterol 1999 Dec
PMID:Hepatitis C virus and hepatocellular carcinoma. 1065 17

Lack of efficacy and significant side effects have severely limited the use of interferon-alpha (IFN-alpha) as the standard therapy for non-A non-B hepatitis (NANBH) caused by hepatitis C virus (HCV) and alternative, improved therapies are urgently sought. Attempts have been made to improve the potency and tolerability of IFN-alpha by adjusting dosing regimens, methods of delivery and length of treatment. Furthermore, a number of different agents have been used in combination wit IFN-alpha and, from these studies, therapeutic options have been galvanized by the synergistic effects of IFN-alpha and ribavirin. Nevertheless, the majority of patients with HCV still do not sustain lasting therapeutic benefit from this combination and continuing research is required to identify new therapeutic candidates that will have more potent antiviral activity and less severe side effects. This review focuses on the progress that has been made in this area and the prospects for new effective therapies in the near future.
Baillieres Best Pract Res Clin Gastroenterol 2000 Apr
PMID:New drugs for hepatitis C virus (HCV). 1089 Mar 23

Hepatitis C virus (HCV) related chronic liver disease is now the leading cause for liver transplantation in many centres. Virological recurrence is inevitable following liver transplantation. Excellent patient and graft survival are seen in the short-term, equivalent to that in patients transplanted for other causes of liver disease. However, histological evidence of disease recurrence or hepatitis is present in over half the patients within a year of transplantation, although a small percentage develop progressive cholestatic hepatitis with graft loss within a year. Cirrhosis can develop in the first year after transplantation and 28% of patients have evidence of cirrhosis by 5 years. There is little agreement over the factors that predict the recurrence of disease, development of cirrhosis within the graft and graft or patient survival. Graft loss due to HCV occurs in up to 9% at 5 years and the long-term prognosis may not be comparable to groups transplanted for other diseases. Patients with hepatocellular carcinoma may benefit from liver transplantation if the tumour is small and without vascular invasion. There are, as yet, no clear guidelines regarding the best combination of immunosuppressants in patients with HCV but viral clearance has been achieved with the use of interferon and ribavirin therapy post-operatively.
Baillieres Best Pract Res Clin Gastroenterol 2000 Apr
PMID:Liver transplantation for hepatitis C virus related cirrhosis. 1089 Mar 24

Primary biliary cirrhosis (PBC) is characterized by an immune mediated, irreversible destruction of the small intrahepatic bile ducts leading to progressive liver cirrhosis and frequently to liver failure. The course of the disease is variable and an early diagnosis is desirable to identify individuals with rapidly progressing disease, to initiate adequate therapeutic measures and to evaluate the necessity of liver transplantation. Serological tests represent the single most important diagnostic feature of PBC because liver histology, biochemistry, or clinical syndrome alone are not reliable in this respect. The molecular definition of the autoantigen targets of antimitochondrial antibodies (AMA) has resulted in the development of reproducible and effective serological testing strategies. AMA directed against the ketoacid dehydrogenase complex are highly disease-specific but not directed against liver-specific target structures. Despite a high disease specificity, their usefulness for predicting the course of disease, the timing of liver transplantation, or disease recurrence after transplantation is limited. The realization that about 5% of patients with PBC do not display AMA has led to the identification of PBC-specific antinuclear autoantibodies directed against the nuclear pore complex and other targets. The overlap of PBC with autoimmune hepatitis and primary sclerosing cholangitis represents a diagnostic challenge in which autoantibody determinations play a central role and contribute to the administration of suitable treatment options.
Baillieres Best Pract Res Clin Gastroenterol 2000 Aug
PMID:Autoimmune tests in primary biliary cirrhosis. 1097 16

Although primary biliary cirrhosis (PBC) is generally a progressive disease, the rate of progression varies greatly from one patient to another. The terminal phase is characterized by hyperbilirubinaemia (>100 micromol/l), a major decrease in the number of intrahepatic bile ducts, and extensive fibrosis or cirrhosis. It is now well established that orthotopic liver transplantation is the treatment of choice for patients entering the terminal phase of the disease.A variety of therapeutic agents have been proposed for treatment of patients with PBC. However, most have been found ineffective or too toxic to be widely used. In contrast, there is accumulating evidence from large therapeutic trials that long-term administration of ursodeoxycholic acid (UDCA) is safe and prolongs survival free of liver transplantation. Treatment with UDCA slows the histological progression and delays the onset of cirrhosis. In patients who have a sub-optimal response to UDCA therapy alone, the combination of colchicine or methotrexate with UDCA has minimal or no additional benefit, whereas that with corticosteroids is more promising but not yet demonstrated. Among causes of non-response to UDCA therapy, the most common is the PBC-autoimmune hepatitis overlap syndrome. The benefit from the combination of corticosteroids and UDCA in this setting is obvious.Further studies are needed to define the patients who are most likely to respond to UDCA therapy and to assess the benefit of combined medical treatments.
Baillieres Best Pract Res Clin Gastroenterol 2000 Aug
PMID:Treatment of primary biliary cirrhosis. 1097 18

The halogenated inhalational anaesthetics halothane, enflurane, isoflurane and desflurane can produce metabolic hepatocellular injury in humans to a variable extent. During metabolism of these anaesthetics, tissue acetylation occurs due to the formation of reactive intermediates. Proteins modified by acetylation may constitute neo-antigens with a potential for triggering an antibody-mediated immune response. The likelihood of suffering post-operative immune hepatitis depends on the amount of the anaesthetic metabolized and is thereby considerably less with enflurane, isoflurane or desflurane compared with halothane. Plasma inorganic fluoride concentrations are regularly increased after sevoflurane. Elevated inorganic fluoride concentrations have been associated with nephrotoxicity following methoxyflurane anaesthesia but not after sevoflurane. Another source of concern is the products of degradation from reactions with carbon dioxide absorbents. Most important is compound A, which has been shown to exhibit nephrotoxicity in rodents. However, no significant changes in renal function parameters have been reported in surgical patients.
Best Pract Res Clin Anaesthesiol 2003 Mar
PMID:Halogenated inhalational anaesthetics. 1275 47

Current strategies for treating hepatitis B focus on clearance of active HBV infection through suppression of viral replication by interferon-alpha (IFN-alpha) and the nucleoside analogs (lamivudine and adefovir). Lamivudine therapy for 1 year leads to HBeAg seroconversion in 16-18% of patients compared to 4-6% of untreated controls, to histological improvement in 49-56% treated patients and in 23-25% controls. HBeAg seroconversion rates increase with the duration of lamivudine therapy from 17% at 1 year to 27, 40, 47 and 50% at 2, 3, 4 and 5 years, respectively. When prescribing lamivudine, drug resistance due to the emergence of tyrosine-methionine-aspartate-aspartate (YMDD) mutations that increases with duration of therapy and the potential risk of a severe flare of hepatitis with sudden cessation of therapy, probably greatest in patients with cirrhosis, are realistic concerns. After 48 weeks of treatment with 10 or 30 mg of adefovir dipivoxil per day, significantly more patients with HBeAg-positive chronic hepatitis B than those on placebo had histologic improvement (53, 59 and 25%, respectively), a reduction in serum HBV DNA levels (by a median of 3.52, 4.76 and 0.55 log copies/ml), undetectable levels of serum HBV DNA (21, 39 and 0%), normalisation of ALT levels (48, 55 and 16%) and HBeAg seroconversion (12, 14 and 6%). In HBeAg negative patients treated with adefovir dipivoxil (10mg/day) for 48 weeks, ALT levels had normalised in 72% (29% in the placebo group), serum HBV DNA levels were reduced to fewer than 400 copies/ml in 51% (none in the placebo group), liver histology improved in 64% (33% in the placebo group). No adefovir-associated resistance mutations of viral DNA were detected. Ongoing studies investigate combination therapy with lamivudine or IFN.
Best Pract Res Clin Gastroenterol 2004
PMID:Treatment of chronic viral hepatitis. 1558 3

The development of hepatocellular carcinoma (HCC), the mechanisms of hepatocarcinogenesis, the prevention of HCC, and screening for HCC will be discussed. Cirrhosis has been considered as a pre-neoplastic condition for the development of HCC. The worldwide incidence of HCC differs according to different hepatitis viruses, and information is lacking. Hepatocarcinogenesis is a multistep process involving a number of different genetic alterations and is poorly understood. Interferon should help prevent the development of HCC in patients with chronic hepatitis C. Screening is the only practical approach for improving the management of HCC patients, as early detection increases the application of curative treatments. However, the cost-effectiveness of various screening strategies needs to be analysed.
Best Pract Res Clin Gastroenterol 2007
PMID:Hepatocellular carcinoma development in cirrhosis. 1722 3


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