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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

So far the treatment of chronic hepatitis B has been based on the use of numerous agents, particularly interferon alpha which proved the most effective. Attempts are made to introduce new therapeutic methods (antiviral agents--nucleoside analogues, immunotherapy--anti HBV vaccine, gene therapy) in order to obtain higher percentage of patients with durable inhibition of HBV replication than it is observed after treatment with interferon alpha. The current work has been devoted to the presentation of the experiences with interferon alpha, lamivudine and anti HBV vaccine used in subjects with chronic type B hepatitis, with special reference to paediatric patients.
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PMID:Current knowledge on treatment of chronic hepatitis B in children. 1120 10

So far seven hepatotropic viruses were identified. They are described by letters A,B,C,D,E, G and TTV. The virus of hepatitis F is so far speculative. Virus of hepatitis A and E are transmitted by the orofaecal route and cause only acute hepatitis. The remaining hepatotropic viruses are transmitted by the parenteral route and have a longer incubation period than viruses A and E. The infection with the virus of hepatitis B develops into the chronic stage in about 10% and that of virus C in 50-90%. At least one third of chronic carriers of the virus of hepatitis B or C develop within 10-20 years liver cirrhosis or hepatocellular carcinoma. The objective of therapeutic regimes is eradication of the viruses or at least arrest or retarding of the activity of the disease. Corticoids are not used. The basis of therapeutic regimes is interferon alpha or lamivudine in hepatitis B and interferon alpha with ribavirine in hepatitis C. There is a permanent therapeutic response only in cca 40-50%. Active immunisation is possible against virus of hepatitis A and B. The virus of hepatitis D is a false virus, i.e. a so-called virold, and the cause is a super- or co-infection with the virus of hepatitis B. In this country it is practically not encountered, similarly as the virus of hepatitis E. The assembled findings on virus of hepatitis G are not applied so far very much in practice.
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PMID:[Characteristics of still unknown hepatotropic viruses and a clinical picture of the disease]. 1122 77

The hepatitis C virus (HCV) causes an acute but very often chronic liver disease. An estimated 3% of the world population is chronically infected with HCV. Chronic hepatitis C is the major cause of cirrhosis and hepatocellular carcinoma (HCC), which most often lead to liver transplantation. HCV is a single-stranded enveloped RNA virus; it belongs to the flaviviridae family. The virus has been classified into six genotypes, some of which are distributed worldwide, others of which are confined to more restricted areas. The genotype is an independent predictor of response to antiviral treatment. Blood transfusion was a major risk factor for acquiring HCV infection before donor screening for surrogate marker testing for non-A, non-B (NANB) hepatitis began in the mid-1980s, followed by screening for antibody to HCV in 1990. Today, intravenous drug use and high-risk sexual activity are the most frequently identified risk factors associated with HCV infection. The prevalence of people with unknown HCV infection worldwide is high, so it is necessary to screen people with risk factors. The treatment of patients with chronic HCV infection who have not been treated previously should consist of interferon alpha (IFN-alpha) and ribavirin.
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PMID:Hepatitis C virus infection: 10 years after the discovery of the virus. 1139 24

Cases of porphyria cutanea tarda (PCT) are occasionally reported in hemodialysis patients. Recently, hepatitis C virus has been recognized as a precipitating factor of PCT. The activity of the liver disease may be critical for the appearance of PCT. In this regard, liver disease reactivation after treatment with interferon alpha (IFN-alpha) is a well-known phenomenon. We report the case of a hemodialysis patient who developed PCT coincidentally with reactivation of liver disease, immediately after treatment with IFN-alpha. Therefore, in the present case, reactivation of hepatitis after IFN-alpha withdrawal could be the triggering factor. The occurrence of a bout of PCT should be considered as a possible complication at the end of IFN-alpha therapy, if reactivation of the disease exists.
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PMID:Development of porphyria cutanea tarda in a hemodialysis patient after reactivation of hepatitis C virus infection. 1139 22

We present the case of a 66-year-old woman with a diagnosis of chronic active viral C hepatitis, for whom a course of interferon alpha-2A was prescribed at a dose of 4.5 MU per day for a 2 month period, followed by the same dose on alternate days for 4 months. After completion of a month of therapy, the patient presented with painful oral lesions that made normal oral food intake impossible. These lesions persisted, in spite of withdrawal of interferon therapy. Intraoral examination revealed erosive intraoral lesions in both yugal mucosae, the upper vestibular gum, the floor of the mouth, the ventral region of the tongue, and the lower lip. A diagnosis of erosive lichen planus induced by interferon therapy was established. The prescribed treatment was 0.1% triamcinolone acetonide in orabase applied 3 times a day for 4 weeks. Following the therapeutical course, the erosive lesions disappeared, and the symptoms stopped, although the reticular lesions remained visible.
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PMID:Presence of lichen planus during a course of interferon alpha-2a therapy for a viral chronic C hepatitis. 1169 69

A 56-year-old male patient with chronic C type hepatitis had HCC which invaded right portal vein trunk (Vp3). In August 2000, we performed intrahepatic artery infusion chemotherapy with CDDP and 5-FU under subcutaneous interferon alpha treatment. In addition, we used chemoradiation therapy for portal tumor thrombus in HCC. As the result of such therapy, the size of HCC and portal tumor thrombus reduced and the level of PIVKA-II decreased. There were no side effects except fever due to interferon alpha treatment. In February 2001, we performed devascularization and RFA therapy for HCC in S7 of liver under laparoscope. The level of PIVKA-II was within the normal range. It is important to perform interdisciplinary therapy appropriate for the HCC status.
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PMID:[Good response in case of hepatocellular carcinoma with portal tumor thrombs--a case report of interdisciplinary local therapy]. 1170 14

Treatment of active chronic viral hepatitis type C with interferon alpha has proved effective and therefore its use is being extended to a large number of patients. Common side effects include respiratory manifestations. One side effect attributable to the immunomodulatory effect of interferon is the possible triggering or exacerbation of systemic or cutaneous sarcoidosis. We report a new case and offer an exhaustive review of the literature. A 49-year-old man with type C chronic, active hepatitis developed new respiratory symptoms and pulmonary infiltrates with hilar and mediastinal adenopathy after 4 months of treatment with pegylated interferon and ribavirin. The transbronchial biopsy showed multiple sarcoid granulomas. When the patient was diagnosed, he had already taken the total dose of interferon and no specific treatment was started. His hepatitis did not respond to therapy and his viral load and transaminase levels remained high.
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PMID:[Sarcoidosis following combined ribavirin and interferon therapy: a case report and review of the literature]. 1471 22

The on-treatment impact of interferon-based therapies on quality of life (QOL), work productivity, and medical resource utilization has not been systematically studied. We evaluated the effects of treatment with peginterferon alpha (pegIFNalpha) 2a monotherapy and the combination of interferon alpha (IFNalpha) 2b plus ribavirin (RBV) on health-related QOL, work productivity and resource utilization. A total of 412 patients with hepatitis C infection were randomized to open-label treatment with either pegIFNalpha 2a (n = 206) or IFNalpha 2b/RBV (n = 206). PegIFNalpha 2a was administered subcutaneously at a dose of 180 microg once weekly for 48 weeks; and IFNalpha 2b/RBV at doses of 3 MU thrice weekly subcutaneously and 1000-1200 mg/day orally. Outcome measures included the SF-36 Health Survey Questionnaire and additional generic and specific scales. During treatment, for all SF-36 summary and Hepatitis Quality of Life Questionnaire (HQLQ)-specific scales, the pegIFNalpha 2a group experienced less impairment than did the IFNalpha 2b/RBV patients. The between-treatment differences were significant for many of the scores particularly in the first 24 weeks of treatment. Across all measures of work functioning and productivity at each visit, patients randomized to pegIFNalpha 2a treatment showed less impairment relative to the group treated with IFNalpha 2b/RBV. Hence treatment with pegIFNalpha 2a relative to IFNalpha 2b/RBV minimizes the adverse impact of therapy on health-related QOL. Patients randomized to pegIFNalpha 2a had improved work productivity, less activity impairment, decreased need for prescription drugs to treat adverse effects, and better adherence to therapy.
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PMID:Comparison of quality of life, work productivity and medical resource utilization of peginterferon alpha 2a vs the combination of interferon alpha 2b plus ribavirin as initial treatment in patients with chronic hepatitis C. 1499 51

In patients with HIV coinfection, chronic hepatitis B was initially treated with interferon alpha, but the long-term results were disappointing. Currently, pegylated interferon is being investigated in an ongoing study. The nucleoside analogues lamivudine and adefovir may well become established as alternatives to interferon alpha. Treatment of hepatitis C in HIV coinfection with interferon alpha plus ribavirin also proved less efficacious compared to HCV-monoinfection. Initial preliminary results of studies on pegylated interferon alpha indicate an advantage over conventional interferon. Under treatment for hepatitis metabolic acidosis and hepatic decompensation may occur--in particular with didanosine and/or stavudine--and these substances may therefore be avoided as antiretroviral therapy in dual infection with hepatitis and HIV.
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PMID:[Viral hepatitis B/C and HIV. Therapy of double infections]. 1501 79

Chronic hepatitis B virus (HBV) infection is a well-recognized risk factor for the development of hepatocellular carcinoma (HCC), which is becoming a more prevalent clinical problem, especially in HBV-endemic areas. It is estimated that 1.25 million people in the United States and more than 300 million people worldwide are chronically infected with HBV. Despite the introduction of universal vaccination against hepatitis B in over 100 countries, persistent HBV infection is still a serious problem worldwide, causing an estimated annual death rate of one million. It may take several decades until the effect of vaccination will be translated into reduced transmission and morbidity. Meanwhile, patients with persistent HBV infection require better antiviral therapeutic modalities than are currently available. It is well accepted that antiviral therapy for chronic hepatitis B is effective to improve prognosis of patients with HBV by preventing development of hepatitis state and HCC. The therapeutic endpoints for hepatitis B treatment are: 1) sustained suppression of HBV replication, as indicated by HBsAg and HBeAg loss, 2) decrease of serum HBV DNA of an undetectable level by a non-PCR method, 3) remission of disease, as shown by normalization of ALT, 4) improvement in liver histology, and 5) reduction of the acute exacerbation, cirrhosis, and HCC. In the present, the antiviral treatment of hepatitis B consists of either interferon alpha or oral lamivudine alone or in combination with existing therapy. Each major antiviral drug of interferon alpha and lamivudine has pros and cons, and effect of combination therapy of both drugs is also still limited. More powerful and safe new antiviral therapies are required to achieve final goal of these therapeutic endpoints. Management of chronic hepatitis B requires significant knowledge of approved pharmacotherapeutic agents and their limitations. Therapeutic options for managing hepatitis infection after liver transplantation (LT) are also evolving.
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PMID:Antiviral therapy for chronic hepatitis B: a review. 1503 42


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