Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunostimulating and anti-cancer action of interferons (IFNs) has been known for many years. However, IFNs have not been introduced widely into the schemes of oncological treatment because of serious side effects potentiating untoward effects of chemotherapy. In addition using high doses of IFNs by parental routes the cost of such therapy is prohibitively high. Natural human interferon alpha lozenges produced from lymphoblastoid cell line by the Hayashibara Biochemical Lab. Okayama Japan (nHuIFN-alpha, HBL) is used in small doses delivered on oral mucosa. Thus, it might be expected not to cause severe side effects, and is less expensive. Children given antineoplastic and immunostimulatory treatment for cancer were also given nHuIFN-alpha--HBL lozenges containing 50-200 units of IFN per lozenge. Children treated age varied from 3-14 years. The average time of observation was 188 days. In 6 patients nHuIFN-alpha therapy was introduced at the time of the intensive oncological treatment during break periods. Those children had advanced malignant solid tumors. For the other children the IFN therapy was used after the successfully completed oncological treatment. The reason of using nHuIFN-alpha in this group was a long lasting hepatitis B virus antigenemia. The drug was well tolerated by children from both groups and a positive immunostimulating effect was observed. One prominent effect of the nHuIFN-alpha--HBL in children was a reduction of frequency of infections, improvement of appetite and psychological feeling of well being. It seems to us that IFN oral therapy may improve the tolerance of chemotherapy and radiotherapy.
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PMID:Evaluation of the efficacy of natural human interferon alpha lozenges on the clinical course of childhood neoplasia and in chronic hepatitis B virus infection in patients who were successfully treated for pediatric malignancies. 812 65

A retrospective review was undertaken on all renal biopsies performed in Chinese children under 13 years of age in Queen Mary Hospital, Hong Kong from 1980 to 1990. Of 172 renal biopsies, 18 cases were diagnosed to be membranous glomerulonephritis. All were associated with hepatitis B virus infection. Fourteen patients presented with, and 3 others developed later nephrotic syndrome. Hematuria was a common feature (83%). Complement C3 was low in 5 cases and they became normal later. At last observation, 10 patients (59%) remitted, usually within 3 years. One had persistent proteinuria and 5 had nephrotic syndrome. One patient developed end-stage renal failure 12 years after onset of illness. All three female patients completely remitted. Of the 15 boys, 50% remitted whether they received steroid treatment or not. Two patients received interferon alpha-2a therapy. One achieved remission but HBsAg and HBeAg persisted. The other had transient seroconversion and clinical improvement but nephrotic syndrome returned after stopping treatment.
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PMID:Hepatitis B virus associated membranous glomerulonephritis in children--experience in Hong Kong. 840 68

A 31-year-old male patient with an asymptomatic HIV infection but with a hepatitis B (HBV) related membraneous glomerulonephritis with nephrotic syndrome was given interferon alpha-2b subcutaneously 3 times weekly for 7.5 months. Zidovudine was added at the 10th week due to low CD4+ cell counts. Before the 6th week of treatment the patient reported a reduced need for diuretics to keep his lower limb edemas at a minimum. This response was partially sustained even after the 7.5 months interferon treatment course. The titers of HBV-DNA decreased markedly during the treatment with interferon but rose to pretreatment levels after discontinuation of the interferon treatment. The serum albumin increased but the proteinuria and hematuria were unaffected. Adverse reactions like fever, myalgias and anemia were tolerable and did not require dose reduction of either interferon or zidovudine. This treatment regimen, at least temporarily, improved the situation for the patient and can be worthwhile to try in HIV-infected patients with HBV related nephritis with nephrotic syndrome.
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PMID:Interferon alpha-2b treatment in an HIV-infected patient with hepatitis B virus induced nephrotic syndrome. 846 Mar 37

A literature review of patients chronically infected with hepatitis B virus (HBV) treated with natural human interferon alpha (nHuIFN-alpha) given parenterally every day for 28 days revelated that even the daily dose of (5 x 10(6)IU) of IFN-alpha inhibits cellular metabolism. As a result of metabolic block, the number of blood elements were diminished. Furthermore treated patients recorded several different adverse reactions. In contrast, among patients treated with the oral form of nHuIFN-alpha non metabolic block occurred and no adverse reactions were seen, even though the therapy lasted much longer. Two years after initiation of parenteral IFN-alpha therapy, the loss of HBV-BeAg was 53.8% and 28.8% of the patients had undergone seroconversion. In contrast, 77% of patients on oral interferon lost HBV-BeAg and 74% serconverted and normalized their biochemical liver function. The results suggest that the nHuIFN-alpha given orally and parenterally activate two different mechanisms responsible for virus elimination.
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PMID:Natural human interferon alpha may act differently when given parenterally or orally to patients chronically infected with hepatitis B virus. 887 64

During therapy of chronic viral hepatitis B (CVHB), some patients treated with natural human interferon alpha (nHuIFN-alpha) lozenges failed to respond. These observations triggered studies aimed to determine whether there are markers predicting patients' response to therapy with nHuIFN-alpha lozenges. In these studies, 32 patients with CVHB were involved: 20 males and 12 females, 16-61 years of age with proven persistent hepatitis B viremia (HBV). Patients were evaluated for clinical, biochemical liver function, and virological markers of disease. During 300 days of treatment of the patients received 75-150 IU nHuIFN-alpha daily in form of lozenges. The responders to oral interferon therapy were those who had initially alanine amino transferase (ALAT) level higher than 100 IU (85.7% cure rate) and weak responses were observed among patients who had an initial ALAT level below 100 IU (9.0% response rate). Therefore, ALAT test in patients with CVHB may serve as a predicting indicator of the outcome of IFN lozenges therapy.
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PMID:Natural human interferon alpha given orally has different effects on patients with distinct forms of chronic viral hepatitis B. 891 25

We report the case of a 51-year-old renal transplant patient, treated by interferon alpha (5MUI, three times a week) since he presented a coinfection by hepatitis B (HBV) and hepatitis C (HCV) virus for more than 7 years, associated with a chronic increase in serum alanine aminotransferase (ALT) levels and a chronic active hepatitis. The 4-month treatment was associated with a sustained normalization of ALT, a disappearance of HBV replication and a transient clearance of HCV viremia. Side effects were moderate and included thrombopenia (90,000/mm3), leucopenia (2200/mm3), an increase in serum creatinine (178 mumol/l). The withdrawal of alpha interferon was associated with the correction of these parameters. No rejection was observed on kidney biopsy. Meanwhile, liver histology was not affected by the treatment. To date, nineteen months after the end of alpha interferon therapy HBV DNA was still negative; ALT remained normal despite the early recurrence of HCV viremia; this emphasized the fact that HBV infection was certainly the most important factor involved in the patient's chronic hepatitis. It is concluded that alpha interferon therapy is able to decline HBV replication for a prolonged period in renal transplant patient although its use should be performed with caution due to the potential renal side effects.
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PMID:Treatment of chronic hepatitis B and C with alpha interferon in a renal transplant patient. 900 30

MxA protein is interferon inducible, and its role as an antiviral mediator is being studied in various viral diseases. Several cytokines, including type 1 interferons (alpha and beta), interleukins 2 and 12, and granulocyte, macrophage, and granulocyte-macrophage colony-stimulating factors, were tested for their ability to induce human MxA protein synthesis in peripheral blood mononuclear cells from 15 chronic hepatitis B virus-infected patients and 6 healthy subjects as controls. Constitutive MxA expression was scarce in patients and controls but increased significantly in response to type I interferons. MxA responsiveness to interferon alpha was diminished significantly in chronic hepatitis B patients, compared with healthy donors (P < 0.05); this effect was more marked in patients with high viremia levels. Interleukins 2 and 12, and none of the colony-stimulating factors tested, induced low, but detectable, MxA protein levels. These results indicate that chronic infection by hepatitis B virus may impair activation of the immune cells and their capacity to respond to type 1 interferons.
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PMID:Impaired interferon induction of human MxA protein in chronic hepatitis B virus infection. 909 49

It is admitted that viral infections can be responsible for systemic vasculitides. Viruses can be responsible for various types of vasculitis that affect vessels of different sizes. Clinical manifestations are the same as those observed in previously described vasculitides such as polyarteritis nodosa or cryoglobulinemia. When viral infection is diagnosed and considered to be responsible for vasculitis, a specific therapeutic approach must be prescribed. Treatment is based on the combination of antiviral agents and symptomatic or immunomodulating therapies. Antiviral therapy facilitates virus clearance and seroconversion to specific antibodies. In systemic vasculitides, plasma exchanges are a powerful treatment that clears circulating immune complexes. In the case of digital ischemia, vasodilators are also useful. Conversely, steroids and cytotoxic agents stimulate virus replication and favor disease chronicity and deleterious effects due to the presence of the virus. Hepatitis B virus-related polyarteritis nodosa can be cured with the combination of antiviral agents (mainly interferon alpha) and plasma exchanges. Hepatitis C virus-related cryoglobulinemia responds to interferon alpha and sometimes to plasma exchanges, but responses are usually partial and relapses occur in the majority of cases. In HIV-related vasculitides, currently available antiretroviral agents are not able to definitively eradicate the virus but their combination with plasma exchanges can cure the vasculitis. Due to common epidemiologic factors, several viruses can be present in the same patient, and determining their responsibility in the vasculitic process requires careful clinical and virologic analysis and then the selection of a specifically adapted therapeutic regimen. The therapeutic strategy applied in virus-associated vasculitides is therefore based on the etiologic investigations and the choice of a treatment is adapted to the pathogenetic mechanisms.
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PMID:The spectrum and treatment of virus-associated vasculitides. 911 Jan 31

The intercellular adhesion molecule 1 (ICAM-1, CD54) and the lymphocyte associated antigen 3 (LFA-3, CD58) have been found in soluble form (sCD54 and sCD58) in human sera. Data concerning their role in chronic liver disease and their usefulness in disease monitoring are contradictory. We addressed the question whether elevated sCD54/sCD58 correlated either with disease activity or with decreased elimination secondary to reduced liver function in chronic hepatitis B. We studied 31 patients with chronic hepatitis B undergoing interferon alpha therapy in a longitudinal fashion. Serum concentrations of sCD54 and sCD58 were measured at four weeks interval by specific Sandwich ELISA during a follow-up period of ten months. The maximal difference in concentration of each biochemical parameter, e.g., delta AST, delta gGt, delta bilirubin, was determined for each patient during the whole follow-up period. These differences were correlated with the variation in sCD54 (delta sCD54) and sCD58 (delta sCD58) at the respective time points. Using this method, we were able to eliminate interindividual differences in serum concentrations for sCD54 and sCD58 and to avoid bias due to preselection of patients. We found that delta sCD54 correlated with delta AST (p = 0.001) and delta ALT (p = 0.002), whereas there was no such correlation for delta sCD58. Interferon therapy did not affect sCD54 or sCD58 levels. Neither hepatitis B viremia nor the immune response to hepatitis B during the time of seroconversion to anti-HBe did significantly increase sCD54 or sCD58 levels. However, delta sCD54 was associated with delta gamma GT (p = 0.005) and delta sCD58 correlated with delta bilirubin (p = 0.037); a negative correlation was found for delta sCD54 with delta cholinesterase (p = 0.007). Our findings imply that sCD54 and sCD58 may be associated with a decrease in liver function that accompanies hepatic disease activity. sCD54 and sCD58 did not prove useful to monitor disease activity or response to interferon therapy in chronic hepatitis B. From our data we conclude, that decreased elimination of soluble adhesion molecules sCD54 and sCD58 in advanced liver disease may be responsible for increased serum concentrations detected.
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PMID:Circulating ICAM-1 (sCD54) and LFA-3 (sCD58) in chronic hepatitis B--a longitudinal study in patients treated with interferon-alpha. 923 90

Fifty percent of healthy hepatitis B surface antigen carriers may have histologically proven chronic hepatitis. Our aim was to study the benefit of interferon-alpha in healthy patients. Twenty-nine hepatitis B surface antigen carriers with normal liver enzymes and with serum hepatitis B virus DNA were randomized into two groups: Group I, 14 patients treated with 9 megaunits of interferon alpha-2a thrice weekly for six months, and Group II, 15 control patients. A liver biopsy was obtained from each patient at study initiation. A second biopsy was available in nine treated patients and six controls. During treatment, a significant increase in alanine amino transferase levels was observed in treated patients as compared with the controls (P < 0.05). After treatment, transaminase levels decreased to normal values. No differences between treated and control patients were observed in clearance of hepatitis B virus markers. A significant increase in the total histological activity index between base line and final liver biopsies was observed in treated patients (P < 0.05). It is concluded that interferon alpha treatment may induce a biochemical and histological activation of liver disease. Accordingly, interferon alpha should not be administered to healthy hepatitis B surface antigen carriers, at least with the schedule used in this work.
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PMID:Activation of liver disease in healthy hepatitis B surface antigen carriers during interferon-alpha treatment. 929 36


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