potential role of APOBEC3G in limiting replication of hepatitis B virus

Recent findings introduced APOBEC3G [A3G] as a host factor that blocks viral replication. It induces G to A hypermutations in viral DNA at the step of reverse transcription and in response to interferon. This study aimed to investigate the expression of liver A3G protein in association with both replication of hepatitis B virus [HBV] and frequency of G to A mutations in BCP [basal core promoter]-PC [pre-core] region. Fifty-one liver biopsies of naive chronic hepatitis B [CHB] patients enrolled for the expression of A3G were done by immunohistochemistry [IHC] standard method. The presence of HBV DNA and sequences of BCP-PC region at the time of liver biopsy was investigated in all patients. Among 34 patients with detectable HBV DNA, 31 carried 1-5 G to A mutations in the BCP-PC region. IHC results showed that the expression level of A3G in CHB patients' liver was very low. Of all patients, A3G is expressed in three undetectable HBV DNA subjects and a patient with 2.24 x 10[4] copies ml[-1] of HBV DNA. G to A mutated residues were indicated at positions 1727, 1757 and 1896 of the HBV genome of this patient. This study indicates that despite very low levels of both A3G in liver and the number of positive subjects, A3G has a potential role to restrict the in vivo replication of HBV

19-year survival in a patient with rectosigmoid liver metastasis

We present the case of an 82-year-old man diagnosed with rectosigmoid cancer and liver metastasis who survived for 19 years following treatment. At the age of 64, the patient twice experienced mucus excretion for which he underwent a colonoscopy that resulted in a diagnosis of rectosigmoid cancer the patient underwent surgery for resection of the tumor and liver metastasis. Histopathology was notable for a diagnosis of rectal adenocarcinoma that infiltrated the entire thickness of the wall, with metastasis to the liver and no lymph node involvement. Post-operative chemotherapy was administered for about four months. The patient remained asymptomatic for 19 years which at that time he presented with liver metastasis, ascites and renal failure

Validity, reliability and factor structure of hepatitis B quality of life questionnaire version 1.0: findings in a large sample of 320 patients

Background: Quality of life is of significant importance in chronic hepatitis B [CHBV]. We aimed to assess the psychometric properties of the Hepatitis B Quality of Life Questionnaire v1.0 [HBQOL] in a large sample of 320 Iranian patients with CHBV

Methods: After adapting the Iranian version through forward-backward translation and expert panel discussion, we administered HBQOL together with Short-Form 36 [SF-36], Medical Outcome Study Social Support Questionnaire [MOS-SS], Hospital Anxiety and Depression Scale [HADS], and the Iowa Fatigue Scale [IFS] to 320 non-cirrhotic Iranian patients. We used principal component analysis with Varimax rotation to determine the factor structure. To evaluate the psychometric properties of HBQOL, test-retest and internal consistency reliabilities, divergent and convergent validity with other instruments, and discriminatory power were calculated

Results: Thirty-one questions loaded on to six factors [Anticipation anxiety, Stigma, Psychological well-being, Vitality, Transmissibility and Vulnerability] which explained 63.6% of total variance. Test-retest reliability was 0.66. Cronbach's alpha was 0.94 for the overall scale and between 0.7 and 0.9 for subscales, with the exception of the Vulnerability subscale. HBQOL and its subscales showed acceptable convergent and divergent validity with other instruments. Furthermore, Vulnerability subscale of HBQOL discriminated between patients with chronic active and chronic inactive hepatitis

Conclusion: The Iranian version of HBQOL is reliable, valid, and sensitive to the clinical conditions of the patients. This instrument has acceptable factor structure to measure several aspects of quality of life in patients with chronic HBV

Hepatitis B virus infection during pregnancy: transmission and prevention

Hepatitis B virus [HBV] infection is a global public health problem. In endemic areas, HBV infection occurs mainly during infancy and early childhood, with mother to child transmission [MTCT] accounting for approximately half of the transmission routes of chronic HBV infections. Prevention of MTCT is an essential step in reducing the global burden of chronic HBV. Natal transmission accounts for most of MTCT, and providing immunoprophylaxis to newborns is an excellent way to block natal transmission. Prenatal transmissions is responsible for the minority of MTCT not preventable by immunoprophylaxis. Because of the correlation between prenatal transmission is responsible for the minority viremia, some authors find it sound to offer lamivudine in women who have a high viral load [more than 8 to 9 log 10 copies/ mL]. In addition to considerations regarding the transmission of HBV to the child, the combination of HBV infection and pregnancy raises several unique management issues. Chronic HBV infection during pregnancy is usually mild but may flare after delivery or with discontinuing therapy. Management of chronic HBV infection in pregnancy is mostly supportive with antiviral medications indicated in a small subset of HBV infected women with rapidly progressive chronic liver disease

Liver histology and HBV DNA levels in chronically HBV infected patients with persistently normal alanine aminotransferase

Data on histological activity and HBV DNA levels in patients with chronic HBV infection and persistently normal alanine aminotransferase levels are sparse. We aimed to investigate the histological activity and HBV DNA levels in these patients. There were 132 patients with HBeAg negative chronic HBV infection and persistently normal alanine aminotransferase levels that were included prospectively. Data were dichotomized according to the median levels. Associations of histology with HBV DNA and other variables were assessed. A total of 80 patients were male. The median age was 36 years. The median baseline HBV DNA was 2.9Log10 IU/mL. There were 50 cases [38%] with a total score >/= 5, 53 cases [40.2%] had grade >/= 4 and 40 cases [30.3%] had stage >/= 2. A baseline HBV DNA <2000 IU/mL was seen in 24 cases [48%] of those with total score >/= 5, 28 cases [53%] of those with grade >/= 4 and 9 cases [22.5%] with stage >/= 2. Multivariate analysis of baseline HBV DNA above the median level significantly predicted the total score, grade and stage with an adjusted odds ratio of 5.43, 3.47, and 4.23, respectively when compared to below median values. A second liver biopsy was performed in 61 patients. The median time interval between the two biopsies was 40 months. Total scores of 23 cases [38%] progressed by >/= 2 scores and the HBV DNA of 18 cases [22.5%] increased by >/= 1 Log[10] IU when compared to baseline values. HBeAg negative chronic HBV infection with persistently normal alanine aminotransferase is not a silent disease. Active liver disease may be seen in such patients with viral loads less than 2000 IU/mL

Efficacy of hepatitis B virus surface antigen vaccine as a therapeutic tool, in inactive hepatitis B virus carriers

Available drugs are not able to eradicate intracellular viral DNA in patients with hepatitis B virus [HBV] infections. HBsAg vaccine could induce immunity and subsequently eradicate Hepatitis B virus in proportions of these patients. Our aim was to evaluate the efficacy of HBsAg as a mode of therapy in inactive carriers. Forty two consecutive patients of inactive carriers were enrolled. All patients underwent liver biopsies. The modified Ishak score of all cases were less than 4. Twenty microgram of recombinant HBsAg vaccine injected intradermally 3 times [at 0, one and 6 months]. Biochemical and serological variables evaluated initially and 6 months after the last injection. The mean age was 39.6 +/- 11.12. Male/female ratio was [67.4%]. Two out of 42 cases lost their HBsAg [4.74%]. The difference was significant comparing to one percent annual spontaneous HBsAg loss [p=0.014]. In addition serum albumin level was significantly increased after vaccination [p=0.009]. Rest of the biochemical and serological variables had no significant changes comparing pre and post vaccination. Intradermal injection of HBV surface antigen vaccine could induce significant HBsAg loss. This mode of therapy is cheap, physiologic and without complication. However, the results of this study should be confirmed in further large controlled trial