Central obesity and advanced liver stiffness in Hepatitis B: Result from golestan hepatitis B cohort study

Background: Chronic infection with the hepatitis B virus and obesity may both contribute synergistically to liver disease, although relatively few studies have investigated this hypothesis. Therefore, in this study, we evaluated the relationship between central obesity and the liver stiffness in the Golestan Hepatitis B cohort study (GHBCS). Methods: Our study included 304 chronic hepatitis B (CHB) patients enrolled from GHBCS. Liver stiffness measurement (LSM) and laboratory tests were performed after a follow-up of 4 years (2012). The hepatitis B viral load was measured at the baseline and follow-up using the real-time PCR method. Waist circumference ≥102 cm in men and ≥ 89 cm in women (central obesity) was considered to be abnormal. Advanced liver stiffness (ALS) was defined as LSM≥8 KPa. Statistical analysis was performed using SPSS-V17. Logistic regression was used to test predictors of advanced liver stiffness (LSM ≥ 8 KPa). Linear regression was used to test the predictive value of variables in ALT (as a continuous variable). P-value of less than 0.05 was considered statistically significant. Results: Among these CHB patients, 19 (7.4%) cases with a mean (±SD) age of 49.5 (±6.3) developed ALS after 4 years of follow-up. Multivariate analysis showed a significant predictive role of central obesity and viral load in ALS. Conclusions: Central obesity is related to the liver stiffness in chronic hepatitis B patients. © 2015, Academy of Medical Sciences of I.R. Iran. All rights reserved

Association of mutations in the basal core promoter and pre-core regions of the hepatitis B viral genome and longitudinal changes in HBV level in HBEAG negative individuals: Results from a cohort study in northern Iran

Background: Although certain HBV mutations are known to affect the expression of Hepatitis e antigen, their association with HBV viral level or clinical outcomes is less clear. Objectives: We evaluated associations between different mutations in the Basal Core promoter (BCP) and Pre-core (PC) regions of HBV genome and subsequent changes in HBV viral DNA level over seven years in a population of untreated HBeAg negative chronic hepatitis B (CHB) participants in Northeast of Iran. Materials and Methods: Participants in the current study were drawn from the Golestan Hepatitis B Cohort Study (GHBCS), a cohort of approximately 2590 HBsAg positive subjects (living in Gonbad city) embedded in the Golestan Cohort Study (GCS). At baseline, HBsAg was measured in all participants and revealed 2590 HBsAg positive cases. We randomly selected 304 participants who their blood sample were taken at both baseline and seven years later in follow-up and had not been treated for HBV during this time. HBV viral load were assessed at baseline and at year 7. The BCP and PC regions of the HBV DNA, at baseline, were amplified via hemi-nested PCR and sequenced by cycle sequencing. At year 7, liver stiffness was assessed by fibroscan; also, other parameters of liver disease were assessed following standard clinical protocols. Associations were assessed via tabulation, chi-square, t-tests and logistic regression. P values < 0.05 were considered statistically significant and all tests were two-sided. Results: Among 304 HBsAg positive participants, 99 had detectable HBV DNA at study baseline. Of these, 61.6% had PC mutations (48.5% A1896 and 25.2% G1899). In contrast to other mutations, A1896 was associated with a higher proportion of detectable HBV DNA at year 7 (39.6%) compared to patients with the wild type (13.7%) (OR: 4.36, CI95% = 1.63-11.70; P Value = 0.002). Although participants with the A1896 mutation had higher year-7 HBV viral load than participants with G1896 (2.30 ± 1.66 IU/mL vs. 1.76 ± 1 IU/mL among patients with detectable HBV; P value = 0.052), no association was observed with either serum level ALT or liver stiffness. Interestingly, mutations in the basal core promoter (BCP) region had no significant effect on virus DNA detection. Conclusions: In this population with chronic HBeAg negative hepatitis B, an association was observed between the G1896A mutation in the Pre-core region of HBV and subsequent level of HBV DNA seven years later, which indicated that mutations in this region of HBV genome may contribute to disease progression in these patients and play an important role in HBV natural course of disease. © 2015, Kowsar Corp

On the massless contributions to the vacuum polarization of heavy quarks

Recently Groote and Pivovarov have given notice of a possible fault in the use of sum rules involving two-point correlation functions to extract information on heavy quark parameters, due to the presence of massless contributions that invalidate the construction of moments of the spectral densities. Here we show how to circumvent this problem through a new definition of the moments, providing an infrared safe and consistent procedure.Comment: 1+9 pages, 3 figures. Discussion on QCD sum rules applications added. Conclusions unchanged. Version to be published in Journal of Physics