Diagnostic value of fecal calprotectin in patient with ulcerative colitis

Ulcerative colitis [UC] is characterized by recurrent episodes of inflammation limited to the mucosal layer of the colon. Calprotectin is a zinc and calcium binding protein derived from neutrophils and monocytes. It is easily detectable in tissue samples, body fluids, and stools, which makes it a potentially valuable marker of inflammation. The aim of the current study is to evaluate the value of fecal calprotectin [FC] as a marker of disease activity in patients with UC. Seventy three eligible subjects underwent ileocolonoscopy and multiple biopsies were obtained from different parts of the colon and terminal ileum. All patients underwent blood and stool sampling as well as an interview to assess the disease severity utilizing ulcerative colitis activity index [UCAI], subjectively. The diagnostic value of the FC in comparison with Mayo disease activity index as the gold standard technique, was then evaluated. Mean FC level increased linearly according to Mayo disease activity index [r=0.44, p<0.001] and was significantly different between levels of Mayo disease activity index [p=0.003]. In multivariate analysis, Mayo disease activity index, positive CRP and ESR were associated with FC level. FC level > 21.4 ng/ml was able to discriminate between active and inactive phases of UC according to Mayo disease activity index>2 with 72.3% sensitivity and 73.1% specificity. The combination of FC > 21.4 ng/ml and UCAI score of 7 had a 46.8% sensitivity and 88% specificity to diagnose Mayo disease activity index >2. Furthermore, FC level <21.4 ng/ml in combination with UCAI score of <3 showed a highly considerable specificity of 98% to discriminate the remission phase of UC [Mayo disease activity index <2], although with a low sensitivity [31%]. FC appears to be a non-invasive biomarker with moderate accuracy to discriminate the active phase of inflammatory bowel disease [IBD]. The value of FC especially in combination with UCAI is highly considerable to rule out the Mayo disease activity index >2

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

Hepatitis B virus genome asymmetry in Hepatocellular Carcinoma

The association between hepatitis B virus [HBV] mutations and hepatocar-cinogenesis were reported in the literature. Preference for G over C in the leading DNA strand has been reported to account for the asymmetry in nucleotide [nt] composition. The aim of this study was to analyze the complete genome sequence and compositional asymmetry of HBV in different stages of hepatitis B. Full genome sequencing of 24 patients with chronic hepatitis B, some of whom also had cirrhosis and hepatocellular carcinoma [HCC] was performed. Mutations analysis was implemented in a comparison with a HBV genotype D reference from an international DNA database. CpGProD, a web-based application, was used to evaluate CG content and predict CpG islands. All strains were 3182 base pairs [bp] in length, except for two cases of HCC in which 9 and 21 nt, respectively, were deleted in preS2. The genetic relatedness of these isolates was 97%-100%. There were common CpG-rich regions in all 24 isolated full genome sequences, however a strong negative GC skew for forming a CpG island in the minus strand were exhibited in overlap with enhancer I in three HCC patients, a cirrhotic patient and three with chronic hepatitis. The high percentage of sequence identity between HBV isolates in our patients demonstrates that genomic factors, except for genotype, are involved in hepatocarcinogenesis. Variations in GC content which were caused by a different spectrum of mutations may affect DNA compositional asymmetry and epigenetic modification of HBV DNA in HCC