Influence of laboratory-related and endoscopy-related factors on the assessment of serum pepsinogens and gastrin-17

Background and aim Serum pepsinogen I (PGI) and pepsinogen II (PGII) are noninvasive parameters in the detection of atrophic gastritis. The diagnostic add-on value of serum gastrin-17 (G-17) remains uncertain. The aim of this study was to assess the stability of these serum parameters over time and to evaluate the influence of clinical factors, such as upper gastrointestinal (GI) endoscopy and bowel cleansing, on serum PGI, PGII, and G-17 assessment. Patients and methods A prospective study was carried out in healthy individuals and patients. For the stability analyses, the plasma and serum samples from 23 individuals were processed at different time points with and without the addition of a stabilizer. Ten patients were included to evaluate the influence of upper GI endoscopy and 18 patients to evaluate the effect of bowel cleansing before colonoscopy. Results PGI, PGII, and G-17 levels were not statistically different in the serum and plasma. PGI and PGII serum levels were stable over time. G-17 is associated with time-dependent degradation (P = 0.0001). The addition of the G-17 stabilizer showed no improvement in stability. Upper GI endoscopy and bowel preparation before colonoscopy were associated with minimal variations in PGI and PGII, whereas G-17 showed patient-specific alterations. Conclusion PGI and PGII serum levels are stable over time. However, G-17 stability is strongly dependent on the time of processing and storage;therefore, samples for G-17 analysis need to be processed no later than 6 h after blood collection. Upper GI endoscopy and colonoscopy preparation lead to minimal nonsignificant changes in basal PGI, PGII, and G-17 levels

Helicobacter Pylori Serology in Relation to Hepatitis C Virus Infection and IL28B Single Nucleotide Polymorphism

The aim of the study was to evaluate the serological rate of Helicobacter pylori (H. pylori) infection in patients with chronic hepatitis C virus (HCV) infection and determine any correlations with liver damage and IL28B single-nucleotide polymorphism (SNP). One hundred eighty-nine patients with chronic HCV infection were included in the study, and H. pylori status was defined based on anti-H. pylori-IgG or anti-CagA-IgG antibodies using enzyme-linked immunosorbent assay (ELISA). Liver damage was assessed using histology or transient elastography. IL28B C/T polymorphism (rs12979860) was evaluated in circulating blood cells using a PCR-based restriction fragment length polymorphism assay. Overall H. pylori serology was positive in 38.1% of our HCV-infected subjects. Among those, the anti-CagA-IgG positivity rate was 43.1% and was within the range of previously described populations of the same region. Highest prevalence of H. pylori was found in patients between 31 and 40 years compared to other age subgroups. The seropositivity rate was higher in the non-cirrhotic group than the cirrhotic one (45.4% vs. 20.0%, p < 0.05). No difference was found in IL28B genotype between H. pylori-positive and -negative cohorts. However, we observed a trend for the lower anti-CagA-IgG expression level in relation to the IL28B T-allele. Our results do not support an association between HCV and H. pylori infection. Whether IL28B SNP has a functional role in modulation of serological response to H. pylori CagA needs further investigation

LINE-1 hypomethylation is not a common event in preneoplastic stages of gastric carcinogenesis

Article Number: 4828. PubMed ID: 28684753. Funding Agency - BMBF of ERA-NET PathoGenoMics. Grant Number BMBF-0315905DLINE-1 hypomethylation is widely accepted as marker for global genomic DNA hypomethylation, which is a frequent event in cancer. The aim of the study was to evaluate LINE-1 methylation status at different stages of gastric carcinogenesis and evaluate its prognostic potential in clinical settings. LINE-1 methylation was analyzed in 267 tissue samples by bisulfite pyrosequencing including primary colorectal cancer tissues (T-CRC) with corresponding adjacent colon mucosa (N-CRC), gastric cancer tissues (T-GC) with corresponding gastric mucosa (N-GC), normal gastric tissues (N), chronic non-atrophic and atrophic gastritis (CG). LINE-1 methylation level was lower in both T-GC and T-CRC when compared to paired adjacent tissues. No difference was observed for LINE-1 methylation status between patients with normal gastric mucosa, CG and N-GC. LINE-1 methylation in T-GC but not N-GC tended to correlate with age. Subgroup stratification analysis did not reveal significant differences in LINE-1 methylation status according to tumor stage, anatomical location, histological subtype, differentiation grade. We observed similar overall survival data between patients with high or low LINE-1 levels. In summary, LINE-1 hypomethylation is a characteristic feature in GC but not very common in early preneoplastic stages of gastric carcinogenesis. Prognostic role of LINE-1 hypomethylation in GC patients could not be confirmed in this cohortLietuvos sveikatos mokslų universitetas. Medicinos akademijaSocialinių tyrimų centrasVilniaus universiteto Onkologijos instituto Vėžio registrasVytauto Didžiojo universiteta

Helicobacter pylori vacA genotype is a predominant determinant of immune response to Helicobacter pylori CagA.

To evaluate the frequency of Helicobacter pylori (H. pylori) CagA antibodies in H. pylori infected subjects and to identify potential histopathological and bacterial factors related to H. pylori CagA-immune response