The presence of autoantibodies to cytoplasmic rod and ring particles in the serum of patients with chronic hepatitis C virus infection

Background: Chronic hepatitis C virus (HCV) is associated with extra hepatic autoimmune disorders, while peg-IFNa-2a/RBV combination therapy may exacerbate these conditions. Autoantibodies to cytoplasmic structures, called rod and ring particles (RR), have strong associations with these patients and are identified by HEp-2 cells. Objectives: Our purpose was to study the correlation of autoantibodies to cytoplasmic rod and ring particles in the serum of patients with chronic HCV infection with their response to standard therapy. Methods: Serum samples were gathered from 120 patients with HCV infection (40 naive treatments, 40 with sustained virological response (SVR), and 40 with relapse response) during peg-IFNa-2a/RBV combination therapy and analyzed for the presence of RR antibodies by IIF on commercially available HEp-2 cell substrate slides from Euroimmun (Lu beck, Germany). Results: Anti-rod and ring (anti-RR) autoantibodies were detected in only the serum of 1 out of 120 patients (0.8), which belonged to a patient (out of 40) with relapse response (2.5). No correlation was found between the types of response to peg-IFNa-2a/RBV combination therapy and the presence of anti-RR autoantibodies. Conclusions: The only HCV patient with RR autoantibodies previously had received IFN/ribavirin antiviral therapy. The presence of these autoantibodies is extremely rare in Iranian HCV patients. Further studies are warranted to determine the role of genetic background and geographical pattern in the prevalence of these novel autoantibodies worldwide. � 2016, Kowsar Corp

Serological assessment of gastric mucosal atrophy in gastric cancer

<p>Abstract</p> <p>Background</p> <p>Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the performance of these serological tests in the presence of gastric neoplasia.</p> <p>Methods</p> <p>Histological and serological samples of 118 patients with gastric cancer have been assessed for tumor specific characteristics (Laurén type, localisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological parameters (PG1, PG2, PG1/2-ratio, G17, <it>H. pylori </it>IgG, CagA status). Association of the general factors to the different serological values have been statistically analyzed.</p> <p>Results</p> <p>Patients with intestinal type gastric cancer had lower PG1 levels and a lower PG1/2-ratio compared to those with diffuse type cancer (<it>p </it>= 0.003). The serum levels of PG2 itself and G17 were not significantly altered. <it>H. pylori </it>infection in general had no influence on the levels of PG1, PG2 and G17 in the serum of gastric cancer patients. There was a trend towards lower PG1 levels in case of positive CagA-status (<it>p </it>= 0.058). The degree of both intestinal metaplasia and atrophy correlated inversely with serum levels for PG1 and the PG1/2-ratio (p < 0.01). Laurén-specific analysis revealed that this is only true for intestinal type tumors. Univariate ANOVA revealed atrophy and CagA-status as the only independent factors for low PG1 and a low PG1/2-ratio.</p> <p>Conclusions</p> <p>Glandular atrophy and a positive CagA status are determinant factors for decreased pepsinogen 1 levels in the serum of patients with gastric cancer. The serological assessment of gastric atrophy by analysis of serum pepsinogen is only adequate for patients with intestinal type cancer.</p

Serum Pepsinogen I, Pepsinogen II, and Gastrin 17 in Relatives of Gastric Cancer Patients: Comparative Study With Type and Severity of Gastritis

Background & Aims: First-degree relatives of gastric cancer patients are at risk for developing precancerous conditions. The aim of this study was to investigate the potential of biomarkers pepsinogen I (PGI), pepsinogen II (PGII), their ratio (PG I:II), as well as gastrin 17 for screening of precancerous conditions and corpus predominant gastritis. Methods: First-degree relatives of gastric cancer patients underwent endoscopy. Three biopsy specimens from the antrum and 3 from the corpus were evaluated according to the Sydney classification. Serum was taken for the measurement of fasting PGI, PGII, and gastrin 17 by enzyme-linked immunosorbent assay kits. Results: A total of 481 patients were examined (age, 47.8 ± 6.7 y). With the extension of gastritis, PGII was increased up to 2.5 times (6.6 ± 2.8 μg/mL in normal mucosa, 9.5 ± 6.7 μg/mL in antral gastritis, and 16.9 ± 12.4 μg/mL in corpus-predominant gastritis; P 17 pmol/mL) together were 9.4 and 99 for screening corpus-predominant gastritis and 14.8 and 97.8, respectively, for screening intestinal metaplasia in the corpus. Conclusions: PGII is a suitable marker for screening any gastritis from normal mucosa, but neither PGI, the PG I:II ratio, gastrin 17, nor their combination were able to select those with precancerous conditions and corpus-predominant gastritis among the first-degree relatives of gastric cancer patients. © 2008 AGA Institute