Assessing GastroPanel serum markers as a non-invasive method for the diagnosis of atrophic gastritis and <i>Helicobacter pylori</i>infection

Gastric colonization by Helicobacter pylori increases the risk of gastric disorders, including atrophic gastritis which can be diagnosed based on levels of serum biomarkers like Gastrin and Pepsinogen. We therefore examined the efficacy of a serological-based method namely GastroPanel Blood kit, in diagnosing and scoring gastritis associated to Helicobacter pylori infection. Patients with dyspeptic symptoms were prospectively recruited on voluntary basis at the Yaounde Central Hospital and University Teaching Hospital, from March to July 2011. The degree of atrophy was classified according to levels in patient serum of pepsinogens I and II (PGI and PGII) and Gastrin 17 (G17) and compared with histological profiles as reference method. A specific ELISA test was used for the detection of H. pylori IgG antibodies. In total, 86 volunteers from 21 to 83 years old (mean = 46.4 ± 3.3) were enrolled, including 74.4% of women and 25.6% of men. The prevalence of gastritis was statistically similar between Gastro Blood Panel test and histology used as reference method (89.5% versus 83.7%: p > 0.20). Diagnosis based on serum makers showed high sensitivity (93.1%) in comparison with the reference method. However, the serological based method has diagnosed more atrophic gastritis than the reference (17.4% versus 7.0%: p 0.05). Furthermore, the prevalence of H. pylori infection did not differ significantly between serological method (84.9%) and reference method (81.4%). These results suggest that diagnosis of atrophic gastritis and H. pylori infection obtained with an optional serological method (GastroPanel) is in a strong agreement with the biopsy findings, and thus can be a useful non endoscopic assessment of stomach mucosal atrophy in patients with dyspepsia.

Highly Prevalent SARS-CoV-2 Antigenemia in COVID-19 Patients

Background:Many issues,such as severity assessment and antibody responses,remain to be answered eagerly for evaluation and understanding of COVID-19.Immune lesion is one of key pathogenesis of the disease.It would be helpful to understand the disease if an investigation on antigenemia and association was conducted in the patients with SARS-CoV-2 infection.Methods:A total of 156 patients admitted to the First People’s Hospital of Hefei or Anhui Provincial Hospital on January to February 2020 were involved in this study.SARS-CoV-2 nucleocapsid(NP)antigen,specific IgM/IgG antibodies,and RNA were detected in sequential sera from three COVID-19 patients,and additional 153 COVID-19 patients by means of NP-antigen capture enzyme-linked immunosorbent assay,colloidal gold quick diagnosis,and real-time RT-PCR,respectively.The clinical types of COVID-19 patients were classified into asymptomatic,mild,moderate,severe,and critical,following on the Chinese guideline of COVID-19 diagnosis and treatment.The demographic and clinical data of patients were obtained for comparable analysis.Results:NP antigen was detected in 5 of 20 sequential sera collected from three COVID-19 patients with typically clinical symptoms,and 60.13%(92/153)expanded samples collected within 17days after illness onset.No SARS-CoV-2 RNA segment was detected in these sera.The NP positive proportion reached a peak(84.85%,28/33)on 6 to 8days after illness onset.Both NP concentration and positive proportion were increased with the increase of clinical severity of COVID-19.Compared to NP negativepatients,NP positive patients had older age[years,medians(interquartileranges(IQR)),49(6)vs.31(11)],lowerpositive proportion of NP specific IgM[27.17%(25/92)vs.59.02%(36/61)],and IgG[21.74%(20/92)vs.59.02%(36/61)]antibodies,and longer duration[days,medians(IQR),24(10)vs.21(13)]from illness to recovery.Conclusions:SARS-CoV-2 NP antigenemia occurred in COVID-19,and presented highly prevalent at early stage of the disease.The antigenemia was related to clinical severity of the disease,and may beresponsible for the delay of detectable SARS-Cov-2IgM.