Corpus Atrophy Research Articles

Effectiveness of serological markers of gastric mucosal atrophy in the gastric precancer screening and in cancer prevention.

New markers are needed to improve the effectiveness of serological screening for atrophic gastritis. To develop a cost-effective method for serological screening of atrophic gastritis with a high level of sensitivity. Of the 169 patients with atrophic gastritis, selected by the visual endoscopic Kimura-Takemoto method, 165 showed histological mucosal atrophy using the updated Kimura-Takemoto method. All 169 patients were examined for postprandial levels of gastrin-17 (G17) and pepsinogen-1 (PG1) using GastroPanel® (Biohit Plc, Helsinki, Finland). We used the histological standard of five biopsies of the gastric mucosa, in accordance with the Kimura-Takemoto classification system to assess the sensitivity of G17 in detecting gastric mucosal atrophy. We also compared the morpho-functional relationships between the detected histological degree of gastric mucosal atrophy and the serological levels of G17 and PG1, as the markers of atrophic gastritis. The sensitivity of postprandial G17 was 62.2% for serological levels of G17 (range: 0-4 pmol/L) and 100% for serological G17 (range: 0-10 pmol/L) for the detection of monofocal severe atrophic gastritis. No strong correlation was found between the levels of PG1 and degree of histological atrophy determined by the Kimura-Takemoto classification system to identify the severity of mucosal atrophy of the gastric corpus. In the presented clinical case of a 63-year-old man with multifocal atrophic gastritis, there is a pronounced positive long-term dynamics of the serological marker of atrophy - postprandial G17, after five months of rennet replacement therapy. Serological screening of multifocal atrophic gastritis by assessment of postprandial G17 is a cost-effective method with high sensitivity. Postprandial G17 is an earlier marker of regression of atrophic gastritis than a morphological examination of a gastric biopsy in accordance with the Sydney system. Therefore, postprandial G17 is recommended for dynamic monitoring of atrophic gastritis after treatment.

B12 deficiency-related glossitis is highly associated with high gastrin-17 and low pepsinogen I.

The causes of vitamin B12 (B12) deficiency are varied and mainly related to gastric disorders. Glossitis is a common oral manifestation of B12 deficiency and is often first seen by dentists. This study aimed to investigate the correlation between B12 deficiency-related glossitis (B12-def glossitis) and gastric serum biomarkers [gastrin-17(G17), pepsinogen I (PGI), pepsinogen II (PGII), and anti-Helicobacter pylori (H. pylori) antibodies], and preliminarily discuss the etiology of B12-def glossitis. A cross-sectional study was conducted in patients complaining of glossodynia, burning sensation, or severe recurrent oral ulcers, but patients with a history of gastrectomy were excluded. All subjects underwent a uniform oral examination and hematological tests. Of 243 patients, 133 with B12-def glossitis were in the case group, and 110 with other oral mucosal diseases (non-glossitis) and normal B12 levels were in the control group. In the case group, 84.2% (112/133) showed high G17 and low PGI levels (G17hi PGIlow ). Univariate logistic regression showed that G17hi PGIlow was a high-risk factor for B12-def glossitis (OR: 92.44; 95% CI: 35.91, 238.02). Subgroup analyses in the case group showed that the G17hi PGIlow group presented with lower B12 levels and a lower positive rate of anti-H. pylori antibodies compared to the non-G17hi PGIlow group. Gastric serum biomarkers in patients with B12-def glossitis generally showed G17hi PGIlow , suggesting possible atrophy of gastric corpus and fundus mucosa. The G17hi PGIlow and non-G17hi PGIlow groups may represent different etiologies of B12 deficiency.

Comparison between the GastroPanel test and the serum pepsinogen assay interpreted with the ABC method-A prospective study.

This study aimed to validate Helicobacter pylori serological and pepsinogen (PG) assays for detecting infection and gastric neoplasm. Individuals who underwent serum Chorus H. pylori and HBI PG assays were included from May to September 2023. The GastroPanel test was performed using the same blood sample. HBI assay findings were interpreted with the ABC method using the criteria of corpus atrophy (PG I ≤ 70 ng/mL & I/II ≤3) and advanced corpus atrophy (PG I ≤ 30 ng/mL & I/II ≤2). A total of 144 H. pylori-infected and 184 non-infected Koreans were analyzed. The Chorus test (sensitivity 97.2%, specificity 89.1%) showed higher area under the curve (0.993 vs. 0.972, p = 0.003) than the GastroPanel test (sensitivity 95.8%, specificity 86.4%). Using the GastroSoft application, the incidence of gastric neoplasms was highest in the corpus atrophy group (50%), followed by the low acid-output (25.8%), H. pylori infection (11.6%), and antral atrophy (9.1%) groups. There were no gastric neoplasms in the normal and high acid output groups. Using the ABC method, the incidence of gastric neoplasms was highest in the corpus atrophy groups (23.8% in Groups C and D), followed by Group B (12.3%) and Group A (2.4%). Corpus atrophy interpreted with the GastroSoft showed poor agreement (k = 0.225) with corpus atrophy interpreted with the ABC method, whereas it showed excellent agreement (k = 0.854) with advanced corpus atrophy. Although the Chorus test was more accurate than the GastroPanel test, both assays discriminated high-risk individuals by detecting atrophy or infection. There were no gastric neoplasms in the normal or high acid-output groups (GastroSoft application), and gastric neoplasm incidence was lowest in Group A (ABC method). Corpus atrophy determined by GastroSoft application is more consistent with advanced corpus atrophy determined by the ABC method than is corpus atrophy.

Erektil disfonksiyonda Trombositten Zengin Plazma (TZP) tedavisi

Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. The prevalence of ED increases with age. The etiological causes of ED may be vasculogenic, neurogenic, anatomic, hormonal, drug-induced and/or psychogenic. Phosphodiesterase-5 enzyme inhibitors (PDE5-i) are used as the first-line treatment for ED. Recently, regenerative therapies have become popular in the treatment of ED. PRP therapy is one of the most popular regenerative ED treatments. Various growth factors and cytokines secreted from the α-granules contained in platelets have been shown to provide tissue regeneration in PRP treatment. These cytokines play important roles in cell proliferation, chemotaxis, cell differentiation and angiogenesis. Animal studies have shown that PRP improves myelin regeneration, reduces corporal atrophy, and improves erectile function. Although clinical studies have shown the positive effects of PRP on ED, the data are not yet sufficient to make a clear recommendation. Keywords: erectile dysfunction, platelet rich plasma, regenerative therapy

Update on Serum Biomarkers in Autoimmune Atrophic Gastritis.

Autoimmune atrophic gastritis (AAG) is a persistent, corpus-restricted immune-mediated destruction of the gastric corpus oxyntic mucosa with reduced gastric acid and intrinsic factor secretion, leading to iron deficiency and pernicious anemia as a consequence of iron and cobalamin malabsorption. Positivity toward parietal cell (PCA) and intrinsic factor (IFA) autoantibodies is very common. AAG may remain asymptomatic for many years, thus making its diagnosis complex and often delayed. Due to the increased risk of gastric neoplasms, a timely diagnosis of AAG is clinically important. The gold standard for AAG diagnosis is histopathological assessment of gastric biopsies obtained during gastroscopy, but noninvasive, preendoscopic serological screening may be useful in some clinical scenarios. Serum biomarkers for AAG may be divided into 2 groups: gastric autoimmunity-related biomarkers, such as PCA and IFA, and gastric corpus atrophy/reduced gastric acid secretion-related biomarkers, such as serum gastrin and pepsinogens. The present review focuses on the clinical significance and pitfalls of serum biomarkers related to gastric autoimmunity and gastric corpus atrophy, including some discussion of analytical methods. Serum assays for PCA, IFA, gastrin, and pepsinogen I show good diagnostic accuracy for noninvasive diagnostic work-up of AAG. Diagnostic performance may increase by combining >1 of these tests, overcoming the problem of seronegative AAG. However, appropriately designed, comparative studies with well-characterized patient cohorts are needed to better define the reliability of these biomarkers in the diagnosis of patients with AAG. Currently, positive serum tests should always be followed by the state-of-art diagnostic test, that is, histopathological assessment of gastric biopsies obtained during gastroscopy to definitively confirm or rule out AAG and eventually neoplastic complications.

Characteristics of Helicobacter pylori-Seropositive Subjects According to: A) The Stool Antigen Test Findings. B) Serum Pepsinogen Level. C) Upper Endoscopic Findings

Abstract Background Helicobacter pylori infection can be diagnosed by invasive methods using the gastric biopsied specimens or non-invasively by examining serum, urine, breath, or stool. Histological examination by Giemsa staining is usually recommended for the diagnosis, but it is difficult to visualize the bacterium when there is alow density of H.Pylori on the gastric mucosa with atrophic and metaplastic changes, Limitations of histological examination include increased false negative test findings due to various density of H. pylori at a different sites, high cost, long turn-around time, and inter observer variability. Therefore, in endemic countries like Egypt with s higher risk of chronic atrophic gastritis (CAG), intestinal metaplasia, and gastric cancer, noninvasive tests need to be added for a more reliable diagnosis of H.Pylori infection. Aim of the Work The aim of this study is to compare between the prevalence of chronic atrophic gastritis (CAG) and gastric corpus atrophy in Helicobacter pyloriseropositive subjects according to the stool antigen test, serum pepsinogen(PG) level and upper endoscopic findings. Patients and Methods The current study represents Cross- sectional study -Descriptive -Diagnostic study. This study had been carried at Ain Shams University and Abbasia fever hospital on 80 seropositive- patients attending to endoscopy ward for a regular check-up, All patients subjected to full history, clinical examination and investigation in the form of; complete blood count, serum antiH.Pylori immunoglobulin G (IgG), stool antigen test and serum pepsinogen. Results The current study showed that there was a significant difference between positive and negative H. pylori regarding pepsinogen I & II and endoscopic finding regarding CAG and CSG. Conclusion In conclusion, there is a link between positive stool H. pylori antigen test findings and a serum PG assay and upper endoscopic findings in seropositive subjects. Positive stool H. pylori antigen test findings are common in seropositive subjects with increased serum PG I levels indicating an ongoing H. pylori infection. Our study findings further suggest that, to reduce the infected subjects with H. pylori in their fecal material, seropositive subjects with increased gastric secreting ability need to be treated.

Autoimmune Gastritis Accompanied by a Schwannoma Presenting as a Subepithelial Tumor

Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.

Type A, Type B, and Non-atrophic Gastritis

The gastric cancer risk varies based on the etiology and severity of gastritis, which depends on a history of Helicobacter pylori infection and the secretory capacity of the stomach. Type A gastritis is associated with reverse atrophy of the corpus and type B with progressive atrophy extending from the antrum to the corpus. Diffuse or spotty redness in the corpus together with high serum pepsinogen (PG) II levels and a low PG I/II ratio are observed in patients with H. pylori infection when secretory capacity of the stomach is intact. Diffuse-type gastric cancer may develop near the gastric folds, which is a rare site of atrophy. Low serum PG I levels are associated with progressive gastric corpus atrophy and intestinal metaplasia in patients with chronic and previous H. pylori infections. This clinical scenario predisposes patients to intestinal-type gastric cancer, which originates in the atrophic and metaplastic gastric mucosa. Conversely, a high PG I/II ratio is observed in patients without H. pylori infection. Serum PG I levels and the PG I/II ratio are high in patients with acute H. pylori-negative gastritis, including drug-induced gastritis but are significantly low in autoimmune gastritis. Gastric neuroendocrine tumors may develop in patients with autoimmune gastritis or in those with long-term acid suppressant use. Fasting serum gastrin levels and the risk of neuroendocrine tumors are high in both cases. In this review, types of gastritis are summarized along with evaluation performed to determine the secretory capacity of the background gastric mucosa.

A.6 CSF1R-related adult-onset leukodystrophy with axonal spheroids and pigmented glia (ALSP) presenting as corticobasal syndrome (CBS): a case report and literature review

Background: Colony stimulating factor 1 receptor (CSF1R) mutations have various clinical, often overlapping, phenotypes. Methods: Case report and literature review. Results: We present a case of a previously independent 49-year-old woman with a 3-year history of early- and insidious-onset, rapidly progressive symptoms resembling CBS (parkinsonism, severe apraxia, global cognitive impairments, personality changes, depression, and functional decline). Brain MRI showed severe atrophy with frontoparietal predilection, asymmetric ex vacuo dilatation, atrophic corpus callosum, and patchy, asymmetric T2/FLAIR hyperintensities in the subcortical white matter. Spine MRI showed no cord signals. Brain MR spectroscopy revealed elevated choline with reduced N-acetyl-aspartate levels. The vasculitis screening, and leukodystrophy and CADASIL workups were all unremarkable. Finally, whole exome sequencing was done and a heterozygous variant of CSF1R (c.1735C>T, p.Arg579Trp) was found. Conclusions: Our patient’s novel CSF1R variant was found to be associated with ALSP. This report supports the utility of a comprehensive genetic testing in adult patients clinically presenting as CBS but with white matter abnormalities on T2-weighted MRI. Given that ALSP has several other clinical and radiologic mimickers, whole exome sequencing proves fundamental and can improve the diagnostic rates and understanding of ALSP. A well-informed diagnosis can lead to appropriate preventive genetic counseling to affected families.

Incidence and Predictors of Gastric Neoplastic Lesions in Corpus-Restricted Atrophic Gastritis: A Single-Center Cohort Study.

Corpus-restricted atrophic gastritis is a chronic inflammatory disorder leading to possible development of type 1 neuroendocrine tumors (T1gNET), intraepithelial neoplasia (IEN), and gastric cancer (GC). We aimed to assess occurrence and predictors of gastric neoplastic lesions in patients with corpus-restricted atrophic gastritis at long-term follow-up. A prospective single-center cohort of patients with corpus-restricted atrophic gastritis adhering to endoscopic-histological surveillance was considered. Follow-up gastroscopies were scheduled according to the management of epithelial precancerous conditions and lesions of the stomach guidelines. In case of new/worsening of known symptoms, gastroscopy was anticipated. Cox regression analyses and Kaplan-Meier survival curves were obtained. Two hundred seventy-five patients with corpus-restricted atrophic gastritis (72.0% female, median age 61 [23-84] years) were included. At a median follow-up of 5 (1-17) years, the annual incidence rate person-year was 0.5%, 0.6%, 2.8%, and 3.9% for GC/high-grade IEN, low-grade IEN, T1gNET, and all gastric neoplastic lesions, respectively. All patients showed at baseline operative link for gastritis assessment (OLGA)-2, except 2 low-grade (LG) IEN patients and 1 T1gNET patient with OLGA-1. Age older than 60 years (hazard ratio [HR] 4.7), intestinal metaplasia without pseudopyloric metaplasia (HR 4.3), and pernicious anemia (HR 4.3) were associated with higher risk for GC/HG-IEN or LG-IEN development and shorter mean survival time for progression (13.4, 13.2, and 11.1, respectively, vs 14.7 years, P = 0.01). Pernicious anemia was an independent risk factor for T1gNET (HR 2.2) and associated with a shorter mean survival time for progression (11.7 vs 13.6 years, P = 0.04) as well as severe corpus atrophy (12.8 vs 13.6 years, P = 0.03). Patients with corpus-restricted atrophic gastritis are at increased risk for GC and T1gNET despite low-risk OLGA scores, and those aged older than 60 years with corpus intestinal metaplasia or pernicious anemia seem to display a high-risk scenario.

Morphometric features of gastric mucosa in atrophic gastritis: A different pattern between corpus and antrum.

Atrophic gastritis can cause mucosa thinning, while detailed metrological evidence is lacking. We aimed to compare the morphological features of full-thickness gastric mucosa in antrum and corpus and evaluate the diagnostic performance for atrophy. Gastric cancer patients were prospectively enrolled (N = 401). Full-thickness gastric mucosa was obtained. Foveolar length, glandular length and musculus mucosae thickness were measured. Pathological assessment was conducted using the visual analogue scale of the updated Sydney system. Areas under the receiver operating characteristic curves (AUCs) were calculated for different atrophy degrees. In corpus mucosa, foveolar length and musculus mucosae thickness were positively correlated with the atrophy degree (spearman's correlation coefficient [rs] = 0.231 and 0.224, respectively, P < .05); glandular length and total mucosal thickness were negatively correlated (rs = -0.399 and -0.114, respectively, P < .05). Total mucosal thickness did not correlate with antral atrophy degree (P = .107). The AUCs of total mucosal thickness for corpus and antral atrophy were 0.570 (P < .05) and 0.592 (P < .05), respectively. The AUCs for corpus atrophy, moderate and severe, and severe atrophy were 0.570 (P < .05), 0.571 (P = .003), and 0.584 (P = .006), respectively. The corresponding AUCs for antral atrophy were 0.592 (P = .010), 0.548 (P = .140), and 0.521 (P = .533), respectively. The tendency for mucosal thickness to thin with atrophy occurred in the corpus rather than in the antrum. The diagnostic performance of corpus and antral mucosal thickness was limited for atrophy.

What’s Hidden Under the Gastric Intestinal Metaplasia? Diffuse-Type Adenocarcinoma Discovered by Targeted Biopsies: A Case-Report

Gastric corpus atrophy and intestinal metaplasia are two well established gastric precancerous conditions and scientific evidence shows a confidential relationship between this precancerous condition and intestinal type gastric cancer, according to Lauren classification. Differently, the background histological gastric mucosa characteristics from whom diffuse type gastric cancer may arise, need to be clarified. In this case, report we present a case of an 81-year-old female with corpus atrophic gastritis in whom we arrived at the diagnosis of diffuse type gastric cancer by following specific guidelines related to the characterization and the endoscopic-histological surveillance of gastric precancerous conditions.

Chronic atrophic gastritis in different ages in South China: a 10-year retrospective analysis

ObjectivesTo explore the prevalence, characteristics, age distribution and etiology changes of chronic atrophic gastritis (CAG) in South China.MethodsThis study included all patients who underwent endoscopy examinations from 2011 to 2020 in our hospital. Patients were divided into groups 1 (2011–2015) and 2 (2016–2020). The prevalence, characteristics, age distribution and etiology changes of CAG were compared between groups.ResultsOverall CAG prevalence was 20.92% (24,084/115,110) from 2011 to 2020; prevalence significantly differed between groups (18.78%, 8468/45,087, in group 1 and 22.30%, 15,616/70,023, in group 2). Patients with CAG had significantly younger age (under 45) and more corpus atrophy and more autoimmune atrophic gastritis (AAG) in group 2 than in group 1. AAG prevalence in group 2 was 30.11% (4702/15,616) significantly higher than 13.57% (1149/8468) in group 1. 82 patients with AAG later exhibited gastric cancer without obvious clinical features over the decade.ConclusionsCAG is increasing and seems starting earlier among people during the study period. We need to focus on diagnosis and treatment of corpus related atrophy and AAG, especially for the young. Laboratory examination, endoscopic biopsy and surveillance are important for CAG.

Novel Helicobacter pylori-associated hemolysis Hp0499 and Hp1490 and its association with severity of gastritis

Background: Gastritis is an inflammation of the stomach lining often caused by Helicobacter pylori infection. Among three H. pylori genes coding for hemolytic toxins, the clinical outcome of hp0499 and hp1490 is unclear. We conducted molecular and histological analyses to evaluate the correlation between these genes and gastritis severity. Methods: We analyzed the hp0499 and hp1490 variants of 116 Indonesian samples using next generation sequencing and validated them using polymerase chain reaction (PCR). The updated Sydney system was used to grade gastritis through histological analyses. We then calculated the influence of hp0499 and hp1490 on the gastritis severity, using multivariate analysis and cagA and vacA as major H. pylori virulence factors. Results: Two variants of each gene were identified and named hp0499-1 and -2, and hp1490-1 and -2. We noted that hp0499 expression was significantly correlated with corporal atrophy (p = 0.037). H. pylori hp1490 significantly correlated with antral acute and chronic inflammation as well as corporal density (p = 0.025, p = 0.07, p = 0.010, respectively). After adjusting for age and sex, we found that vacA s1m1 was an independent risk factor for acute antral inflammation (p = 0.032). hp1490 and vacA s1m1 were independent risk factors for chronic antral inflammation (p = 0.030 and p = 0.031, respectively). Conclusions: We identified the variants hp0499-1 and -2 and hp1490-1 and -2 and demonstrated that hp0499 plays a significant role in the severity of corporal atrophy. Moreover, hp1490 was characterized as an independent risk factor for chronic inflammation in the antral region. Therefore, hp0499 and hp1490 are new potential targets for therapeutics.

A clinical case of POL3A-associated hypomyelinating leukodystrophy with spinal cord lesion with a debut in early childhood

Leukodystrophies are a group of hereditary progressive diseases of the central nervous system characterized by selective lesions in white matter with specific involvement of glial cells. There are hypomyelinating (absence of myelin deposition), demyelinating (loss of previously deposited myelin), dysmyelinating (deposition of structurally or biochemically abnormal myelin), and myelinolytic leukodystrophies (myelin vacuolization). Hypomyelinating leukodystrophies (HL), like most leukodystrophies, debut in childhood or adolescence and are characterized by a progressive course of the disease. HL occurs as a result of impaired synthesis of proteins responsible for the development, structure, and integrity of the myelin sheath, involved in the processes of transcription and translation. In the latter group, the main role is assigned to HL associated with biallelic mutations in the genes of the RNA polymerase III transcription complex, POLR3: POLR3A, POLR3B, POLR1C, and POLR3K. The diagnosis can be confirmed by magnetic resonance imaging of the brain. POLR3A-associated HL is manifested by hypomyelination, hypodontia, and hypogonadotropic hypogonadism. The magnetic resonance features of POLR3-associated HL include diffuse hypomyelination with relative preservation of the dentate nuclei, anterolateral nuclei of the thalamus, globus pallidus, pyramidal tracts at the level of the posterior part of the internal capsules, and the corona radiata. In some cases, thinning of the corpus callosum and atrophy of the cerebellum were also noted. The article presents a clinical case of a patient with POL3A-associated HL with spinal cord injury with the debut in early childhood.

Pontocerebellar Hypoplasia Type 9: A New Case with a Novel Mutation and Review of Literature.

Pontocerebellar hypoplasia type 9 (PCH-9) is a very rare autosomal recessive neurodegenerative disorder. Affected infants present early with severe developmental delay, spasticity, with the unique magnetic resonance imaging picture of thin corpus callosum, atrophied pons, and cerebellum. It is caused by loss of function mutations in the AMPD2 gene, encoding for the adenosine monophosphate deaminase enzyme-paralog 2. This gene is expressed in different somatic tissues with high level of expression in cerebellum and its encoded enzyme catalyzes a critical step in de novo biosynthesis of purines and its deficiency in the developing neurons severely affects neuronal differentiation and cell viability. We clinically evaluated an Emirati patient presented with severe developmental and growth delay, as well as corpus callosum agenesis and atrophy of brainstem and cerebellum. We performed exome sequencing, Sanger sequencing, and segregation analysis to identify the genetic cause of the phenotype, followed by in silico and in vitro analysis. We identified the novel variant (NM_004037.9:c.1471G > A) in AMPD2 gene leading to a single amino acid substitution (p.Gly491Arg) in adenosine monophosphate deaminase-2 enzyme. This variant is predicted to be pathogenic using several in silico tools, and resulted in a decrease in the enzyme function in the patient's polymorphonuclear cells by 82% (95% confidence interval: 73.3-91.7%, p = 0.029) compared with the control. This data establishes that the affected child is affected by PCH-9. Furthermore, we review all reported cases in literature to summarize the main clinical features of this rare disease.

Increase of Deep Intraepithelial Lymphocytes in the Oxyntic Mucosa of Patients With Potential and Overt Autoimmune Gastritis.

Pathological correlates of potential autoimmune gastritis (AIG), defined by anti-parietal cell antibody (PCA) positivity in the absence of gastric atrophy, have never been described. We herein aimed to assess intraepithelial lymphocyte (IEL) infiltration in gastric corpus of AIG patients. From 2000 to 2021, among 53 potential AIG patients, we focused on nine (median age 61 years, IQR 53-82; four females) who subsequently developed overt AIG. IEL infiltration of the oxyntic mucosa was assessed before and after developing overt AIG by measuring deep and superficial CD3+ IEL. AIG patients with different degrees of corpus atrophy, healthy controls (HC), active H. pylori gastritis, celiac disease (CD), and Hashimoto’s thyroiditis patients were included as controls. Of note, deep, but not superficial, CD3+ IEL count was higher (p<0.001) in potential AIG compared to HC and H. pylori gastritis. Deep CD3+ IEL infiltration did not change before or after the evolution into atrophy (median 9.6, IQR 8.8-12.4, vs 11.3, IQR 9.4-12.9). No difference was found in deep CD3+ IEL infiltration among potential, mild, and severe AIG, and compared to Hashimoto’s thyroiditis or CD. A deep CD3+ IEL cut-off of >7/100 epithelial cells allowed discrimination of any AIG stage and severity (AUC=0.842). We conclude that an increased deep CD3+ IEL infiltration of the oxyntic mucosa could represent a marker of potential AIG. Prospective studies including a larger number of potential AIG patients are needed.

Serum Assay Findings after Successful Helicobacter pylori Eradication

Serum pepsinogen (PG), anti-Helicobacter pylori (H. pylori) immunoglobulin G (IgG), and gastrin-17 (G-17) are plasma biomarkers for gastritis. H. pylori serology titers and PG levels increase during active H. pylori infection; moreover, elevated PG II levels indicate a high risk for diffuse-type gastric cancer in East Asian populations. Serum PG I/II ratios and PG I levels decrease with the progression of gastric corpus atrophy; thus, a combination of serum PG I levels ≤70 ng/mL and a PG I/II ratio ≤3 (serologic atrophy) indicates a high risk of intestinal-type gastric cancer. Serum G-17 is often not used as an indicator in H. pylori-seroprevalent populations because it is usually elevated in subjects with H. pylori infections. When H. pylori is eradicated, most patients show a rapid decrease in serum PG II levels and anti-H. pylori IgG titers within a few months. Seroreversion is required for several months to years after regression of H. pylori. Moreover, seroreversion may not always be achieved in all eradicated cases. The serum PG I/II ratio starts to increase after eradication; therefore, serologic atrophy improves accordingly, unless severe atrophy is present. Thus, some eradicated patients may show normal serum assay findings but have a higher risk for developing gastric cancer than H. pylori-naive subjects. Furthermore, serum PG levels decrease after gastrectomy and increase with the intake of certain drugs (e.g., aspirin or acid suppressants) or in renal failure patients. Due to such wide variations, serum assays are inadequate for the confirmation of H. pylori eradication. It is useful when interpreted with gastroscopy and other H. pylori test findings.

Are all the polyps in the stomach the same?

The article presents a clinical case of a 38-year-old patient with revealed polyps of the stomach body and iron deficiency anemia on the background of chronic atrophic gastritis. On the example of this observation, variants of the course were demonstrated, including endoscopic and histological manifestations of autoimmune (atrophic corpus) gastritis (AIG). In parallel, the issues of diagnosis and management of patients with the most common polyps in the stomach are discussed. The problem of timely diagnosis of AIG and the advantages of non-invasive methods for assessing the functional state of the stomach is also being actualized.

Pseudopyloric Metaplasia Is Not Associated With the Development of Gastric Cancer.

Corpus atrophic gastritis (CAG) is associated with intestinal metaplasia (IM) and pseudopyloric metaplasia (PPM). Prospective data on corpus mucosa PPM and its link to the development of gastric cancer (GC) are lacking. This study aimed to investigate the relationship between the presence of corpus mucosa PPM at baseline and the development of GC at follow-up in patients with CAG. A longitudinal cohort study was conducted on patients with consecutive CAG adhering to endoscopic-histological surveillance. Patients were stratified for the presence/absence of corpus PPM without concomitant corpus IM at baseline, and the occurrence of gastric neoplastic lesions at the longest available follow-up was assessed. A total of 292 patients with CAG with a follow-up of 4.2 (3-17) years were included. At baseline, corpus PPM without corpus IM was diagnosed in 62 patients (21.2%). At the follow-up, GC was detected in 5 patients (1.7%) and gastric dysplasia (GD) in 4 patients (1.4%). In all these 9 patients with GC/GD at the follow-up, corpus IM was present at baseline and follow-up. Age <50 years (odds ratio [OR] 2.5), absence of pernicious anemia (OR 4.3), and absence of severe corpus atrophy (OR 2.3) were associated with corpus PPM without corpus IM. At the 4.2-year follow-up, in patients with CAG characterized at baseline with corpus PPM without corpus IM, GC or GD was not observed because these lesions were consistently associated with corpus IM. Corpus PPM without corpus IM was associated with younger age, absence of pernicious anemia, and severe corpus atrophy, suggesting a lower stage of disease progression. Corpus PPM alone seems not to be associated with GC, whose development seems to require the presence of corpus IM as a necessary step.