Atrophic Body Gastritis Research Articles

Ghrelin- and preproghrelin-immunoreactive cells in atrophic body gastritis

INTRODUCTION: Ghrelin is a 28 amino acid peptide mainly secreted by endocrine cells of the gastric mucosa, which is believed to have a modulating effect on cell growth. OBJECTIVE: To assess the presence of ghrelin and its precursor preproghrelin molecule in endocrine hyperplasias associated with atrophic body gastritis (ABG). MATERIAL AND METHODS: Endoscopic biopsies from 54 patients with ABG were processed for immunohistochemistry and specific antibodies against ghrelin, preproghrelin and chromogranin were applied. We assessed the immunoreactive cells in endocrine hyperplasia from the atrophic mucosa and intestinal and pseudo-antral metaplasia areas. RESULTS: There was ghrelin expression in a variable number of hyperplastic endocrine cells from all patients studied. There was a statistically significant difference in the number of hyperplastic nodules with more than 50% immunostained cells for chromogranin and ghrelin and for chromogranin and preproghrelin. The mean number of hyperplastic nodules identified by chromogranin was 8.6 per patient. Most nodules were immunoreactive to ghrelin and preproghrelin. The presence of ghrelin and preproghrelin expression was uncommon in glands showing intestinal metaplasia: four (9.5%) and nine (21.4%) cases, respectively. In contrast, they were relatively frequent in pseudo-antral metaplasia areas: 37 (72.5%) and 26 (50.9%) cases, respectively. CONCLUSION: Ghrelin- and preproghrelin-immunoreactive cells are frequently present in endocrine hyperplasias associated with ABG. However, further studies are required to determine to what extent these hormones act as modulators of hyperplastic nodular growth and evolution.

Diagnosis and Management of Pernicious Anemia

Pernicious anemia is a macrocytic anemia due to cobalamin deficiency, which is the result of intrinsic factor deficiency. Pernicious anemia is associated with atrophic body gastritis, whose diagnostic criteria are based on the histologic evidence of gastric body atrophy associated with hypochlorhydria. Serological markers suggesting the presence of oxyntic mucosa damage are increased levels of fasting gastrin and decreased levels of Pepsinogen I. Without the now obsolete Schilling's test, intrinsic factor deficiency may not be proven, and gastric intrinsic factor output after pentagastric stimulation has been proposed. Intrinsic factor autoantibodies are useful surrogate markers of pernicious anemia. The management of patients with pernicious anemia should focus on the life-long replacement treatment with cobalamin and the monitoring to early diagnose an eventual onset of iron deficiency. Moreover, these patients should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.

Type I Gastric Carcinoids: A Prospective Study on Endoscopic Management and Recurrence Rate

Background: Type I gastric carcinoids (TIGCs) are neuroendocrine neoplasms arising from enterochromaffin-like cells in atrophic body gastritis. Data regarding their evolution in prospective series are scarce, thus treatment and follow-up are not codified. Our aim was to evaluate clinical outcome and recurrence in TIGCs managed by endoscopic approach. Methods: 33 patients (24 females; median age 65 years, range 23–81) were included and managed through endoscopic follow-up every 6–12 months, with lesion removal and multiple gastric biopsies. Baseline clinical and histological features were analyzed as risk factors by Cox regression. Results: At diagnosis, 7 tumors were intramucosal carcinoids and 26 were polyps (median diameter 5 mm, range 2–20), multiple in 17 patients. Associated severe atrophy was present in 21 cases (63.6%), while mild atrophy was found in 6 cases (18.2%). During a 46-month median follow-up, survival was 100% and no metastases occurred. One patient developed a less-differentiated carcinoid that was radically treated by surgery. 21 patients (63.6%) had recurrence after a median of 8 months, 14 of these (66.6%) had a second recurrence after a median of 8 months following the previous carcinoid removal. Median recurrence-free survival was 24 months. Neither clinical nor biochemical recurrence-predicting factors were found. Conclusions: Although about 60% of TIGCs had recurrence after endoscopic resection, endoscopic management may be considered safe and effective.

Type I Gastric Carcinoids: A Prospective Study on Endoscopic Management and Recurrence Rate

Background: Type I gastric carcinoids (TIGCs) are neuroendocrine neoplasms arising from enterochromaffin-like cells in atrophic body gastritis. Data regarding their evolution in prospective series are scarce, thus treatment and follow-up are not codified. Our aim was to evaluate clinical outcome and recurrence in TIGCs managed by endoscopic approach. Methods: 33 patients (24 females; median age 65 years, range 23–81) were included and managed through endoscopic follow-up every 6–12 months, with lesion removal and multiple gastric biopsies. Baseline clinical and histological features were analyzed as risk factors by Cox regression. Results: At diagnosis, 7 tumors were intramucosal carcinoids and 26 were polyps (median diameter 5 mm, range 2–20), multiple in 17 patients. Associated severe atrophy was present in 21 cases (63.6%), while mild atrophy was found in 6 cases (18.2%). During a 46-month median follow-up, survival was 100% and no metastases occurred. One patient developed a less-differentiated carcinoid that was radically treated by surgery. 21 patients (63.6%) had recurrence after a median of 8 months, 14 of these (66.6%) had a second recurrence after a median of 8 months following the previous carcinoid removal. Median recurrence-free survival was 24 months. Neither clinical nor biochemical recurrence-predicting factors were found. Conclusions: Although about 60% of TIGCs had recurrence after endoscopic resection, endoscopic management may be considered safe and effective.

Reversal of atrophic body gastritis after H. pylori eradication at long-term follow-up

Background The effect of Helicobacter pylori treatment on the potential reversal of atrophic body gastritis (ABG) is controversial. Body atrophy reversal was evaluated in a cohort of H. pylori-negative and treated H. pylori-positive ABG patients. Methods Observational long-term follow-up cohort study including 300 ABG patients with at least one follow-up gastroscopy with three biopsies from the antrum and three from the body performed no earlier than 1 year after diagnosis was included. H. pylori was diagnosed by Giemsa-stain and serology. H. pylori-positive patients ( n = 192) were treated with bismuth-based triple regimen. Results After a mean follow-up of 5.2 years, body atrophy reversal was observed in 42/300 patients (14%). Body atrophy reversal occurred more frequently in patients treated for H. pylori than in H. pylori-negative ones (21.3% vs 0.9%, p < 0.00001) and was observed between 2 and 8 years after treatment in 52% of cases. Predictive factors for body atrophy reversal at Cox-regression analysis were mild atrophy (HR 2.14; 95% CI 1.12–4.1), moderate–severe inflammation (HR 5.3; 95% CI 1.64–17.3), and absence of intestinal metaplasia (HR 2.4; 95% CI 1.2–4.8). Conclusion Body atrophy reversal was observed in about 20% of ABG patients treated for H. pylori infection, and about 50% of reversals occurred during long-term follow-up.

Immunoproteomics of Helicobacter pylori infection in patients with atrophic body gastritis, a predisposing condition for gastric cancer

Atrophic body gastritis is considered an outcome of H. pylori infection at high risk for gastric cancer. Immunoproteomics has been used to detect H. pylori antigens, which may act as potential markers for neoplastic disease and may be used in specific serological tests. We used immunoproteome technology to identify H. pylori antigens, recognized by sera from patients with atrophic body gastritis. Here, we performed 2DE protein maps of H. pylori strain 10K, probed against single sera from 3 groups of H. pylori-positive patients (atrophic body gastritis; intestinal-type gastric cancer; peptic ulcer) and negative controls. Immunoreactive spots were identified by MALDI-TOF–MS. A total of 155 immunoreactive spots were detected corresponding to 14.1% of total spots detected in our reference map of H. pylori strain 10K. Sera from atrophic body gastritis (40.5 ± 2%) and gastric cancer patients (25.9 ± 1.8%) showed a significantly higher and stronger mean immunoreactivity versus H. pylori antigens compared to peptic ulcer patients (11.2 ± 1.3%). The average intensity of immunoreactivity of sera from atrophic body gastritis and gastric cancer patients was significantly stronger compared to peptic ulcer patients. Sera from atrophic body gastritis and gastric cancer patients differentially recognized 17 H. pylori spots. Immunoproteome technology may discriminate between different H. pylori-related disease phenotypes showing a serological immunorecognition pattern common to patients with gastric cancer and atrophic body gastritis, its precursor condition. This tool may be promising for developing specific serological tests to identify patients with gastritis at high risk for gastric cancer, to be evaluated in prospective investigations.

Ghrelin and pre-proghrelin immunoreactive cells in gastric neuroendocrine tumors associated with atrophic body gastritis

INTRODUCTION: Ghrelin is a 28 amino acid peptide secreted mainly by endocrine cells present in the gastric mucosa and acknowledged as an endogenous releaser of growth hormone. The immunohistochemical expression of ghrelin has been described in neuroendocrine tumors, and it is believed that may exert modulating action related to the growth of these tumors. OBJECTIVE: To study the presence of ghrelin and preproghrelin immunoreactive cells in gastric neuroendocrine tumors associated with atrophic body gastritis. METHODS: Endoscopic biopsies from 15 patients with neuroendocrine tumor of the gastric mucosa associated with atrophic body gastritis were performed for immunohistochemistry, and specific chromogranin, ghrelin and preproghrelin antibodies were applied. The immunohistochemical expression was assessed in tumor cells and endocrine micronodular hyperplasia present in mucosa adjacent to the tumor, and it was classified in relation to the number of stained cells. RESULTS: Chromogranin was positive in 14 out of 15 tumors. Ghrelin and preproghrelin immunoreactive cells were detected in 11 (73%) and 13 (87%) tumors, respectively. There was a significant correlation between the immunohistochemical results of both antigen expressions (kappa = 81%). Ghrelin and preproghrelin expression was detected in hyperplastic nodules present in the mucosa adjacent to the tumor in seven and eight cases, respectively. There was no correlation between these results and those observed in neoplastic cells. CONCLUSION: Ghrelin and preproghrelin immunoreactive cells may be found in variable number in Type I neuroendocrine gastric tumors and in hyperplastic nodules associated with these tumors. However, it remains unclear what role these peptides play on the development of these tumors.

Type 1 gastric carcinoids: Efficacy and safety of endoscopic management.

e14577 Background: Type I gastric carcinoids (TIGC) are “rare” neuroendocrine neoplasms arising from ECL cells in the background of atrophic body gastritis, due to gastrin growth effects. Diagnosis is often accidental, as patients may be asymptomatic, and these tumors are usually indolent. Data regarding their evolution in prospective series are scanty, and thus treatment and follow-up programs are not codified. Our aim was to assess clinical outcome and recurrence in a series of TIGC patients managed by endoscopic approach. Methods: We enrolled in this prospective study consecutive patients with TIGC (diagnosis of gastric well-differentiated endocrine tumor associated with atrophic body gastritis) who had at least one gastroscopy after the first diagnosis. Exclusion criteria were treatments other than endoscopical resection (polypectomy or mucosectomy). Results: 33 patients (24 females), median age 65 (23-81), 75.7% with anemia (40% pernicious). 7 tumors (22.2%) were microcarcinoids, 26 polyps (median diameter: 5 mm; 2-20) multiple in 17 (65.4%) patients. Associated severe atrophy in 21 cases (63.6%), mild in 18.2%. During 46-month median follow-up, survival was 100% and no local/distant invasion occurred. 21 patients (63.6%) had recurrence after a median of 8 months, 12 of these (57.1%) had second recurrence after a median of 7 months from previous TIGC removal. Median recurrence-free survival was 15 months. Nor clinical neither biochemical factors predicting for recurrence were found. Conclusions: Although about 60% of TIGC patients underwent recurrence after endoscopic resection, no tumor progression was observed during follow-up. In patients with TIGC, endoscopic management may be considered safe and effective, while radiological stadiation is not mandatory. No significant financial relationships to disclose.

Helicobacter pylori immunoproteomics in gastric cancer and gastritis of the carcinoma phenotype

Helicobacter pylori infection is linked to the development of gastric cancer. Atrophic body gastritis is considered the first important step in the histogenesis of such neoplasia. H. pylori infection is involved in the induction of atrophic body gastritis, but documentation of H. pylori infection is difficult because of the progressive disappearance of the bacterium. Host–pathogen interactions may be investigated by means of immunoproteomics, which provides global information regarding the host humoral response to H. pylori infection and allows the identification of relevant specific and nonspecific antigens, and can be used for diagnostic or prognostic purposes. In the present review, we describe how several research groups used H. pylori immunoproteomics to investigate highly immunoreactive bacterial antigens related to the development of gastric cancer.

Reassessment of Intrinsic Factor and Parietal Cell Autoantibodies in Atrophic Gastritis With Respect to Cobalamin Deficiency

Atrophic body gastritis (ABG) is an autoimmune condition eventually manifesting itself as pernicious anemia (PA). Parietal cell autoantibodies (PCAs) and intrinsic factor autoantibodies (IFAs) are considered characteristics of these conditions. Recent studies on IFA and PCA frequency with respect to cobalamin deficiency in biopsy-proven ABG patients are lacking. We addressed this issue using new enzyme-linked immunosorbent assay (ELISA)-based assays. Sera from 165 patients with histologically diagnosed ABG and 113 controls were tested for IFA and PCA using ELISA. A total of 81 ABG patients had cobalamin deficiency and macrocytic anemia (Group 1-PA), 36 had cobalamin deficiency without macrocytic anemia (Group 2), and 48 had normal cobalamin levels (Group 3). IFAs were detected in 44/165 ABG patients (27% sensitivity) and in 0/113 controls (100% specificity). PCAs were detected in 134 ABG patients (81% sensitivity) and in 11 controls (90% specificity). In Group 1, IFAs showed 37% sensitivity and 100% specificity, whereas PCAs showed 81% sensitivity and 90% specificity. Combining IFA and PCA testing increased the sensitivity to 61% in all ABG patients and to 73% in Group 1, while maintaining 100% specificity. IFAs are 100% specific for biopsy-proven ABG and occurred in 27% of patients. PCAs occurred in 81% of ABG patients and in 10% of controls. Combining IFA and PCA testing significantly increases their diagnostic performance for ABG and PA, yielding a 73% sensitivity for PA. The non-invasive combined PCA and IFA assessment may be useful in selecting patients at risk for autoimmune gastritis to be confirmed by gastroscopic-histologic examination.

M1060 Regression of Atrophy in Patients with Atrophic Body Gastritis Following Helicobacter pylori Treatment: Occurrence and Predictor Factors

M1060 Regression of Atrophy in Patients with Atrophic Body Gastritis Following Helicobacter pylori Treatment: Occurrence and Predictor Factors

Endoscopic Management of Type I Gastric Carcinoid and Recurrence Rate

Background: Type I gastric carcinoids (TIGC) are “rare” neuroendocrine neoplasms arising from ECL cells in the background of atrophic body gastritis, due to gastrin growth effects. Diagnosis is often accidental, as patients may be asymptomatic, and these tumors are usually benign. Data regarding the evolution of TIGC in prospective series are scanty, and thus treatment and follow-up programs are not codified. Aim: To assess the safety of a conservative management of TIGC patients, and their recurrence rate after endoscopic removal. Materials and Methods: We enrolled in this prospective study consecutive patients with TIGC (diagnosis of gastric well-differentiated neuroendocrine tumor associated with atrophic body gastritis) who had at least one gastroscopy after the first diagnosis. Exclusion criteria were treatments other than endoscopical resection (polypectomy or mucosectomy). Results: 29 patients (69% females), median age 65 (23-81), median fasting gastrin 625 pg/ml (43,6-2800; nv<40 pg/ml). 68% had dyspepsia, 76% had anaemia (45% pernicious anaemia). 21 patients (72%) had polypoid carcinoids (median diameter: 6 mm; 2-20) and 8 (28%) had intramucosal carcinoid. Multiple polypoid lesions in 13 patients (45%). Associated severe atrophy in 19 cases (65%), but also mild atrophy in 14%. Median follow-up was 43 months (3-99). No patients died and of the 26 patients who had at least 1 CT-scan or MRI, none had evidence of either local or distant invasion/metastasis. A median of 5 endoscopies performed per patient (2-9) after diagnosis. The recurrence rate of TIGC was 55% (16/29). The median time of first recurrence was 6 (3-54) months from diagnosis; all the patients with recurrence had polyps, 50% multiple. A second recurrence occurred in 10/29 patients (34,5%), after a median of 14,5 (5-51) months from diagnosis and 7 (2-19) from previous carcinoid removal. Neither demographics, biochemical (gastrin, chromogranin-A values)or histological features could distinguish between the 16 recurrent and the 13 non-recurrent patients. Conclusions: TIGC is a benign condition despite the high recurrence rate. Endoscopic polyp removal and subsequent follow-up with is safe and is recommended in the first three years after diagnosis, while radiological evaluation is not necessary.

Pernicious anemia: New insights from a gastroenterological point of view

Pernicious anemia (PA) is a macrocytic anemia that is caused by vitamin B(12) deficiency, as a result of intrinsic factor deficiency. PA is associated with atrophic body gastritis (ABG), whose diagnosis is based on histological confirmation of gastric body atrophy. Serological markers that suggest oxyntic mucosa damage are increased fasting gastrin and decreased pepsinogen I. Without performing Schilling's test, intrinsic factor deficiency may not be proven, and intrinsic factor and parietal cell antibodies are useful surrogate markers of PA, with 73% sensitivity and 100% specificity. PA is mainly considered a disease of the elderly, but younger patients represent about 15% of patients. PA patients may seek medical advice due to symptoms related to anemia, such as weakness and asthenia. Less commonly, the disease is suspected to be caused by dyspepsia. PA is frequently associated with autoimmune thyroid disease (40%) and other autoimmune disorders, such as diabetes mellitus (10%), as part of the autoimmune polyendocrine syndrome. PA is the end-stage of ABG. Long-standing Helicobacter pylori infection probably plays a role in many patients with PA, in whom the active infectious process has been gradually replaced by an autoimmune disease that terminates in a burned-out infection and the irreversible destruction of the gastric body mucosa. Human leucocyte antigen-DR genotypes suggest a role for genetic susceptibility in PA. PA patients should be managed by cobalamin replacement treatment and monitoring for onset of iron deficiency. Moreover, they should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.

T1077 Occurrence of Intrinsic Factor and Parietal Cell Autoantibodies in Atrophic Body Gastritis Patients with or Without Pernicious Anemia

T1077 Occurrence of Intrinsic Factor and Parietal Cell Autoantibodies in Atrophic Body Gastritis Patients with or Without Pernicious Anemia

Occurrence and Risk Factors for Autoimmune Thyroid Disease in Patients with Atrophic Body Gastritis

Purpose To investigate the occurrence of and risk factors for autoimmune thyroid disease in atrophic body gastritis patients. Methods Cross-sectional study on 401 consecutive outpatients with atrophic body gastritis. Diagnostic work-up of thyroid disease was completed in 319 atrophic body gastritis patients (225 women, median age 55.5 years [range 17-95 years]). Data on anagraphics, lifestyle, family history, and biochemical and histological items were obtained at baseline, and associations between atrophic body gastritis and autoimmune and nonautoimmune thyroid diseases were explored through descriptive statistics and logistic regression analyses. Results Of the 319 atrophic body gastritis patients, 169 (53%) had an associated thyroid disorder, and 89 (52.7%) of these were unaware of it. The thyroid disease was autoimmune in 128 patients (75.7%) and nonautoimmune in 41 patients. Logistic regression showed that risk factors for having autoimmune thyroid disease in atrophic body gastritis patients were female sex (odds ratio [OR] 5.6, 95% confidence interval [CI], 2.6-12.1), presence of parietal cell antibodies (OR 2.5, 95% CI, 1.1-5.5), and presence of metaplastic atrophy (OR 2.2, 95% CI, 1.0-5.0). Conclusions Autoimmune thyroid disease and atrophic body gastritis occur in a closely linked fashion, suggesting that atrophic body gastritis patients should be investigated for an occult autoimmune thyroid disease, in particular women and those with positive parietal cell antibodies.

Artificial neural networks in the recognition of the presence of thyroid disease in patients with atrophic body gastritis

To investigate the role of artificial neural networks in predicting the presence of thyroid disease in atrophic body gastritis patients. A dataset of 29 input variables of 253 atrophic body gastritis patients was applied to artificial neural networks (ANNs) using a data optimisation procedure (standard ANNs, T&T-IS protocol, TWIST protocol). The target variable was the presence of thyroid disease. Standard ANNs obtained a mean accuracy of 64.4% with a sensitivity of 69% and a specificity of 59.8% in recognizing atrophic body gastritis patients with thyroid disease. The optimization procedures (T&T-IS and TWIST protocol) improved the performance of the recognition task yielding a mean accuracy, sensitivity and specificity of 74.7% and 75.8%, 78.8% and 81.8%, and 70.5% and 69.9%, respectively. The increase of sensitivity of the TWIST protocol was statistically significant compared to T&T-IS. This study suggests that artificial neural networks may be taken into consideration as a potential clinical decision-support tool for identifying ABG patients at risk for harbouring an unknown thyroid disease and thus requiring diagnostic work-up of their thyroid status.

Relation of atrophic gastritis with Helicobacter pylori -CagA+ and interleukin-1 gene polymorphisms

To determine the association of Helicobacter pylori (H pylori) CagA(+) infection and pro-inflammatory polymorphisms of the genes interleukin (IL)-1RN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay (ELISA). Infection with H pylori CagA(+) was determined by serology and polymerase chain reaction (PCR). IL-1B and IL-1RN polymorphisms genotyping was performed by PCR-restriction fragment length polymorphism (PCR-RFLP) and PCR respectively. In this dyspeptic population, 86% were H pylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis (AAG) was associated with CagA(+) status [odd ratio (OR) = 4.1; P < 0.000] and fruit consumption (OR = 0.3; P < 0.00). Atrophic body gastritis (ABG) was associated with pepsinogen PGI/PGII < 3.4 (OR = 4.9; P < 0.04) and alcohol consumption (OR = 7.3; P < 0.02). Duodenal ulcer was associated with CagA(+) (OR = 2.9; P < 0.04) and smoking (OR = 2.4; P < 0.04). PGI < 60 microg/L as well as PGI/PGII < 3.4 were associated with CagA(+). In a dyspeptic population in Costa Rica, H pylori CagA(+) is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine polymorphisms IL-1B + 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.

La maladie de Biermer : une cause possible d’anémie microcytaire chez l’adolescent

A teenager was admitted with an iron-deficiency anemia. The gastroscopy found an atrophic body gastritis, which revealed a pernicious anemia. This diagnosis is rare in paediatric patients, the frequency of pernicious anemia increasing with age. Iron-deficiency anemia is mainly described in young people.

Is interleukin‐1 genotyping useful for the clinical management of patients with atrophic body gastritis?

Atrophic body gastritis patients are at increased risk for gastric cancer. IL-1B/IL-1RN polymorphisms have been associated with gastric cancer susceptibility. The relationship between these polymorphisms and the long-term outcome of atrophic body gastritis patients is not known. To investigate whether the genotyping of IL-1B-511/IL-1RN polymorphisms is useful to characterize atrophic body gastritis patients at increased risk for gastric neoplasms. IL-1B-511/IL-1RN polymorphisms were compared between 110 atrophic body gastritis patients and 110 age- and gender-matched controls, and patients were followed up (median 4.1 years) according to a cohort study design. Genotype frequencies of IL-1B-511/IL-1RN were similar between patients and controls. Atrophic body gastritis patients harbouring the wild type of IL-1B-511/IL-1RN polymorphisms were not different from those harbouring the proinflammatory pattern as far as regards gender, age, gastric cancer family history and metaplastic atrophy. Sixteen atrophic body gastritis patients developed a gastric neoplastic lesion at follow-up: eight were IL-1B-511-T carriers and eight were IL-1RN-allele-2 carriers. Harbouring the proinflammatory genotypes was not significantly associated with developing gastric neoplastic lesions. In atrophic body gastritis patients, IL-1B-511 and IL-1RN polymorphisms do not appear to be associated either with specific clinical, biochemical or histological features or with the development of gastric neoplastic lesions at long-term follow-up.

Serum Ghrelin as a Marker of Atrophic Body Gastritis in Patients with Parietal Cell Antibodies

Autoimmune gastritis is frequently associated with autoimmune thyroiditis and other organ-specific autoimmune diseases, and may lead to atrophic body gastritis (ABG). We studied the diagnostic use of the measurement of serum ghrelin compared with other markers of gastric damage in predicting the presence of ABG in patients with autoimmune gastritis. We studied 233 patients with autoimmune gastritis and 211 control subjects. All patients and control subjects were screened for circulating parietal cell antibodies (PCAs) and were tested for serum ghrelin, gastrin, pepsinogen I and II, and anti-Helicobacter pylori antibody levels. A total of 52 patients and 28 control subjects underwent a gastric endoscopy. In PCA/positive patients, mean (+/-sd) serum ghrelin levels were significantly lower (238 +/- 107 pmol/liter), and mean (+/-sd) serum gastrin levels were significantly higher (81.2 +/- 128.3 ng/ml), with respect to PCA/negative patients (282 +/- 104 pmol/liter and 20.7 +/- 13.3 ng/ml, respectively; P < 0.0001). Serum ghrelin and gastrin levels were inversely correlated (P = 0.004). A total of 40 patients had ABG documented by the gastric biopsy (90% in PCA/positive patients and 10% in PCA/negative patients). The receiver operating characteristic curve analysis revealed that a cutoff value for serum ghrelin of 188 pmol/liter was associated with the highest sensitivity and specificity (97.3 and 100%, respectively) in detecting gastric atrophy and was superior to gastrin (P = 0.012), PCA (P = 0.002), and the pepsinogen I/II ratio (P = 0.016) measurements. Our study demonstrates that ghrelin secretion is negatively affected by autoimmune gastritis, and its serum level represents the most sensitive and specific noninvasive marker for selecting patients at high risk for ABG.