Low Serum Pepsinogen Research Articles

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.

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.

Low serum pepsinogen II levels are closely linked with a risk of metabolic syndrome among healthy individuals with asymptomatic Helicobacter pylori infection: a cross-sectional study.

Aim:Helicobacter pylori (Hp) infection has a connection with metabolic syndrome (MetS). Pepsinogen II (PGII) is a marker for gastric epithelial function. The present research was aimed at determining the associations among serum PGII levels, Hp infection and MetS in healthy subjects. Methods: This cross-sectional study enrolled 1242 healthy people, including 545 subjects with asymptomatic Hp infection and 697 subjects without Hp infection. Based on the number of MetS components present, subjects with Hp infection were assigned to the following groups: group 1, no component (126 subjects); group 2, one or two components (260 subjects); and group 3, three or more components (159 subjects). Physical measurements and biochemical indices were recorded. Serum PGII levels were recorded using ELISA. SPSS and GraphPad Prism were used for statistical analyses. Results: Among subjects with Hp infection, serum PGII was evidently downregulated in group 3 compared with group 1 (14.95±8.24 vs 17.97±9.08μg/l; p=0.015). Serum PGII levels were correlated with an increased risk of MetS (odds ratio: 0.867; 95% CI: 0.772-0.974; p=0.016), as indicated by the multivariate logistic regression analysis. Grouping subjects with Hp infection according to quartiles of serum PGII levels identified an evident difference in MetS prevalence among the four quartile-based groups (p=0.047). Conclusions: Among healthy subjects with asymptomatic Hp infection, serum PGII levels were lower in those with MetS than in those without MetS. Serum PGII levels showed an independent and negative correlation with the risk of MetS in healthy subjects with Hp infection.

Five Autoimmune Gastritis Patients with Positive Findings of Serum Anti-parietal Cell Antibodies

Autoimmune gastritis is a corpus-dominant type of gastritis with positive serum anti-parietal cell antibodies (APCA) and/or anti-intrinsic factor antibodies. Serum APCA and pepsinogen (PG) assays were performed in subjects with corpus-dominant gastritis detected by endoscopy. Serum APCA was positive in five patients. All these patients were postmenopausal women (four Koreans and one Caucasian from the Russian Federation) with a mean age of 59.0±3.2 years. They displayed low PG I levels ranging from 8.1 to 18.8 ng/mL (mean, 11.4±4.8 ng/mL) and low PG I/II ratios ranging from 0.7 to 2.4 (mean, 1.2±0.7). Three of the patients were being treated for autoimmune thyroiditis. Multiple gastric neuroendocrine tumors were observed in two Helicobacter pylori (H. pylori)-naive patients with high serum gastrin levels exceeding 700 pg/mL and serum chromogranin A levels exceeding 1,000 ng/mL. In the remaining three patients, intestinal metaplasia was observed in the biopsied specimens from the antrum, suggesting a history of H. pylori infection. Our findings indicate the value of positive serum APCA findings, low serum PG I levels, and low serum PG I/II ratios in confirming autoimmune gastritis in patients showing corpus-dominant atrophy, regardless of their H. pylori infection status.

Gastric Cancer Screening in Common Variable Immunodeficiency.

Individuals with common variable immunodeficiency (CVID) have an increased risk of gastric cancer, and gastrointestinal lymphoma, yet screening for premalignant gastric lesions is rarely offered routinely to these patients. Proposed screening protocols are not widely accepted and are based on gastric cancer risk factors that are not applicable to all CVID patients. Fifty-two CVID patients were recruited for screening gastroscopy irrespective of symptoms or blood results and were compared to 40 controls presenting for gastroscopy for other clinical indications. Overall, 34% of CVID patients had intestinal metaplasia (IM), atrophic gastritis or moderate to severe non-atrophic gastritis, which can increase the risk of gastric cancer, compared to 7.5% of controls (p< 0.01). Focal nodular lymphoid hyperplasia, a precursor lesion for gastrointestinal lymphoma, was seen in eight CVID patients (16%), one of whom was diagnosed with gastrointestinal lymphoma on the same endoscopy. High-risk gastric pathology was associated with increased time since diagnosis of CVID, smoking, Helicobacter pylori, a low-serum pepsinogen I concentration, and diarrhea, but not pepsinogen I/II ratio, iron studies, vitamin B12 levels or upper gastrointestinal symptoms. There was a lower rate of detection of IM when fewer biopsies were taken, and IM and gastric atrophy were rarely predicted by the endoscopist macroscopically, highlighting the need for standardized biopsy protocols. The prevalence of premalignant gastric lesions in patients with CVID highlights the need for routine gastric screening. We propose a novel gastric screening protocol to detect early premalignant lesions and reduce the risk of gastric cancer and gastric lymphoma in these patients.

The histologic detection of Helicobacter pylori in seropositive subjects is affected by pathology and secretory ability of the stomach.

Helicobacter pylori is unevenly distributed in hypochlorhydric environments. The study aim was to elucidate the risk factors for a negative Giemsa staining finding in seropositive subjects by measuring the secretory ability of the stomach. Subjects aged over 18years were included consecutively after endoscopic biopsy at gastric lesions with color or structural changes. Blood was sampled for the serum pepsinogen (PG) assay and H.pylori serology test. After excluding the subjects with past H.pylori eradication, the risk factors for a negative Giemsa staining finding in seropositive subjects were analyzed. Among 872 included subjects, a discrepancy between the serum anti-H.pylori IgG and Giemsa staining findings was found in 158 (18.1%) subjects, including 145 Giemsa-negative, seropositive subjects. Gastric adenocarcinoma/adenoma (OR=11.090, 95% CI=3.490-35.236) and low serum PG II level (OR=0.931, 95% CI=0.899-0.963) were the independent risk factors for a negative Giemsa staining finding in seropositive subjects. The cutoff value of serum PG II level was 7.45ng/mL (area under curve [AUC]=0.904, 95% CI=0.881-0.927). Follow-up studies of Giemsa staining at different sites of the stomach revealed that 75% of the Giemsa-negative seropositive subjects with adenocarcinoma are positive, whereas none of those with low serum PG II level of <7.45ng/mL revealed positive findings. The risk of a negative Giemsa staining finding in seropositive subjects is increased in gastric adenocarcinoma/adenoma specimens and in subjects with a diminished gastric secretory ability with low serum PG II level of <7.45ng/mL. A false-negative Giemsa staining finding is common in subjects with adenocarcinoma, and therefore, additional biopsies at different sites should be performed in these subjects.

Blood biomarkers for early diagnosis of oesophageal cancer: a systematic review.

Oesophageal cancer prognosis remains poor owing to the inability to detect the disease at an early stage. Nontissue (serum, urinary or salivary) biomarkers potentially offer less invasive methods to aid early detection of oesophageal cancer. We aimed to systematically review studies assessing the relationship between nontissue biomarkers and subsequent development of oesophageal cancer. Using terms for biomarkers and oesophageal cancer, Medline, EMBASE and Web of Science were systematically searched for longitudinal studies, published until April 2016, which assessed the association between nontissue biomarkers and subsequent oesophageal cancer risk. Random effects meta-analyses were used to calculate pooled relative risk (RR) and 95% confidence intervals (CIs), where possible. A total of 39 studies were included. Lower serum pepsinogen I concentrations were associated with an increased risk of oesophageal squamous cell carcinoma (n=3 studies, pooled RR=2.20, 95% CI: 1.31-3.70). However, the association for the pepsinogen I : II ratio was not statistically significant (n=3 studies, pooled RR=2.22, 95% CI: 0.77-6.40), with a large degree of heterogeneity observed (I=68.0%). Higher serum glucose concentrations were associated with a modestly increased risk of total oesophageal cancer (n=3 studies, pooled RR=1.27, 95% CI: 1.02-1.57). No association was observed for total cholesterol and total oesophageal cancer risk (n=3 studies, pooled RR=0.95, 95% CI: 0.58-1.54). Very few studies have assessed other biomarkers for meta-analyses. Serum pepsinogen I concentrations could aid early detection of oesophageal squamous cell carcinoma. More prospective studies are needed to determine the use of other nontissue biomarkers in the early detection of oesophageal cancer.

Family history of cancer in first-degree relatives and risk of gastric cancer and its precursors in a Western population.

Family history may inform risks of gastric cancer and preneoplastic lesions. We examined associations with history of cancer in first-degree relatives for 307 incident gastric cancer cases among 20,720 male smokers in a prospective study in Finland. Cox regression was used to calculate gastric cancer hazard ratios (HR) and 95% confidence intervals (95% CI). Logistic regression was used to estimate odds ratios (OR) and 95% CIs for low serum pepsinogen, a marker of gastric atrophy. Gastric cancer risk was associated with gastric cancer history in first-degree relatives overall (HR 1.56, 95% CI 1.15-2.12), in fathers (HR 1.67, 95% CI 1.09-2.55) and in siblings (HR 2.05, 95% CI 1.25-3.38). Associations were significant for noncardia (HR 1.83, 95% CI 1.30-2.57) but not cardia (HR 0.93, 95% CI 0.46-1.87) cancers, and marginal for both intestinal-(HR 1.53, 95% CI 0.92-2.55) and diffuse-type (HR 1.47, 95% CI 0.72-3.03) histologies. Family history of other cancer types was not associated with gastric cancer risk. Family history of gastric cancer was associated with low pepsinogen (OR 1.29, 95% CI 1.11-1.50). Family history of gastric cancer is strongly associated with specific subtypes of gastric cancer as well as with gastric atrophy, a risk factor for developing this malignancy.

Serum pepsinogens and Helicobacter pylori are not associated with esophageal squamous cell carcinoma in a high-risk area in China.

The role of serum pepsinogen level and Helicobacter pylori infection in esophageal carcinoma remains controversial. It may be a risk or protective factor, or without association with esophageal carcinoma. We prospectively examined associations between serum pepsinogen status, H pylori infection and the risk of esophageal squamous cell carcinoma in the Chinese population. In the present study, 1501 subjects from a community-based general population of Northern China were included. The incidence of esophageal carcinoma among the subjects was registered during a 15-year follow-up period by annual home visit, and the risks of low serum pepsinogen level and H pylori infection in the development of ESCC were evaluated using logistic regression. The total accumulated incidence of ESCC in the cohort was 666/100,000 during the 15-year follow-up. Notably, all the cases were verified to be ESCC. Logistic regression analysis showed that age ≥60 (OR = 9.67; 95% CI, 2.797-33.423) was the only risk factor for esophageal squamous cell carcinoma in the population. There was no significant association between sex, H pylori infection, pepsinogen level (PG I ≤70 ng/ml alone, PG I/II ratio ≤3 alone, or PG I ≤70 ng/ml and PG I/II ratio ≤3) and esophageal squamous cell carcinoma. In this prospective study, neither H pylori infection nor abnormal pepsinogen status had a predictive role for the development of esophageal squamous cell carcinoma in the rural population of China.

The corpus-predominant gastritis index can be an early and reversible marker to identify the gastric cancer risk of Helicobacter pylori-infected nonulcer dyspepsia.

Corpus-predominant gastritis index (CGI) is an early histological marker to identify Helicobacter pylori-infected gastric cancer relatives at risk of cancer. This study validated whether CGI is more prevalent in H. pylori-infected nonulcer dyspepsia (NUD) subjects than in duodenal ulcer (DU) controls and whether it is reversible after H. pylori eradication or is correlated with noninvasive biomarkers. In this longitudinal cohort study, 573 H. pylori-infected subjects were enrolled, including 349 NUD and 224 DU. Gastric specimens were provided to assess CGI, spasmolyic polypeptide-expressing metaplasia (SPEM), and Operative Link on Gastric Intestinal Metaplasia assessment (OLGIM). Serum pepsinogen I and II levels were assessed using enzyme-linked immunosorbent assay. CGI subjected were followed up at least 1year after H. pylori eradication. NUD subjects had higher prevalence rates of CGI (47.0% vs 29.9%, P<.001) and OLGIM stages III-IV (24.1% vs 15.2%, P=.01) than controls. CGI was highly prevalent in NUD subjects after the age of 40, which was 10 years earlier than atrophic gastritis and intestinal metaplasia. NUD subjects with CGI had higher risk of SPEM (OR 2.86, P<.001) and lower serum pepsinogen I/II ratios (P<.001) than those without CGI. Serum pepsinogen I/II ratios <9 could predict CGI modestly (AUROC 0.69, 95% CI: 0.63-0.74). CGI was regressed after eradication (P<.001). CGI was more prevalent in H. pylori-infected NUD subjects than in controls, was correlated with SPEM, and may serve as a marker earlier than OLGIM to indicate risk of gastric cancer. Moreover, CGI could be regressed after eradication.

The Impact of Gastric Atrophy on the Incidence of Diabetes

Gastric atrophy results in lower plasma ghrelin, higher gastrin secretion, a change in gut microbiota, and altered dietary nutrient absorption, which may be associated with the incidence of diabetes. Helicobacter pylori (H. pylori) infection is a major cause of gastric atrophy and is associated with diabetes in some reports. Since there is no study which investigates the impact of gastric atrophy on diabetes, we conduct a prospective cohort study to examine the relationship between H. pylori infection, gastric atrophy, and incident diabetes. In this study, subjects with gastric atrophy had a lower risk of incident diabetes, compared to those without gastric atrophy. The extent of gastric atrophy, measured by serum pepsinogen (PG) I/II ratio, was correlated with age, H. pylori IgG titer, HOMA2-IR, and HOMA2%B. When gastric atrophy is more extensive, presented as a lower serum PG I/II ratio, the risk of incident diabetes is lower. On the other hand, there was no significant association between H. pylori infection and the incidence of diabetes. In conclusion, the presence and the extent of gastric atrophy, but not H. pylori infection, are associated with incident diabetes. Further studies are needed to investigate the detailed mechanisms and the potential applications of the findings to guide diabetes screening and treatment strategies.

Slow-release L-cysteine capsule prevents gastric mucosa exposure to carcinogenic acetaldehyde: results of a randomised single-blinded, cross-over study of Helicobacter-associated atrophic gastritis

Introduction: Helicobacter-induced atrophic gastritis with a hypochlorhydric milieu is a risk factor for gastric cancer. Microbes colonising acid-free stomach oxidise ethanol to acetaldehyde, a recognised group 1 carcinogen.Objective: To assess gastric production of acetaldehyde and its inert condensation product, non-toxic 2-methyl-1,3-thiazolidine-4-carboxylic acid (MTCA), after alcohol intake under treatment with slow-release L-cysteine or placebo.Methods: Seven patients with biopsy-confirmed atrophic gastritis, low serum pepsinogen and high gastrin-17 were studied in a cross-over single-blinded design. On separate days, patients randomly received 200 mg slow-release L-cysteine or placebo with intragastric instillation of 15% (0.3 g/kg) ethanol. After intake, gastric concentrations of ethanol, acetaldehyde, L-cysteine and MTCA were analysed.Results: Administration of L-cysteine increased MTCA (p < .0004) and decreased gastric acetaldehyde concentrations by 68% (p < .0001). The peak L-cysteine level was 7552 ± 2687 μmol/L at 40 min and peak MTCA level 196 ± 98 μmol/L at 80 min after intake. Gastric L-cysteine and MTCA concentrations were maintained for 3 h. The AUC for MTCA was 11-fold higher than acetaldehyde, indicating gastric first-pass metabolism of ethanol. With placebo, acetaldehyde remained elevated also at low ethanol concentrations representing ‘non-alcoholic’ beverages and food items.Conclusions: After gastric ethanol instillation, slow-release L-cysteine eliminates acetaldehyde to form inactive MTCA, which remains in gastric juice for up to 3 h. High acetaldehyde levels indicate a marked gastric first-pass metabolism of ethanol resulting in gastric accumulation of carcinogenic acetaldehyde. Local exposure of the gastric mucosa to acetaldehyde can be mitigated by slow-release L-cysteine capsules.

Associated factors of atrophic gastritis diagnosed by double-contrast upper gastrointestinal barium X-ray radiography: a cross-sectional study analyzing 6,901 healthy subjects in Japan.

BackgroundDouble-contrast upper gastrointestinal barium X-ray radiography (UGI-XR) is one of the most widely conducted gastric cancer screening methods. It has been executed to find gastric cancer, but has not been usually executed to detect premalignant atrophic mucosa of stomach. To understand the meaning of UGI-XR-based atrophic gastritis, we analyzed its association with several causative factors including Helicobacter pylori (HP) infection.MethodsWe evaluated 6,901 healthy adults in Japan. UGI-XR-based atrophic gastritis was diagnosed based on the irregular shape of areae gastricae and its expansion in the stomach.ResultsOf the 6,433 subjects with no history of HP eradication and free from gastric acid suppressants, 1,936 were diagnosed as UGI-XR-based atrophic gastritis (mild: 234, moderate: 822, severe: 880). These were univariately associated with serum HP IgG and serum pepsinogen I/II ratio with statistical significance. The multiple logistic analysis calculating standardized coefficients (β) and odds ratio (OR) demonstrated that serum HP IgG (β = 1.499, OR = 4.48), current smoking (β = 0.526, OR = 1.69), age (β = 0.401, OR = 1.49), low serum pepsinogen I/II ratio (β = 0.339, OR = 1.40), and male gender (β = 0.306, OR = 1.36) showed significant positive association with UGI-XR-based atrophic gastritis whereas drinking and body mass index did not. Among the age/sex/smoking/drinking-matched 227 pairs derived from chronically HP-infected and successfully HP-eradicated subjects, UGI-XR-based atrophic gastritis was detected in 99.1% of the former but in only 59.5% of the latter subjects (p<0.0001). Contrastively, UGI-XR-based atrophic gastritis was detected in 13 of 14 HP-positive proton pump inhibitor users (92.9%) and 33 of 34 HP-positive histamine H2-receptor antagonist users (97.1%), which are not significantly different from gastric acid suppressant-free subjects.ConclusionsThe presence of UGI-XR-based atrophic gastritis is positively associated with Helicobacter pylori infection, current smoking, age, decreased serum pepsinogen I/II ratio, and male gender. Eradication of Helicobacter pylori seems to superficially improve UGI-XR-based atrophic gastritis whereas intake of gastric acid suppressants does not.

A possible association of low pepsinogen I and pepsinogen I/II with low and high body weight in Japanese men

BackgroundIt is unknown whether low serum pepsinogen I and pepsinogen I/II ratio (PGI–PGI/II), a marker for chronic atrophic gastritis, is associated with low or high body weight. MethodsWe investigated the association between low PGI–PGI/II and both ends of the spectrum of body mass index (BMI) in 819 apparently healthy Japanese men aged 20–75years who received a medical check-up in 2008. ResultsIn univariate analysis, serum pepsinogen I, but not pepsinogen II or pepsinogen I/II, was significantly reduced across the increasing BMI categories. Multivariate regression analysis showed that, compared with BMI 21.0–22.9kg/m2, BMI of 20.9kg/m2 and less or 25.0kg/m2 and above was significantly associated with low PGI–PGI/II (pepsinogen I<50ng/ml combined with PG I/II<3.0), even after adjustment for relevant confounders. These associations showed a J-shaped curve against BMI. ConclusionLow PGI–PGI/II may be independently associated with both low body weight and obesity in Japanese men.

Serum Pepsinogens and Helicobacter Pylori are not Associated with Esophageal Squamous Cell Carcinoma in a High-Risk Area in China

The role of serum pepsinogen level and Helicobacter pylori infection in esophageal carcinoma remains controversial. It may be a risk or protective factor, or without association with esophageal carcinoma. We prospectively examined associations between serum pepsinogen status, H pylori infection and the risk of esophageal squamous cell carcinoma in the Chinese population. In the present study, 1501 subjects from a community-based general population of Northern China were included. The incidence of esophageal carcinoma among the subjects was registered during a 15-year follow-up period by annual home visit, and the risks of low serum pepsinogen level and H pylori infection in the development of ESCC were evaluated using logistic regression. The total accumulated incidence of ESCC in the cohort was 666/100,000 during the 15-year follow-up. Notably, all the cases were verified to be ESCC. Logistic regression analysis showed that age ≥60 (OR = 9.67; 95% CI, 2.797-33.423) was the only risk factor for esophageal squamous cell carcinoma in the population. There was no significant association between sex, H pylori infection, pepsinogen level (PG I ≤70 ng/ml alone, PG I/II ratio ≤3 alone, or PG I ≤70 ng/ml and PG I/II ratio ≤3) and esophageal squamous cell carcinoma. In this prospective study, neither H pylori infection nor abnormal pepsinogen status had a predictive role for the development of esophageal squamous cell carcinoma in the rural population of China.

Serum Pepsinogens, Gastrin-17 and &lt;i&gt;Helicobacter pylori&lt;/i&gt; Antibody in the Residents of Two Cities in China with Distinct Mortality Rates of Gastric Cancer

Gastric cancer is one of the most common malignant tumors causing death in Fujian Province, China. However, the mortality of gastric cancer is greatly varied in different areas in Fujian; for example, the mortality in Changle City is 7.4 times higher than that in Fuan City. In this study, we compared the differences in serological parameters, pepsinogen (PG) I, PG II, gastrin-17 (G-17), and Helicobacter pylori (H. pylori) antibody, between the two cities. It has been reported that low serum PG I is correlated with atrophic gastritis, a high-risk condition for developing gastric cancer, while high serum G-17 has been used for serological detection of atrophic corpus gastritis. We recruited 224 healthy subjects in Changle and 229 healthy subjects in Fuan, matched in age and sex. The serum levels of PG II and G-17 were significantly higher in Changle than those in Fuan. Importantly, the frequency of the subjects with low serum PG I (< 25 μg/L) was significantly higher in Changle than in Fuan, although the serum PG I levels were similar between the two cities. Moreover, the percentage of the subjects with high serum G-17 (≥ 2 pmol/L) and the positive rate of serum IgG antibody against H. pylori were significantly higher in Changle than those in Fuan. The detected differences in these serological parameters are consistent with the notion that the prevalence of atrophic gastritis may be higher in Changle than in Fuan, which results in a higher risk condition for developing gastric cancer in Changle.

Serum ghrelin is inversely associated with risk of subsequent oesophageal squamous cell carcinoma

BackgroundGastric atrophy, as determined by a low serum pepsinogen I:II ratio, may be associated with an increased risk of oesophageal squamous cell carcinoma (OSCC). Ghrelin, a hormone which, is also...

Low serum pepsinogen I and pepsinogen I/II ratio and Helicobacter pylori infection are associated with increased risk of gastric cancer: 14‐year follow up result in a rural Chinese community

The correlation between low serum PG level and H. pylori infection with the development of gastric cancer has caused considerable concerns all over the world. Some authors exclaimed that gastric cancer developed only in patients infected with H. pylori, whereas the other had different findings. In this study, 1,501 adult local residents with determined serum PG levels and anti H. pylori IgG status were followed for 14 years for the development of gastric cancer in a rural community with high risk of gastric cancer in Hebei Province, China. The results showed the accumulated gastric cancer incidence in the subjects with abnormal PG level and those with H. pylori infection were all significantly higher than that in the corresponding normal controls (53.9‰ vs. 12.7‰, p < 0.05 and 23.1‰ vs. 5.93‰, p < 0.05). The highest gastric cancer incidence was seen in the subjects with both abnormal serum PG and positive H. pylori (56.0‰), and followed by the subjects with abnormal PG and negative H. pylori (47.6‰) and those with normal serum PG and positive H. pylori (18.4‰). The abnormal serum PG level (OR 3.029) and H. pylori infection (OR 4.345) were all risk factors for the development of gastric cancer. The results suggested that the subjects with abnormal serum PG level and/or positive H. pylori infection in the rural area of China were all high risk population for gastric carcinoma and the subjects with both abnormal serum PG and positive H. pylori infection were at especially high risk for the development of gastric carcinoma.

Clinical parameters including serum pepsinogen level and management strategy in patients with premalignant gastric dysplasia

Surgical or endoscopic resection is recommended for the management of gastric high-grade dysplasia (HGD). However, there are no proper guidelines for the management of gastric low-grade dysplasia (LGD). We evaluated clinical parameters, histological results, and endoscopic follow-up to find a management strategy of LGD. A total of 590 patients with LGD, HGD, functional dyspepsia (FD), and early or advanced gastric cancer (EGC or AGC, respectively) were consecutively enrolled. We examined the association of clinical parameters including low serum pepsinogen (PG) I/II ratio of 3.0 or less with the disease phenotypes. Histological results between initial forceps biopsy and final endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) specimens were compared. Complications and recurrence were evaluated after EMR or ESD. The PG I/II ratio in FD was 4.2±1.7 (mean±SD), but was significantly lower in LGD (2.8±1.6, P<0.0001). The PG I/II ratio was not any lower in the HGD, EGC, and AGC groups. In patients with FD having a PG I/II ratio of 3.0 or less, multiple logistic regression analysis showed smoking habits and high salt intake were independent risk factors for gastric dysplasia or gastric cancer. About 11% (n=8/70) of LGD lesions were upgraded to HGD (6/70) or EGC (2/70) after EMR or ESD. Neither serious complications nor recurrence at the primary site after EMR or ESD were found in LGD. It is proposed that endoscopic resection followed by endoscopic surveillance might be a beneficial strategy for patients with LGD having a PG I/II ratio of 3.0 or less.

Clinical Parameters Including Serum Pepsinogen Level and Management Strategy in Patients with Gastric Low-Grade Dysplasia

Background/Aims: There are no proper guidelines for the management of gastric low-grade dysplasia (LGD). We evaluated clinical parameters, histological results and follow-up endoscopies to find a management strategy of LGD. Materials and Methods: A total of 590 patients with LGD, high-grade dysplasia (HGD), functional dyspepsia (FD), early or advanced gastric cancer (early gastric cancer [EGC] or advanced gastric cancer [AGC]) were consecutively enrolled. We examined the association of clinical parameters including low serum pepsinogen (PG) I/II ratio ≤3.0 with the disease phenotypes. Histological results between initial forceps-biopsy and endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) specimens were compared. Results: The PG I/II ratio in FD was 4.2±1.7, but was significantly low in LGD (2.8±1.6, P<0.0001). The ratio was not further decreased in the HGD, EGC, and AGC groups. In FD patients with the ratio of ≤3.0, smoking habits and high salt intake were independent risk factors for gastric dysplasia or gastric cancer. In about 11% (n=8/70) of LGD lesions, the pathologic diagnoses were upgraded to HGD or EGC after endoscopic resection. Neither serious complications nor recurrence at the primary site were found. Conclusions: It is proposed that endoscopic resection followed by endoscopic surveillance might be a beneficial strategy for patients with LGD having a PG I/II ratio of ≤3.0. (The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2011;11:52-58)