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Objective:To investigate the application value of pepsinogen, Helicobacter pylori combined with endoscopic Kimura-Takemoto classification in the diagnosis of early gastric cancer. Methods:Sixty patients with gastric cancer who received treatment in the Department of Gastroenterology, the First People's Hospital of Huzhou from January to June 2022 were included in the gastric cancer group. An additional 60 patients with benign gastric lesions (benign gastric lesion group) and 60 patients with precancerous lesions of the stomach (precancerous lesion group) were also included in this study. Serologic testing for pepsinogen and Helicobacter pylori antibody combined with endoscopic Kimura-Takemoto classification was performed to evaluate their application value in the diagnosis of early gastric cancer. Results:Compared with the benign gastric lesion and precancerous lesion groups, the pepsinogen I/pepsinogen II ratio was significantly lower, and the pepsinogen II level and Helicobacter pylori infection rate [71.67% (43/60)] were significantly higher in the gastric cancer group ( F = 108.14, 71.75, 38.43, χ2 = 6.89, all P < 0.05). Compared with the benign gastric lesion and precancerous lesion groups, the Kimura-Takenmoto classification in the gastric cancer group was significantly higher ( H = 38.91, P < 0.05). In the gastric cancer group, pepsinogen I level and pepsinogen I/pepsinogen II ratio decreased and pepsinogen II level increased with the increase of pathological stage ( F = 65.79, 5.66, 53.32, all P < 0.01). There was no significant difference in Helicobacter pylori infection rate between different stages of gastric cancer ( P < 0.05) in the gastric cancer group. There was no significant difference in Kimura-Takenmoto classification between different stages of gastric cancer (all P > 0.05) in the gastric cancer group. The area under the receiver operating characteristic curve plotted for evaluating pepsinogen I, pepsinogen II, and pepsinogen I/pepsinogen II ratio for diagnosis of gastric cancer was 0.865, 0.664, and 0.881, respectively. Conclusion:Serum pepsinogen, Helicobacter pylori combined with endoscopic Kimura-Takemoto classification can increase the diagnostic rate of early gastric cancer. The Kimura Takemoto classification is helpful for risk stratification in the endoscopic screening of gastric cancer, and its results are consistent with pepsinogen levels. The combined application is of a high application value.
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Objective:To explore the effects and underlying mechanisms of azintamide on gastric emptying and gastrointestinal hormone secretion in proton pump inhibitor related low gastric acid environment.Methods:A total of 60 rats were selected and randomly divided into low gastric acid control group, low gastric acid model group, low gastric acid and azintamide intervention group, high gastric acid control group, high gastric acid model group and high gastric acid and azintamide intervention group by random number table, with 10 rats in each group. The rats of low gastric acid control group and high gastric acid control group were all treated with 0.9% sodium chloride solution. The rats of low gastric acid model group and high gastric acid model group were established by intraperitoneal injection of 20 mg/kg omeprazole once per day for seven days, and subcutaneous injection of 2 mg/kg penta gastrin once per day for three days, respectively. The rats of low gastric acid and azintamide intervention group and high gastric acid and azintamide intervention group were gavaged with azintamide 50 mg/kg once per day for three days on the basis of low gastric acid model group and high gastric acid model group, respectively. Only the rats in three low gastric acid groups were analyzed. At Day 0, 2nd, 4th, 6th and 8th after modeling, the body weight of rats were compared. After modeling, the weight of gastric contents and pH of gastric fluid was measured and compared, and the peripheral blood levels of pepsinogen A (PGA), gastrin and cholecystokinin (CCK) were detected by enzyme linked immunosorbent assay. One-way analysis of variance and Tukey′s honestly significant difference post-hoc test were used for statistical analysis.Results:The pH value of gastric fluid in low gastric acid model group and low gastric acid and azintamide intervention group were both higher than that in the low gastric acid control group (2.17±0.53, 2.03±0.69 vs. 1.32±0.17), and the differences were statistically significant ( P=0.026 and 0.041, respectively). While there was no significant difference in pH value between the low gastric acid model group and low gastric acid and azintamide intervention group ( P>0.05). On the Day 0, 2nd, 4th, 6th and 8th after modeling, the body weight of rats of low gastric acid control group, low gastric acid model group and low gastric acid and azintamide intervention group was (285.40±10.86), (283.40±6.38), (282.00±5.04) g; (287.10±10.73), (283.20±5.83), (284.00±5.72) g; (292.20±11.18), (281.90±6.23), (289.00±5.82) g; (296.40±11.12), (277.70±6.96), (292.00±6.82) g; (300.80±11.29), (274.30±8.84), (297.00±4.17) g, respectively. On the Day 6th and 8th after modeling, the body weight of rats of low gastric acid model group was lower than that of the low gastric acid control group; and the body weight of rats of low gastric acid and azintamide intervention group was higher than that of low gastric acid model group, and the differences were statistically significant (both P<0.01). On the Day 0, 2nd, 4th, 6th and 8th, there was no statistically significant difference in body weight of rats between low gastric acid and azintamide intervention group and low gastric acid control group ( P>0.05). On the Day 0, 2nd, 4th, there were no statistically significant differences in body weight of rats between low gastric acid and azintamide intervention group and low gastric acid model group, and between low gastric acid model group and low gastric acid control group (both P>0.05). The weight of gastric contents of low gastric acid model group was heavier than that of low gastric acid control group ((2.36±0.11) g vs. (1.85±0.20) g), the weight of gastric contents of low gastric acid and azintamide intervention group was lighter than that of low gastric acid model group ((1.87±0.42) g vs. (2.36±0.11) g), and the differences were statistically significant ( P=0.019 and 0.016, respectively), and there was no statistically significant difference in weight of gastric contents between the low gastric acid and azintamide intervention group and the low gastric acid control group ( P>0.05). The peripheral blood level of PGA of rats of low gastric acid model group was lower than that of low gastric acid control group ((551.80±190.00) ng/L vs. (857.00±164.80) ng/L), while the peripheral blood level of PGA of the low gastric acid and azintamide intervention group was higher than that of the low gastric acid model group ((799.90±97.80) ng/L vs. (551.80±190.00) ng/L), and the differences were statistically significant ( P=0.011 and 0.037, respectively). There was no significant difference in peripheral blood level of PGA between the low gastric acid control group and the low gastric acid and azintamide intervention group ( P>0.05). The peripheral blood level of gastrin of the low gastric acid model group was higher than that of the low gastric acid control group ((49.31±11.93) ng/L vs. (35.59±5.29) ng/L), and the CCK level of the low gastric acid model group was lower than that of low gastric acid control group ((10.26±5.32) ng/L vs. (25.55±11.62) ng/L), and the differences were statistically significant ( P=0.037 and 0.035, respectively). The peripheral blood level of gastrin of the low gastric acid and azintamide intervention group was lower than that of low gastric acid model group ((35.65±6.49) ng/L vs. (49.31±11.93) ng/L), the level of CCK of the low gastric acid and azintamide intervention group was higher than that of low gastric acid model group ((27.59±11.22) ng/L vs. (10.26±5.32) ng/L), and the differences were statistically significant ( P=0.048 and 0.021, respectively). There were no significant differences in CCK and gastrin between low gastric acid and azintamide intervention group and low gastric acid control group (both P>0.05). Conclusion:Azintamide regulates the levels of gastrointestinal hormones CCK and gastrin under the condition of low gastric acid and affects the expression of pepsinogen A, thereby promoting gastric emptying in a low gastric acid environment.
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Objective:To evaluate the clinical efficacy of Wanfu-Qutong Decoction combined with esomeprazole in the treatment of chronic atrophic gastritis (CAG). Methods:A total of 106 CAG patients who met the inclusion criteria from June 2017 to June 2019 were randomly divided into two groups with 53 in each group. The control group took esomeprazole magnesium enteric coated tablets, and the observation group took Wanfu-Qutong Decoction on the basis of the control group. Both groups were treated continuously for 3 months. TCM syndrome score was performed before and after treatment, and the new Sydney system intuitive simulation score method was used to score the histopathology of gastric mucosa. The levels of gastrin 17 (G-17), pepsinogen (PGⅠ , PGⅡ) and the PG Ⅰ/Ⅱ were measured by ELISA. Results:The total effective rate was 96.2% (51/53) in the observation group and 79.2% (42/53) in the control group. There was significant difference between the two groups ( χ2=7.414, P<0.01). After treatment, the scores of epigastric pain, fullness, liking temperature and pressing, vomiting clear water, eating less and staying foolish, and limb burnout in the observation group were significantly lower than those in the control group ( t values were 2.788, 3.632, 3.816, 1.590, 2.183, 2.103, respectively, all Ps<0.05), and the scores of chronic inflammatory reaction, inflammatory activity, atrophy degree, dysplasia and intestinal metaplasia in the mucosa were significantly lower than those in the control group ( t values were 2.983, 2.106, 2.106, 3.773, 1.922, 3.095, respectively, all Ps<0.05). After treatment, the serum G-17 [(14.47 ± 3.06) pmol/L vs. (10.67 ± 2.47) pmol/L, t=10.510] and PG Ⅰ [(130.31 ± 14.79) μg/L vs. (102.36 ± 12.63) μg/L, t=8.178] and PG Ⅰ/Ⅱ [(10.45 ± 0.48) vs. (9.17 ± 0.72), t=2.104] in the observation group were significantly higher than those in the control group ( P<0.01 or P<0.05). Conclusion:Wanfu-Qutong Decoction combined with esomeprazole tablets can effectively improve the clinical symptoms of CAG patients, regulate the levels of G-17, PG Ⅰ , PG Ⅱ and PGⅠ/Ⅱ, and promote the repair of gastric mucosa.
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ABSTRACT BACKGROUND: It has been proposed that the combination of gastrin-17 (G-17), pepsinogens I and II (PGI and PGII), and anti-Helicobacter pylori (H. pylori) antibodies (GastroPanel®, BIOHIT HealthCare, Helsinki, Finland) could serve as biomarkers of atrophic gastritis. OBJECTIVE: This study aimed to ensure the diagnostic accuracy of GastroPanel® and evaluate the effect of proton pump inhibitors (PPIs) on these biomarkers. METHODS: Dyspeptic patients who underwent gastrointestinal endoscopy were enrolled in the present study. Histological findings, which were the gold standard to stratify groups, were as follows: no atrophy (controls); antrum atrophy; corpus atrophy; multifocal atrophy; and neoplasia. G-17, PGI, PGII, and anti-H. pylori immunoglobulin (Ig)G antibodies were assayed using commercially available kits. The ratio of PGI/PGII was calculated. RESULTS: Among 308 patients, 159 (51.6%) were PPI users. The overall prevalence of atrophy was 43.8% (n=135). Ninety-two (29.9%) patients were H. pylori positive according to anti-H. pylori IgG levels. G-17 levels were not low in those with antrum atrophy but were high in those with corpus and multifocal atrophies. PGI levels were significantly lower in those with corpus and multifocal atrophies. The sensitivity of PGI <30 µg/L to detect corpus atrophy was 50% (95% CI 27.8-72.1%), with a specificity of 93.2% (95% CI 84.3-97.5%), a positive likelihood ratio of 7.4 (95% CI 2.9-19.2), and a negative likelihood ratio of 0.5 (95% CI 0.3-0.8). A small number of subjects (n=6) exhibited moderate to intense atrophy (4%), among whom 66.7% exhibited decreased PGI levels. PPI significantly increased the levels of G-17 and PGI, except in those with corpus and multifocal atrophies, in whom PGI levels were not increased by PPIs. CONCLUSION: GastroPanel® (Gastrin-17, PGI, and PGI/PGII ratio) did not demonstrate high sensitivity for detecting gastric atrophy.
RESUMO CONTEXTO: Foi proposto que a combinação de gastrina 17 (G-17), pepsinogênios I e II (PGI e PGII), e anticorpos anti-Helicobacter pylori (H. pylori) (GastroPanel®, BIOHIT HealthCare), poderiam indicar gastrite atrófica. OBJETIVO: Portanto, o objetivo foi averiguar a acurácia diagnóstica do painel gástrico e avaliar o efeito dos inibidores de bomba de prótons (IBP) nesses marcadores. MÉTODOS: Pacientes dispépticos que se submeteram à endoscopia gastrointestinal entraram no estudo. Os achados histológicos foram o padrão ouro para estratificar os grupos: sem atrofia (controles), atrofia de antro, atrofia de corpo, atrofia multifocal e neoplasia. G-17, PGI, PGII, e anticorpos IgG anti-H. pylori foram determinados por kits comerciais. A razão PGI/PGII foi calculada. RESULTADOS: Entre 308 pacientes que foram incluídos, 159 estavam usando IBP (51,6%). A prevalência de atrofia foi de 43,8% (135 pacientes). H. pylori foi positivo em 92 (29,9%) pacientes por IgG anti-H. pylori. G-17 não estava diminuída na atrofia do antro, mas estava elevada nas atrofias do corpo e multifocal. PGI estava significantemente menor nas atrofias de corpo e multifocal. A sensibilidade da PGI <30 µg/L de indicar atrofia do corpo foi 50% (95%IC 27,8-72,1%) com especificidade de 93,2% (95%IC 84,3-97,5%), razão de verossimilhança positiva de 7,4 (95%IC 2,9-19,2) e razão de verossimilhança negativa de 0,5 (95%IC 0,3-0,8). O número de indivíduos com atrofia moderada para intensa foi pequeno (n=6;4%), dos quais 66,7% tinham diminuição dos níveis de PGI. IBP significantemente aumentou os níveis de G-17 e PGI, exceto nas atrofias de corpo e multifocal que não apresentaram aumento de PGI. CONCLUSÃO: O painel gástrico não teve alta sensibilidade de indicar gastrite atrófica.
Subject(s)
Humans , Proton Pump Inhibitors , Gastritis, Atrophic/diagnosis , Brazil , Helicobacter pylori , Helicobacter Infections , Antibodies, BacterialABSTRACT
Objective To explore the relationship between the serum PGⅠ,PGⅡ,PGⅠ/PGⅡ ratio(PGR),IgG anti-HP and gastric cancer and the diagnostic value.Methods The levels of serum PGⅠ,PGⅡ,PGⅠ/PGⅡ ratio(PGR) and IgG anti-HP were detected by emulsio immunoturbidimetry and ELISA in 30 patients with gastric cancer and 30 healthy subjects as controls.Then, the best cut-off value was established to screen gastric cancer.Results The levels of serum PGⅠ,PGⅡ,PGR and IgG anti-HP in the gastric cancer group were (33.72±6.49)ng/L, (8.36±1.26)ng/L, (3.67±0.72), (69.74±15.86)IU,respectively,which in the control group were (111.36±15.86)ng/L, (10.57±1.71)ng/L, (10.53±1.34), (34.62±8.94)IU,respectively.The levels of serum PGⅠ,PGⅡ and PGR in the gastric cancer group were significantly lower than those in the control group(t=25.58,5.60,24.67,all P<0.01),while the level of serum IgG anti-HP was significantly higher than that in the control group(t=10.55,P<0.01).Compare the serum PGⅠ, PGR between IgG anti-HP positive group and IgG anti-HP negative group, there was statistically significant differences(t=5.77,4.02,3.76,all P<0.01).According to the ROC curves, the best cut-off points of PGⅠ, PGⅡ, PGR, IgG anti-HP were 32.54 ng/L[sensitivity 80.7%,specificity 75.0%,area under curve (0.775±0.075)], 7.73 ng/L[sensitivity 75.4%,specificity 70.5%,area under curve (0.742±0.071)],3.48[sensitivity 86.4%,specificity 72.5%,area under curve (0.859±0.067)] and 69.11 IU[sensitivity 59.1%,specificity 75.0%,area under curve (0.667±0.089)].Conclusion Detection of serum PGⅠ, PGR, and IgG anti-HP levels can be useful as a way to screen gastric cancer, the PGR may the best single measure to diagnosis of gastric cancer.
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Objective To investigate the impact and clinical significance of helicobacter pylori (Hp) elimination on ghrelin. Methods Forty patients with chronic superficial gastritis (CSG), 42 patients with chronic atrophic gastritis (CAG), 41 patients with peptic ulcer (PU) and 17 patients with gastric adenocarcinoma (CA) were included in this study. All of pa-tients in four groups were Hp-positive. Forty patients with Hp-negative were used as control. The Hp elimination were only performed in CAG,CSG and PU groups. The serum ghrelin and pepsinogen (PG) levels before and after Hp elimination were detected with ELISA assay in CSG, CAG and PU groups. The correlation between PG and glrelin was also detected. The ex-pression of ghrelin in gastric mucosa was detected by RT-PCR. Results Comparing with control group (30.41 ± 8.97), the ghrelin level was increased in PU group (35.42±9.87), but which were decreased in CAG group (18.59±8.19) and CA group (18.33±6.88). There was no significant difference in ghrelin level between CSG group (26.08±9.14) and control group. After Hp elimination, the serum and gastric mucosa ghrelin levels were significantly increased in CSG group (P＜0.01), but both serum and gastric mucosa ghrelin levels were significantly decreased in PU group (P＜0.01). And no significant difference in the level of ghrelin after Hp elimination in CAG group (P>0.05). A positive correlation was found between serum PGⅠ/PGⅡand serum ghrelin level in CSG, CAG and CA groups (r=0.668,P＜0.01). Conclusion Hp elimination has an impact on ghrelin level in patients with upper gastrointestinal diseases. The changes of ghrelin level related to PGⅠ/PGⅡ. Ghrelin can be used as one of the indexes of diagnostic and prognostic evaluation in Hp related upper gastrointestinal diseases.
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It is confirmed that chronic atrophic gastritis (CAG) caused by Helicobacter pylori is the main cause of gastric precancerous lesions.CAG is also the key determinant in gastric cancer risk assessment,which affects pepsinogen and gastrin-17 secretion.Most of the gastric cancer patients have poor prognosis,and non-invasive tools for gastric cancer screening and diagnosis are lacking.Therefore,the early detection of gastric cancer in order to reduce the disease mortality is necessary.Pepsinogen and gastrin-17 are biomarkers of gastric mucosa and gastric antra.The serological testing for the stomach-specific biomarkers offers the possibility to know preneoplastic gastric mucosal conditions.
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Objective To investigate the effect of folic acid combined with Helicobacter pylori (Hp) eradication therapy on chronic atrophic gastritis.Methods From December 2009 to March 2011 at the First Affiliated Hospital of Nanjing Medical University,184 patients with endoscopic and pathological diagnosis of chronic atrophic gastritis (90 Hp positive and 94 Hp negative) were selected.Hp positive patients were divided into group A and group B.Forty-three patients in group A were treated with standard triple Hp eradication therapy and follow by folic acid therapy for three months.Forty-seven patients in group B and Hp negative patients received three months of folic acid therapy.The clinical symptoms of each group were scored before treatment,one month after folie acid therapy and three months after folic acid therapy and analyzed by t test. Patients of each group received gastroscopy before treatment and three months after medicine withdrawal. Endoscopic scores,pathological scores and t test were recorded.The serum levels of pepsinogen ( Ⅰ,Ⅱ ) and gastrin 17 in venous blood of 55 Hp negative patients were detected by enzyme-linked immunosorbent assay (ELISA) method before treatment and three months after medicine withdrawal.Results Compared with three months therapy (1.15 ± 0.03),after one month folic acid therapy (1.55 ± 0.04) was statistically significant in clinical symptoms score of all patients (t =8.18,P＜0.01).By the end of therapy,clinical symptom score of group A (1.06 ± 0.04) was lower than that of group B (1.56 ±0.08),and the difference was significant (t=6.00,P＜0.01).There was significant difference in endoscopic scores of all patients between before treatment (1.57±0.95) and after treatment (1.00±0.76,t=11.12,P＜0.01).The differences in each pathological score of all patients (inflammatory scoring,active scoring,atrophy scoring,intestinal metaplasia scoring,atypical hyperplasia degree scoring) were significant between before treatment and after treatment (t=5.51,6.90,7.53,6.34,2.90,respectively,all P＜0.01).The serum level of pepsinogen Ⅰ before treatment of 55 Hp negative patients [(1.03±0.19) nmol/L] was lower than that after treatment [(2.24±0.33) nmol/L],and the difference was statistically significant (t=3.19,P＜0.01).After treatment the level of gastrin 17 [(0.86±0.05) nmol/L] was higher than that before treatment [(0.47±0.05) nmol/L],and the difference was statistically significant ( t =5.33,P＜ 0.01 ).Conclusion Folic acid in combination with Hp eradication therapy can be favorable to atrophic gastritis,which may promote the secretion of pepsinogen and gastrin.
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Recently, fundic gland type gastric adenocarcinoma (GA-FG) has been reported as a new entity. This report describes GA-FG among Koreans for the first time. From March 2008 to July 2010 we identified only three cases of GA-FG out of over 6,000 GAs resected by endoscopy or surgery. Cell differentiation by mucin proteins, pepsinogen-I, and H+/K+-ATPase was evaluated. All three cases were male patients and diagnosed as early stage GA. Histologically, GA-FGs were well-differentiated adenocarcinoma with pale gray-blue, basophilic columnar or cuboidal cells and mildly enlarged nuclei, resembling chief cells. All three cases were positive for pepsinogen-I and were classified as gastric mucin phenotype. Among three histologic subtypes of GA-FG, since tumors were mainly composed of chief cells, our three cases were classified as chief cell predominant type. In conclusion, GA-FG is very rare among Koreans and pepsinogen-I and MUC6 expression are typical immunohistochemical findings in GA-FG suggesting differentiation toward fundic glands.
Subject(s)
Male , Humans , AdenocarcinomaABSTRACT
Recently, fundic gland type gastric adenocarcinoma (GA-FG) has been reported as a new entity. This report describes GA-FG among Koreans for the first time. From March 2008 to July 2010 we identified only three cases of GA-FG out of over 6,000 GAs resected by endoscopy or surgery. Cell differentiation by mucin proteins, pepsinogen-I, and H+/K+-ATPase was evaluated. All three cases were male patients and diagnosed as early stage GA. Histologically, GA-FGs were well-differentiated adenocarcinoma with pale gray-blue, basophilic columnar or cuboidal cells and mildly enlarged nuclei, resembling chief cells. All three cases were positive for pepsinogen-I and were classified as gastric mucin phenotype. Among three histologic subtypes of GA-FG, since tumors were mainly composed of chief cells, our three cases were classified as chief cell predominant type. In conclusion, GA-FG is very rare among Koreans and pepsinogen-I and MUC6 expression are typical immunohistochemical findings in GA-FG suggesting differentiation toward fundic glands.