The Relationship of Gastrin, Pepsinogen, and Helicobacter pylori in Erosive Reflux Esophagitis / 대한소화기학회지

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is known as a major cause of atrophic gastritis and is associated with serum gastrin, pepsinogen, and gastric acid secretion. There is still a controversial association between gastroesophageal reflux disease and H. pylori infection. This study was designed to investigate the relationship among serum gastrin, pepsinogen, and H. pylori infection in the erosive reflux esophagitis (ERD) patients. METHODS: Patients who were diagnosed as ERD by one gastroenterologist at the Kangnam St. Marys hospital were prospectively enrolled. The persons without ERD in the control group were matched for age and sex. We examined the gastrin, pepsinogen I (PG I), PG II, PG I/II ratio, and H. pylori infection. RESULTS: Forty five patients were enrolled in ERD group and 66 persons in control group. The H. pylori infection rate in ERD group was lower than that in the control group (11.1% vs. 43.9%, p<0.001). PG I/II ratio in ERD group was higher than that in the control group (7.0+/-3.1 vs. 5.3+/-2.6, p=0.003). The PG II (p=0.016) and gastrin (p=0.029) in ERD group were lower than those in the control group. BMI in ERD group was higher than that in the control group (24.5 vs. 23.1 kg/m(2), p=0.013). CONCLUSIONS: The H. pylori infection rate in ERD group was lower and PG I/II ratio was higher than that in the control group. Reflux esophagitis is thought to be reversely associated with the atrophy of gastric mucosa.

Significance of serum pepsinogens in atrophic gastritis

Chronic atrophic gastritis is a precancerous lesion. A commonly used test for the diagnosis of chronic atrophic gastritis, gastric endoscopy with biopsy collection, and a good serological test would be best include low levels of pepsinogen I [PGI] or a low PGI/PGII ratio. To confirm the use of serum pepsinogens as a screening marker in atrophic gastritis. A study was conducted in the period between December 2005 and March 2006 on 25 patients with artophic gastritis attending Gastroenterology and Hepatology Teaching Hospital in Baghdad, and 25 healyh control subjects. Sera were tested for PGI and PGII by ELISA test the serum PGI were decreased significantly with artophic gastritis and the PGI/PGII ratio were decreased in [78%] of patient group and not affected in healthy people

No association of an SDHC gene polymorphism with gastric cancer.

It is widely reported that reactive oxygen species (ROS) cause apotosis and carcinogenesis. Marked infiltration of activated leukocyte and enhanced production of ROS appear to occur in the gastric mucosa infected with Helicobacter pylori (H. pylori). The previous studies reported that the mutation of the succinate dehydrogenase subunit C (SDHC) gene caused the increase in superoxide anion (O(2)(-)) and oxidative stress. To extend these findings, we epidemiologically investigated the association of a SDHC polymorphism at 3'-untranslated region of exon 6 (JST173800) with H. pylori infection, gastric atrophy and gastric cancer risk in Japan. The subjects consisted of 454 health checkup examinees without a history of cancer and 202 gastric cancer patients. The SDHC polymorphism was not associated with H. pylori infection seropositivity, gastric atrophy, and cancer risk in this study. Although the polymorphism at the 3'-untranslated region could be hypothesized to be functional, this study did not demonstrate any significant association of the SDHC gene polymorphism with gastric atrophy and cancer.

The ACE gene polymorphism is associated with the incidence of gastric cancer among H. pylori seropositive subjects with atrophic gastritis.

Studies of the angiotensin converting enzyme (ACE) I/D polymorphism have provided evidence that the D/D genotype is associated with gastric tumor progression and numbers of lymph node metastases, but not with the overall risk of gastric cancer. The highest levels of circulating and tissue ACE activity were found in carriers of the D/D genotype. Here, we further investigated the association using 454 Japanese subjects undergoing a health checkup and 202 gastric cancer patients. The ACE polymorphism was not found to be linked with H. pylori seropositivity or gastric atrophy. However, among H. pylori seropositive subjects with atrophy, those with the I/D genotype had an increased risk of gastric cancer (OR=1.59; 95% CI, 1.02-2.48). We also established that the polymorphism did not lower the age at diagnosis of gastric cancer. Confirmation of the association between ACE polymorphisms and development of gastric cancer requires much larger studies, and the biological role also needs to be fully elucidated.

Evaluacion de la concentracion serica de pepsinogeno como metodo de tamizaje para gastritis atrofica y cancer gastrico / Evaluation of serum concentration of pepsinogen as screening for athropic gastritis and gastric cancer

El cáncer gástrico en Colombia es un problema de salud pública por su alta incidencia y su diagnóstico tardío, con un porcentaje de cáncer temprano menor de 5 por ciento. Por estas razones, es imprescindible constituir un programa de tamizaje para cáncer gástrico que sea sensible, costo-efectivo y tolerable por los pacientes. El pepsinógeno I y el II han ido sustituyendo en el Japón al método de tamizaje con fluoroscopia ya que, como ha sido demostrado por varios autores, tiene una tasa de detección de cáncer gástrico de 0,168 por ciento comparado con el 0,066 por ciento de la fluoroscopia. Con esto en mente, decidimos evaluar el uso del pepsinógeno I para detectar gastritis crónica atrofia y cáncer gástrico. Para esto se tomaron dos poblaciones: 66 pacientes con cáncer gástrico y 110 tomados de la población general; a todos se les tomó muestra para pepsinógeno I y anticuerpos para Helicobacter pylori (IgG e IgA), con endoscopio y biopsia posterior. Se construyó una curva ROC para definir el mejor punto de corte para el pepsinógeno I, encontrándose que el mejor punto era un valor < 150 ng/ml con una sensibilidad de 84,3 por ciento y una especificidad de 71,3 por ciento. Podemos entonces concluir que el uso de pepsinógeno I es un buen método para detectar gastritis crónica atrófica y cáncer gástrico, y que se debería asociar la determinación del pepsinógeno II en nuestra población por la alta prevalencia de infección por H. pylori que en nuestro estudio fue de 97 por ciento

Serum gastrin and pepsinogen I, II concentrations in children with Helicobacter pylori infection: the role of CagA and VacA

Serum gastrin and pepsinogen concentrations were measured in 51 children infected with Helicobacter pylori, to investigate the clinical significance and influence of CagA and VacA on serum concentrations of these peptides. CagA+ was 44/51 (86%) and VacA+ was 42/51 (82%). Type I (CagA+/VacA+) included 39/51 (76%), type II (CagA-/VacA-) was 4/51 (8%), and intermediate (CagA-/VacA+, CagA+/VacA-) was 8/51 (16%). There was no significant correlation between endoscopic diagnosis and the state of CagA/VacA. Serum gastrin concentrations were not significantly correlated with the state of CagA/VacA. Serum pepsinogen I and II concentrations were significantly higher in CagA+ than in CagA-, but there was no significant difference between VacA+ and VacA-, Serum pepsinogen I/II ratio was not significantly correlated with the state of CagA/VacA. There was no significant difference between serum concentrations of gastrin, pepsinogen I and H. pylori phenotypes. However, pepsinogen II concentration was significantly higher in type I than type II. Pepsinogen I/II ratio was significantly lower in type I and intermediate than in type II. These findings suggest that CagA positively and phenotype of H. pylori could play a role in the development of upper gastrointestinal diseases in children.

Serum pepsinogen levels in patients with gastro-duodenal lesions.

Serum pepsinogen (SP) levels were studied in 100 patients with gastroduodenal lesions, and 100 healthy volunteers. SP levels were significantly elevated in patients with duodenal ulcer (DU) and duodenitis compared to the controls. SP values above 150 ug Tyr/ml/24 hr were highly suggestive of duodenal ulcer disease. Age and sex of patients and controls did not influence SP levels. The mean values of SP in North India were found to be lower in both normal and DU subjects compared to the west.