Relation of gallbladder function and Helicobacter pylori infection to gastric mucosa inflammation in patients with symptomatic cholecystolithiasis

Background. Inflammatory alterations of the gastric mucosa are commonly caused by Helicobacter pylori (Hp) infection in patients with symptomatic gallstone disease. However, the additional pathogenetic role of an impaired gallbladder function leading to an increased alkaline duodenogastric reflux is controversially discussed. Aim:To investigate the relation of gallbladder function and Hp infection to gastric mucosa inflammation in patients with symptomatic gallstones prior to cholecystectomy. Patients: Seventy-three patients with symptomatic gallstones were studied by endoscopy and Hp testing. Methods: Gastritis classification was performed according to the updated Sydney System and gallbladder function was determined by total lipid concentration of gallbladder bile collected during mainly laparoscopic cholecystectomy. Results: Fifteen patients revealed no, 39 patients mild, and 19 moderate to marked gastritis. No significant differences for bile salts, phospholipids, cholesterol, or total lipids in gallbladder bile were found between these three groups of patients. However, while only 1 out of 54 (< 2%) patients with mild or no gastritis was found histologically positive for Hp, this infection could be detected in 14 (74%) out of 19 patients with moderate to marked gastritis. Conclusion: Moderate to marked gastric mucosa inflammation in gallstone patients is mainly caused by Hp infection, whereas gallbladder function is not related to the degree of gastritis. Thus, an increased alkaline duodenogastric reflux in gallstone patients seems to be of limited pathophysiological relevance. Copyright (c) 2006 S. Karger AG, Basel

Serum pepsinogen I in the diagnosis of type A gastritis

La gastrite atrophique sévère du fundus (GASF) associée à des modifications moins sévères de la muqueuse antrale, une achlorbydrie, une gastrinémie élevée et des anticorps anti-cellules pariétales, est dénommée gastrite type A et est considérée comme une étape précédant l'anémie pernicieuse Ce type de gastrite est en règle générale accompagné de métaplasie intestinale et souvent de lésions de dysplasie épithéliale sévère, elle-même considérée comme lésion pré-maligne. La muqueuse gastrique humaine produit deux groupes de pepsinogènes, différents du point de vue immunochimique. Les pepsinogènes du groupe I sont synthétisés au niveau de la muqueuse fundique par les cellules principale; et les cellules du collet des glandes Le débit sécrétoire et le taux sérique de ces pepsinogènes est diminué dans la GASF. Nous avons étudié chez 62 patients atteints d'anémie pernicieuse (AP) et chez 171 parent du premier degré, les sensibilité, spécificité et valeur prédictive de taux bas de pepsinogène PG I, de gastrinémie élevée et de présence d'anticorps anti-cellules pariétales (ACP) en rapport avec l'identification d'une GASF. Parmi les patients atteints d'anémie pernicieuse (AP), 98 % présentaient un taux bas de pepsinogène sériue PG I (100 pmol/l) et 40 % avaient un taux d'anticorps anti-cellules pariétales positif. Parmi les sujets apparentés au premier degré des patients-AP, les taux de sensibilité et de spécificité pour le diagnostic de GASF étaient respectivement pour un taux abaissé de pepsinogène sérique PG I, 91 % et 97 %, pour une gastrinémie élevée, 83 % et 97 % et pour un taux d'anticorps anti-cellules pariétales, 65 % et 87 %. L'association gastrinémie élevée et taux abaissé de pepsinogène sérique PG I présente une spécificité de 100% pour la GASF

DNA Methylation Predicts Progression of Human Gastric Lesions

BACKGROUND: Development of the intestinal subtype of gastric adenocarcinoma is marked by a progression of histopathological lesions. Residents of the Andean regions of Colombia are at high risk for gastric cancer. METHODS: A cohort of 976 Colombian subjects was followed over 16 years examining effects of Helicobacter pylori eradication and treatment with anti-oxidants on progression of lesions. We performed methylation analysis of DNA from baseline antral biopsies from 104 subjects for whom follow-up data were available for at least 12 years. Methylation was quantitated for AMPH, CDKN2A, CDH1, EN1, EMX1, NKX6-1, PCDH10, RPRM, RSPO2, SORCS3, ZIC1, and ZNF610 genes, using Pyrosequencing. RESULTS: Levels of DNA methylation were associated with baseline diagnosis for AMPH, EMX1, RPRM, RSPO2, SORCS3 and ZNF610. After adjusting for baseline diagnosis and H. pylori infection, methylation levels of AMPH, PCDH10, RSPO2 and ZNF610 had progression coefficients that increased and p values that decreased over 6, 12 and 16 years. Methylation for SORCS3 was associated with progression at all 3 time points, but without the continual strengthening of the effect. Scores for mononuclear leukocytes, polymorphonuclear leukocytes or intraepithelial lymphocytes were unrelated to progression. CONCLUSIONS: Methylation levels of AMPH, PCDH10, RSPO2, SORCS3 and ZNF610 predict progression of gastric lesions independent of the effect of duration of H. pylori infection, baseline diagnosis, gender of the patient, or scores for mononuclear leukocytes, polymorphonuclear leukocytes or intraepithelial lymphocytes. IMPACT: DNA methylation levels in AMPH, PCDH10, RSPO2, SORCS3 and ZNF610 may contribute to identification of persons with gastric lesions likely to progress