Chronic use of proton pump inhibitors and the quantity of g, d, and ecl cells in the stomach / Uso crônico de inibidores de bomba de prótons e a quantidade de células g, d e ecl no estômago

ABSTRACT Background: Acid inhibition from chronic proton pump inhibitor use and a possible increase in gastrin can lead to changes in the regulation of hydrochloric acid production. However, it has not known whether such chronic use changes the presence of gastrin, delta, and enterochromaffin-like cells in the stomach or the relationship between gastrin and delta cells. Aim: To analyze the number of gastrin-producing gastrin cells, somatostatin-producing cells, and histamine-producing cells in patients who were chronic users of proton pump inhibitor, with or without related Helicobacter pylori infection. Methods: Biopsies from 105 patients, including 81 chronic proton pump inhibitor users (experimental group) and 24 controls, were processed immunohistochemically and subjected to counting of gastrin, delta, and enterochromaffin-like cells in high-magnification microscopic fields and in 10 glands. Results: Gastrin cell, delta cell, and enterochromaffin-like cells counts were similar across the groups and appeared to be unaffected by Helicobacter pylori infection. The ratio between gastrin cells and delta cells was higher in the chronic users of proton pump inhibitor group than in controls. Conclusion: Chronic users of proton pump inhibitor does not affect gastrin cell, delta cell, and enterochromaffin-like cell counts significantly, but may alter the ratio between gastrin cells and delta cells.

RESUMO Racional: A inibição ácida pelo uso crônico de inibidores de bomba de prótons e o possível aumento da gastrina podem ser seguidos de alterações na regulação da produção do ácido clorídrico. Ainda não está definido se o uso crônico altera a quantidade de células G, D e ECL no estômago ou a razão células G/D. Objetivo: Avaliar o número de células G - produtoras de gastrina -, células D - produtoras de somatostatina - e células ECL - produtoras de histamina -, em pacientes com uso crônico de inibidores de bomba de prótons, com ou sem infecção pelo Helicobacter pylori. Método: Trata-se de estudo retrospectivo avaliando 105 pacientes, 81 usadores crônicos de inibidores de bomba de prótons e 24 controles, através de biópsias com contagem das células G, D e ECL por estudo imunoistoquímico, de forma quantitativa onde havia maior número de células positivas por campo microscópico de grande aumento e em 10 glândulas. Resultados: Não houve diferença estatística comparando-se o número de células G, D e ECL. A razão entre as células G e D foi maior nos pacientes usadores crônicos de inibidores de bomba de prótons. Conclusão: O uso crônico de inibidores de prótons parece não interferir na contagem das células G, D e ECL, porém, interfere na razão entre as células G e D.

Effects of Proton Pump Inhibitors on Atrophic Gastritis and Gastric Cancer: Safe Perspective / 대한내과학회지

Proton pump inhibitors (PPIs) are widely used over 20 years for management of symptoms due to acid related diseases such as peptic ulcer and reflux esophagitis. Serious adverse events are extremely rare for short-term PPIs use. Recently, as long-term PPIs use increase, diverse reports have been reported on adverse event related with long-term PPIs use. Long-term PPIs use is generally referred as use of PPIs more than 1 year. Secondary hypergastrinemia after long-term PPIs use is associated with development of fundic gland polyps (FGP) and hyperplasia of enterochromaffin-like cell (ECL) that might be concerned with gastric carcinoid tumor. Furthermore, several studies have posed the relationship between the risk of gastric cancer and long-term PPIs use with co-existing H. pylori infection. The present review summarize the recent accumulated evidence on neoplasm associated with secondary hypergastrinemia after long-term PPIs use.

Concerns on Atrophic Gastritis and Neoplasia: Unsafe Perspective / 대한내과학회지

Proton-pump inhibitors (PPI) have important roles in the management of acid-related disorders, especially gastro-esophageal reflux disease and peptic ulcer disease. They are considered safe, but some side effects, such as oxyntic cell hyperplasia, glandular cysts, hypergastrinemia and fundic gland polyps, are also reported. Long-term PPI administration in Helicobacter pylori (H. pylori) positive subjects promotes a shift from antral to corpus-predominant gastritis. The shift leads to corpus atrophy eventually that is known predisposing factor of gastric adenocarcinoma. It is recommended that patients being considered for long-term PPI therapy should be tested for H. pylori infection. And if present, H. pylori eradication should be preceded to PPI administration. Also, long-term PPI administration can cause enterochromaffin-like cell hyperplasia. Although the underlying mechanism and pathogenesis are not yet fully understood, it is possible that long-term PPI administration can promote the development of gastric carcinoid tumor. Therefore, to minimize the side effects, it should be used in adequate dose for a precise duration.

Development of carcinoid tumors of the glandular stomach and effects of eradication in Helicobacter pylori-infected Mongolian gerbils.

The relation between Helicobacter pylori (Hp) eradication and prevention of stomach carcinoid development has hitherto remained unclear. We therefore examined this problem using an Hp-infected and Hp-eradicated Mongolian gerbil (MG) model. Enterochromaffin-like (ECL) lesions (hyperplasia/dysplasia and carcinoid) were histopathologically evaluated in the glandular stomachs of Hp-infected and Hp-eradicated MGs. In addition, serum gastrin levels were analyzed. Hp infection induced significant increase in the development of ECL lesions in the glandular stomach, as well as serum gastrin levels as compared with non-infected MGs, while Hp eradication was associated with significant alleviation. The development of ECL lesions in the glandular stomach strongly correlated with titers of anti-Hp antibodies and serum gastrin levels in MGs. In conclusion, Hp infection induces carcinoid development, and Hp eradication prevents its occurrence in the glandular MG stomach, this being strongly linked with reduction in serum gastrin levels.

A case of multiple gastric carcinoid tumors associated with Sjogren's syndrome / 대한내과학회지

Carcinoid tumors are rare endocrine neoplasms arising from the enterochromaffin or enterochromaffin-like cells. Gastric carcinoids associated with autoimmune atrophic gastritis and hypergastrinemia, are usually multiple and the prognosis are better compared to solotary lesions with out hypergastrinemia. Gastric carcinoids are commonly associated with other endocrine disorders or tumors, but any associations with autoimmune disorders other than autoimmune atrophic gastritis have rarely been reported. Sjogren's syndrome is an autoimmune exocrinopathy that primarily affects the salivary glands, but it can also involve almost any other part of the gut. The most common form of gastrointestinal involvement in Sjogren's syndrome is chronic atrophic gastritis, which can lead to hypergastrinemia and the subsequent development of carcinoid. However, gastric carcinoid tumor associated with Sjogren's syndrome has not yet been reported on. To the best of our knowledge, this is the first such case in the world. We report on this case along with review of the related literature.