Gastric histology in children treated with proton pump inhibitors long term, with emphasis on enterochromaffin cell-like hyperplasia

Hassall, Eric; Owen, David A.; Kerr, Wendy; Sturby, Theresa; Richardson, Peter; El–Serag, Hashem B.

doi:10.1111/j.1365-2036.2011.04592.x

Cited by 30 publications

(15 citation statements)

References 20 publications

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“…Although a clear correlation between PPI treatment and g-NETs in humans [18,30,31] is yet to be demonstrated, it has already been established that prolonged PPI-induced acid suppression causes the elevation of circulating gastrin levels in rodents as well as humans [32][33][34][35] and possibly leads to ECL-cell hyperplasia [17,22,36]. In animal safety tests, PPIinduced hypergastrinemia exerts a marked trophic effect on ECL-cell and may induce g-NETs of variable malignancy [22,35,[37][38][39].…”

Section: Discussionmentioning

confidence: 99%

Gastric neuroendocrine neoplasms and proton pump inhibitors: fact or coincidence?

Cavalcoli

Zilli

Conte

et al. 2015

Scandinavian Journal of Gastroenterology

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Section: Discussionmentioning

confidence: 99%

Gastric neuroendocrine neoplasms and proton pump inhibitors: fact or coincidence?

Cavalcoli

Zilli

Conte

et al. 2015

Scandinavian Journal of Gastroenterology

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“…Certaines des réserves formulées chez l'adulte se posent pourtant avec une acuité renforcée chez l'enfant. On citera par exemple le rôle déterminant du métabolisme du calcium pour la constitution de la masse osseuse, ou encore le risque associé à l'apparition de cellules hyperplasiques connues pour pouvoir évoluer vers une gastrite atrophique [67].…”

Section: Contexte Pédiatriqueunclassified

Effets indésirables des inhibiteurs de la pompe à proton : faut-il craindre de les prescrire au long cours ?

Roulet

Vernaz

Giostra

et al. 2012

La Revue de Médecine Interne

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Mots clés :Inhibiteurs de la pompe à proton Fractures ostéoporotiques Infections Cancer gastrique Pharmacodépendance r é s u m é La prévalence des traitements de longue durée par inhibiteurs de la pompe à proton (IPP) est en augmentation. Si leur tolérance à court terme est bonne, des réserves ont vu le jour sur d'éventuels effets indésirables graves associés à une exposition prolongée. Ainsi, l'association avec le risque fracturaire semble être confirmée, notamment au niveau vertébral, ainsi que le risque d'effet rebond sur la sécrétion acide à l'arrêt du traitement. Le risque de pneumopathie communautaire n'est pas établi dans la population générale et semble limité aux patients les plus fragiles. L'association avec le risque d'infection digestive à Clostridium difficile est probable. Les cas de néphrite tubulo-intestitielle sont rares mais peuvent conduire à une insuffisance rénale chronique. Les données disponibles sont encore insuffisantes pour évaluer le risque de carence en vitamine B12, en fer ou en magnésium et le risque de cancer digestif, même si des bases physiopathologiques existent dans le cas du cancer gastrique. Il existe des interactions avec de nombreux autres médicaments, notamment ceux qui sont métabolisés par certaines isoenzymes du cytochrome P450. Enfin, la balance bénéfice-risque de l'utilisation des IPP au long cours chez l'enfant semble défavorable dans la plupart des cas.© 2012 Société nationale française de médecine interne (SNFMI). Publié par Elsevier Masson SAS. Tous droits réservés. Keywords: Proton pump inhibitors Osteoporotic fractures Infection Stomach neoplasms Substance withdrawal syndrome a b s t r a c tLong-term treatment with proton pump inhibitors (PPI) is becoming more prevalent. Although they are well tolerated in the short term, serious concerns about long-term use have arisen. Recent data suggest that the latter is associated with an increased risk for osteoporotic fracture (especially vertebral), Clostridium difficile infection and rebound acid hypersecretion after treatment discontinuation. Acute interstitial nephritis is rare but may progress to chronic renal failure. An increased risk of communityacquired pneumonia has not been established in the general population and seems limited to the most vulnerable patients. Consistent data are still missing to correctly assess the risk of iron deficiency, vitamin B12 deficiency or hypomagnesaemia and the risk of digestive malignant diseases, despite the pathophysiological basis that exists concerning gastric malignancy. Many drug interactions can occur on long-term treatment, including some that imply the cytochrome P450 enzymes. Finally, the risk-benefit balance for a chronic PPI use in children seems unfavorable in most cases.

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“…However, studies have shown that the prolonged of PPIs may lead to an increased risk of an infection due to the suppression of stomach acid, which ordinarily acts as the first line of defense. In addition, long-term use of PPIs increases the risk of a number of other side effects, such as the development of hyperplastic polyps and a reduction in the absorption of certain trace elements and vitamins (2)(3)(4). Therefore, it is necessary to investigate novel anti-ulcer drugs with non-toxic side effects, which may replace antacids.…”

Section: Introductionmentioning

confidence: 97%

Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats

Zhou

et al. 2014

Molecular Medicine Reports

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Curcumin is known to possess anti‑inflammatory properties. Despite the fact that curcumin is known to be a strong inhibitor of H+, K+‑ATPase activity, the mechanism underlying the curcumin‑induced inhibition of the transcription of the H+, K+‑ATPase α subunit in gastric mucosal parietal cells remains unclear. The present study investigated the possible mechanism by which curcumin inhibits stomach H+, K+‑ATPase activity during the acute phase of gastric ulcer disease. A rat model of stress‑induced gastric ulcers was produced, in which the anti‑ulcer effects of curcumin were examined. Curcumin‑induced inhibition of the H+, K+‑ATPase promoter via histone acetylation, was verified using a chromatin immunoprecipitation assay. The results showed that curcumin improved stress‑induced gastric ulcer disease in rats, as demonstrated by increased pH values and reduced gastric mucosal hemorrhage and ulcer index. These effects were accompanied by a significant reduction in the level of histone H3 acetylation at the site of the H+, K+‑ATPase promoter and in the expression of the gastric H+,K+‑ATPase α subunit gene and protein. In conclusion, curcumin downregulated the acetylation of histone H3 at the site of the H+, K+‑ATPase promoter gene, thereby inhibiting the transcription and expression of the H+, K+‑ATPase gene. Curcumin was shown to have a preventive and therapeutic effect in gastric ulcer disease.

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Gastric histology in children treated with proton pump inhibitors long term, with emphasis on enterochromaffin cell-like hyperplasia

Abstract: SUMMARY Background

Cited by 30 publications

References 20 publications

Gastric neuroendocrine neoplasms and proton pump inhibitors: fact or coincidence?

Gastric neuroendocrine neoplasms and proton pump inhibitors: fact or coincidence?

Effets indésirables des inhibiteurs de la pompe à proton : faut-il craindre de les prescrire au long cours ?

Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats

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