Sa1153 - Esophageal Squamous Cells from Eosinophilic Esophagitis Patients Express a Non-Gastric Proton Pump, and their Th2 Cytokine-Stimulated Secretion of Eotaxin-3 can be Blocked by a Potassium-Competitive Acid Blocker and a Histamine H 2 -Receptor Antagonist

Summary Esophageal food impaction (EFI) is often the first presentation for patients with eosinophilic esophagitis (EoE); however, there is significant heterogeneity in the management of EFI. We aimed to study the impact of EFI management, particularly post-EFI medication prescriptions on EoE diagnosis, follow-up, and recurrence in patients with endoscopic features of EoE. In our retrospective study, adults presenting between 2007 and 2017 with EFI requiring endoscopic dis-impaction with endoscopic features of EoE (furrows, rings, and/or exudates) were included. We examined the impact of demographics and EFI management on EoE diagnosis, follow-up (esophagogastroduodenoscopy [EGD] or clinic visit within 6 months), and recurrence. We identified 164 cases of EFI due to suspected EoE. Biopsy was performed in 68 patients (41.5%), and 144 patients (87.8%) were placed on proton pump inhibitor (PPI) and/or swallow corticosteroids after EFI, including 88.5% of those not biopsied. PPI use at time of biopsy was negatively associated with EoE diagnosis (odds ratio: 0.39, confidence interval: 0.17–0.85). Sixty-one (37.4%) patients were lost to follow-up at 6 months. Recurrent EFI at 1 year occurred in 3.7% of patients. Medications, most commonly PPI, are frequently prescribed after EFI when the endoscopic features of EoE are present, which may mask the diagnosis of EoE on follow-up EGD. We estimated that for every five patients biopsied on PPI, one case of EoE is masked. As recurrent EFI within 1 year is uncommon, empiric therapy should be avoided until diagnostic biopsies are obtained. Further efforts to reduce loss to follow-up after EFI are also needed.

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Luminescent Immunoprecipitation System (LIPS) for Detection of Autoantibodies Against ATP4A and ATP4B Subunits of Gastric Proton Pump H+,K+-ATPase in Atrophic Body Gastritis Patients

Clinical and Translational Gastroenterology ◽

10.1038/ctg.2016.71 ◽

2017 ◽

Vol 8 (1) ◽

pp. e215 ◽

Cited By ~ 13

Author(s):

Edith Lahner ◽

Cristina Brigatti ◽

Ilaria Marzinotto ◽

Marilia Carabotti ◽

Giulia Scalese ◽

...

Keyword(s):

Proton Pump ◽

Gastric Proton Pump

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Hypomagnesemia Induced by Long-Term Treatment with Proton-Pump Inhibitors

Gastroenterology Research and Practice ◽

10.1155/2015/951768 ◽

2015 ◽

Vol 2015 ◽

pp. 1-7 ◽

Cited By ~ 22

Author(s):

Simone Janett ◽

Pietro Camozzi ◽

Gabriëlla G. A. M. Peeters ◽

Sebastiano A. G. Lava ◽

Giacomo D. Simonetti ◽

...

Keyword(s):

Receptor Antagonist ◽

Proton Pump Inhibitors ◽

Proton Pump ◽

Term Treatment ◽

Cross Sectional ◽

Magnesium Metabolism ◽

Poor Renal Function ◽

Long Term Treatment

In 2006, hypomagnesemia was first described as a complication of proton-pump inhibitors. To address this issue, we systematically reviewed the literature. Hypomagnesemia, mostly associated with hypocalcemic hypoparathyroidism and hypokalemia, was reported in 64 individuals on long-term proton-pump inhibitors. Hypomagnesemia recurred following replacement of one proton-pump inhibitor with another but not with a histamine type-2 receptor antagonist. The association between proton-pump inhibitors and magnesium metabolism was addressed in 14 case-control, cross-sectional studies. An association was found in 11 of them: 6 reports found that the use of proton-pump inhibitors is associated per se with a tendency towards hypomagnesemia, 2 found that this tendency is more pronounced in patients concurrently treated with diuretics, carboplatin, or cisplatin, and 2 found a relevant tendency to hypomagnesemia in patients with poor renal function. Finally, findings likely reflecting decreased intestinal magnesium uptake were observed on treatment with proton-pump inhibitors. Three studies did not disclose any relationship between magnesium metabolism and treatment with histamine type-2 receptor antagonists. In conclusion, proton-pump inhibitors may cause hypomagnesemia. In these cases, switching to a histamine type-2 receptor antagonist is advised.

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