Management of upper gastrointestinal symptoms in patients with autoimmune gastritis

Abstract

Purpose of reviewAutoimmune gastritis is characterized by atrophy of acid secreting parietal cells resulting in achlorhydria. Upper gastrointestinal symptoms are common in autoimmune gastritis and frequently result in prescriptions for acid suppressant medications despite the inability of the stomach to secrete acid. Evidence-based recommendations for management of gastrointestinal symptoms in autoimmune gastritis are lacking. Recent findingsThe most common symptoms in patients with autoimmune gastritis are dyspepsia, heartburn, and regurgitation. Gastroesophageal reflux should be confirmed by pH-impedance testing and is typically weakly acid or alkaline. Therapy for reflux focuses on mechanical prevention of reflux (i.e., elevation of the head of the bed and alginates) or when severe, antireflux surgery. The etiology of dyspepsia in autoimmune gastritis is unclear and largely unstudied. In the first half of the 20th century, oral administration of acid to ''aid digestion'' was widely used with reported success. However, randomized, placebo-controlled trials are lacking. Here, we provide suggestions for attempting gastric acidification therapy. SummaryUpper GI symptoms are common in autoimmune gastritis. Their pathogenesis and therapy remain incompletely understood. Acid suppressant medications are useless and should be discontinued. A trial of acid replacement therapy is recommended especially in the form of placebo-controlled trials.

Creating a Framework for Treating Autoimmune Gastritis—The Case for Replacing Lost Acid

“…Hypochlorhydria is perhaps the earliest sign of AIG and may precede the development of B12 deficiency by several years [ 39 ]. Hypochlorhydria is typically defined as a gastric pH > 4, with achlorhydria defined as a pH > 7 [ 21 ].…”

“…The increase in nitrosation may also increase the risk of gastric adenocarcinoma, though the Correa model of gastric carcinogenesis refers to multifocal (corpus + antral) atrophy as a requirement, while in AIG, atrophy is confined to the corpus. As such, the increased risk of gastric adenocarcinoma is under debate [ 39 , 51 ]. The risk of developing type 1 NETs in AIG is from 0.4–7%, and the incidence of gastric adenocarcinoma ranges from 0 to 1.8% per year [ 5 ].…”

“…It is well known that the hypochlorhydria of AIG contributes to B12 deficiency, but it is perhaps less known that hypochlorhydria first causes iron deficiency. Approximately 50% of patients with AIG are iron deficient, and 37–60% are B12 deficient [ 39 ]. Given that both are hematopoietic nutrients, it is surprising that anemia is found in only half of AIG patients at diagnosis [ 6 ].…”

“…In 1918, Crohn found that diluted HCL supplementation did not improve protein digestion in patients with achlorhydria; this may be because the HCL solution is rapidly neutralized by the stomach [ 35 ]. In 1942, Westfall studied 300 patients with achlorhydria; 76% of them reported that their symptoms improved with HCL supplementation [ 39 ]. HCL supplementation was not able to improve non-heme iron absorption in patients with atrophic gastritis studied in the 1960s and 1970s [ 18 ].…”

“…Despite the limited scope of BHCL studies in humans, BHCL appears to be tolerated in healthy stomachs and by the majority of subjects with functional dyspepsia. Experts in AIG recommend trials of BHCL to ameliorate the GI side effects of hypochlorhydria [ 10 , 39 ].…”