Gastric Acid-Dependent Diseases: A Twentieth-Century Revolution

Sachs, George; Shin, Jai Moo; Munson, Keith; Scott, David

doi:10.1007/s10620-014-3104-8

Cited by 28 publications

(14 citation statements)

References 62 publications

(58 reference statements)

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“…Nevertheless, the effect of these drugs on the modification of intestinal microflora should be fully clarified in the future. The profound gastric acid suppression induced by long-term PPI treatment may alter intestinal microflora, 43,44 thus PPI administration has been suggested to be a risk factor for development of SIBO, though that relationship remains undetermined. Some studies have found no correlation between PPI use and SIBO as measured by indirect breath tests, whereas others that used small bowel aspirates showed a higher association of SIBO with PPI administration as compared to the least potent gastric antisecretory therapy.…”

Section: Discussionmentioning

confidence: 99%

Small Intestinal Bacterial Overgrowth in Patients with Refractory Functional Gastrointestinal Disorders

Shimura

Ishimura

Mikami

et al. 2015

J Neurogastroenterol Motil

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Background/AimsSmall intestinal bacterial overgrowth (SIBO) is considered to be involved in the pathogenesis of functional gastrointestinal disorders (FGID). However, the prevalence and clinical conditions of SIBO in patients with FGID remain to be fully elucidated. Here, we examined the frequency of SIBO in patients with refractory FGID. MethodsWe prospectively enrolled patients with refractory FGID based on Rome III criteria. A glucose hydrogen breath test (GHBT) was performed using a gas analyzer after an overnight fast, with breath hydrogen concentration measured at baseline and every 15 minutes after administration of glucose for a total of 3 hours. A peak hydrogen value ≥ 10 ppm above the basal value between 60 and 120 minutes after administration of glucose was diagnosed as SIBO. ResultsA total of 38 FGID patients, including 11 with functional dyspepsia (FD), 10 with irritable bowel syndrome (IBS), and 17 with overlapping with FD and IBS, were enrolled. Of those, 2 (5.3%) were diagnosed with SIBO (one patient diagnosed with FD; the other with overlapping FD and IBS). Their symptoms were clearly improved and breath hydrogen levels decreased to normal following levofloxacin administration for 7 days. ConclusionsTwo patients initially diagnosed with FD and IBS were also diagnosed with SIBO as assessed by GHBT. Although the frequency of SIBO is low among patients with FGID, it may be important to be aware of SIBO as differential diagnosis when examining patients with refractory gastrointestinal symptoms, especially bloating, as a part of routine clinical care. (J Neurogastroenterol Motil 2016;22:60-68)

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Section: Discussionmentioning

confidence: 99%

Small Intestinal Bacterial Overgrowth in Patients with Refractory Functional Gastrointestinal Disorders

Shimura

Ishimura

Mikami

et al. 2015

J Neurogastroenterol Motil

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“…Proton pump inhibitors (PPIs) are used by millions of patients for treatment and prevention of peptic ulcers, gastro‐oesophageal reflux disease and NSAID‐induced mucosal damage . There is accumulating evidence that PPIs induce hypomagnesaemia .…”

Section: Introductionmentioning

confidence: 99%

Inulin significantly improves serum magnesium levels in proton pump inhibitor‐induced hypomagnesaemia

Hess

Baaij

Broekman

et al. 2016

Aliment Pharmacol Ther

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“…Acid secretion depends on activation of the gastric H + , K + -ATPase, termed as the acid or proton pump. This enzyme was found uniquely in gastric parietal cells and in renal collecting ducts [ 1 ]. Parietal cells are located at oxyntic gastric gland of the corpus (Fig.…”

Section: + -Atpase With Regard To H Pylori Infectionmentioning

confidence: 98%

“…There are three regulatory molecules (acetylcholine, histamine, and gastrin) that stimulate acid secretion and one regulatory molecule (somatostatin) that inhibits acid secretion [ 1 ] (Fig. 4.1 ).…”

Section: + -Atpase With Regard To H Pylori Infectionmentioning

confidence: 99%

Change of Acid Secretions, Ghrelin and Leptin, by H. pylori

Kim

Choi

2016

Helicobacter Pylori

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When Helicobacter pylori ( H. pylori ) begins to colonize on the surface of gastric epithelium, H. pylori induces strong infl ammatory responses and causes a transitory hypochlorhydria. The main underlying mechanisms are, fi rst, H. pylori represses the activity of promoter of the alpha-subunit (HKα) of H + , K + -ATPase, and second, cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α suppress gastric acid. Third, H. pylori -induced gastritis evokes decrease of parietal cell numbers. In the chronic H. pylori gastritis, the change of gastric acid is mainly determined by the pattern of corpus gastritis. That is, in the antral-predominant gastritis, acid secretion increases due to increase of gastrin secretion. In the situation of corpus-predominant gastritis, acid secretion is decreased similar to the acute gastritis. The acute response after H. pylori eradication includes the increase of gastric acid mainly due to the clearance of H. pylori itself and its secreted proteins, reversed activity of H + , K + -ATPase, and decrease of IL-1β and TNF-α. After this acute response phenomenon, the change of acid secretion depends on gastritis pattern. That is, in the situation of corpus-predominant gastritis, acid secretion increases slowly until 2 years depending on the severity of atrophic gastritis. In the

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Gastric Acid-Dependent Diseases: A Twentieth-Century Revolution

Cited by 28 publications

References 62 publications

Small Intestinal Bacterial Overgrowth in Patients with Refractory Functional Gastrointestinal Disorders

Small Intestinal Bacterial Overgrowth in Patients with Refractory Functional Gastrointestinal Disorders

Inulin significantly improves serum magnesium levels in proton pump inhibitor‐induced hypomagnesaemia

Change of Acid Secretions, Ghrelin and Leptin, by H. pylori

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