Risk of post-stroke pneumonia with proton pump inhibitors, H2 receptor antagonists and mucoprotective agents: A retrospective nationwide cohort study.

Stroke patients are at high risk of developing pneumonia, which is major cause of post-stroke mortality. Proton pump inhibitors and H2 receptor antagonists are anti-ulcer drugs, which may predispose to the development of pneumonia by suppression of the gastric acid with bactericidal activity. Unlike proton pump inhibitors and H2 receptor antagonists, mucoprotective agents have gastroprotective effects with no or less anti-acid property. We aimed to investigate effects of the acid-suppressive medications (proton pump inhibitors and H2 receptor antagonists) and mucoprotective agents on risk for post-stroke pneumonia using the National Health Insurance Service-National Sample Cohort in Korea. This retrospective cohort study included 8,319 patients with acute ischemic stroke. Use of proton pump inhibitors, H2 receptor antagonists, and mucoprotective agents (rebamipide, teprenone, irsogladine, ecabet, polaprezinc, sofalcone, sucralfate, and misoprostol) after stroke were determined based on the prescription records, which were treated as time-dependent variables. Primary outcome was the development of post-stroke pneumonia. During the mean follow-up period of 3.95 years after stroke, 2,035 (24.5%) patients had pneumonia. In the multivariate time-dependent Cox regression analyses (adjusted hazard ratio [95% confidence interval]), there was significantly increased risk for pneumonia with use of proton pump inhibitors (1.56 [1.24-1.96]) and H2 receptor antagonists (1.40 [1.25-1.58]). In contrast to the proton pump inhibitors and H2 receptor antagonists, use of mucoprotective agents did not significantly increase the risk for pneumonia (0.89 [0.78-1.01]). In conclusion, the treatment with proton pump inhibitors and H2 receptor antagonists was associated with increased risk for pneumonia in stroke patients. Clinicians should use caution in prescribing the acid-suppressive medications for the stroke patients at great risk for pneumonia.

Role of mucoprotective agents in endoscopic submucosal dissection-derived ulcers: A systematic review.

BACKGROUND: Currently, it is still unclear whether adding a mucoprotective agent to a proton pump inhibitor (PPI) results in better outcomes compared with using a PPI alone in patients with post-gastric endoscopic submucosal dissection (ESD) ulcers. This study aimed to examine the efficacy of PPI alone versus combination treatment in healing of post-gastric ESD ulcers, as well as on delayed bleeding and amount of blood transfused. METHODS: A systematic search of MEDLINE, EMBASE, Cochrane, and ISI Web of knowledge databases, up until May 2017, for randomized trials comparing PPI alone versus PPI plus a mucoprotective drug in achieving ulcer healing in patients undergoing gastric ESD was performed. The primary outcome is scarring stage on endoscopic assessment at 4 or 8 weeks after gastric ESD. RESULTS: From an initial 3071 citations, eight articles (n = 953 lesions from 934 patients) were analyzed. Patients receiving combination treatment achieved a scarring stage significantly more often than those on a PPIs alone at 4 or 8 weeks after ESD, (risk ratio = 1.36, 95% CI; 1.06-1.75). No study reported amount of blood transfused. There were no significant between treatment-group differences in terms of delayed bleeding (risk ratio = 0.58, 95% CI; 0.17-1.99). Neither location of ulcer nor Helicobacter pylori infection was related to ulcer scarring stage. CONCLUSION: The limited evidences suggested combination treatment may be more effective in accelerating the process of ulcer healing in patients undergoing gastric ESD than the use of PPI alone, but does not appear to alter delayed bleeding risk.

The role of mucoprotectants in the management of gastrointestinal disorders.

INTRODUCTION: The intestinal barrier controls the absorption of nutrients and water whilst helping to prevent the entry of toxins and pathogenic micro-organisms from the lumen into the tissues. Deficiencies in the barrier are associated with various gastrointestinal and extra digestive disorders. Areas covered: This review provides an overview of the relationship between increased intestinal permeability and disease, and considers the role of mucosal protectants (mucoprotectants) in restoring normal intestinal barrier function, with a particular focus on diarrheal disorders. Expert commentary: Impairment of the intestinal barrier characterizes a variety of diseases, and there is ongoing interest in the development of pharmacological approaches targeting the reduction of intestinal permeability. These include corticosteroids, aminosalicylates and anti-tumor necrosis factor-α (TNF-α), which act by reducing inflammation; probiotics, which modulate the production of mucin and epithelial tight junction proteins; and mucoprotectants, which form a protective film over the epithelium. Recently, preclinical and clinical data highlight, the ability of new mucoprotectants, such as gelatin tannate and xyloglucan, to protect the intestinal mucosa and to exert anti-diarrheal effects. In the future the ability of these substances to enhance the intestinal barrier may extend their use in the management of a variety of gastro-intestinal diseases associated with 'leaky gut'.