Opioids are standard for analgesia; however, their effects on gastric dysfunction is relatively poorly studied. The higher incidence of gastric lesions in opioid users resulted in increased hospitalizations. Pain management is an important challenge worldwide. Opioids are the most effective pain killers for cancer and postoperative pain and are also increasingly used in non-cancer diseases.
Although morphine is the main drug for pain relief, morphine use also causes adverse effects, such as nausea, vomiting, and reduced gastrointestinal motility, called opioid-induced intestinal dysfunction (OBD). Reduced gastrointestinal transport causes abdominal distension and idiopathic constipation, which to to esophageal reflux disease. Even clinical doses of opioid analgesics can cause adverse gastrointestinal side effects.
Recently, researchers from the University of Miami are working at Br J Pharmacol. The article titled "Morphine use induces gastric microbial dysbiosis driving gastric inflammation through TLR2 signalling which is attenuated by proton pump inhibition", The study listed morphine-induced gastric acid as a driver of gastric biological dysbiosis and pathology, And suggest using PPI as an inexpensive approach to the clinical treatment of morphine-related pathophysiology.
In this study, the investigators investigated the effects of morphine use on gastric pathology and its underlying mechanisms. The therapeutic benefits of proton pump inhibition in overcoming morphine-mediated gastric inflammation were further investigated. The investigators implanted 25 mg of slow-release morphine and placebo micropills in mice. The gastric microbiome analysis was performed. Detection of gastric damage in rats. The gastric fluid pH value was determined.germ-free and TLR2KO mice were used to investigate the mechanism of action. Gastric protection studies were performed using a proton pump inhibitor (PPI) omeprazole.
Chronic morphine treatment changes the composition of gastric microbes and induces a preferential expansion of pathogenic communities such as Streptococcus and Pseudomonas sp. Morphine leads to disruption of the gastric mucosal layer, increases apoptosis, and increases inflammatory cytokines. Furthermore, in germ-free mice, the morphine-induced gastric lesions were significantly reduced, and the reconstruction of the morphine gastric microbiota in germ-free mice led to gastric inflammation.
Furthermore, morphine-mediated gastric inflammation was also reduced in TLR2KO mice. Morphine causes a drop in pH in the stomach, which leads to biological disorders and inflammation of the stomach. Omeprazole treatment suppresses gastric acid, saves gastric metabolism, and prevents inflammation.
