• A Reappraisal of the Pathophysiology of Cushing Ulcer: A Narrative Review
• Randomised clinical trial: 3-year interim analysis results of the VISION trial to evaluate the long-term safety of vonoprazan as maintenance treatment in patients with erosive oesophagitis
• Laparoscopic versus laparoscopy-assisted suturing of perforated peptic ulcers (meta-analysis)
• Comparison of Concordance of Peptic Ulcer Disease, Non-Adenomatous Intestinal Polyp, and Gallstone Disease in Korean Monozygotic and Dizygotic Twins: A Cross-Sectional Study
• A new model to predict the risk of major gastrointestinal bleeding in patients on direct oral anticoagulants (dabigatran and rivaroxaban)
• Metabolic effects of truncal vagotomy when combined with bariatric-metabolic surgery
• Analysis of Adverse Reactions of Aspirin in Prophylaxis Medication Based on FAERS Database
• The surgical management of complicated peptic ulcer disease: An EAST video presentation

Peptic ulcer disease is a condition in which there are painful sores or ulcers in the lining of the stomach or the first part of the small intestine (the duodenum). Normally, a thick layer of mucus protects the stomach lining from the effect of its digestive juices.

A duodenal ulcer is a peptic ulcer that develops in the first part of the small intestine (duodenum). An esophageal ulcer occurs in the lower part of your esophagus.

Steroid side effects

In 1932, Harvey Cushing described peptic ulceration secondary to raised intracranial pressure and attributed this to vagal overactivity, causing excess gastric acid secretion. Cushing ulcer remains a cause of morbidity in patients, albeit one that is preventable.

Kumaria et al. evaluate the evidence pertaining to the pathophysiology of neurogenic peptic ulceration. A literature review suggests that the pathophysiology of Cushing ulcer may extend beyond vagal mechanisms for several reasons: (1) clinical and experimental studies have shown only a modest increase in gastric acid secretion in head injury patients; (2) increased vagal tone is found in only a minority of cases of intracranial hypertension, most of which are related to catastrophic, nonsurvivable brain injury; (3) direct stimulation of the vagus nerve does not cause peptic ulceration, and; (4) Cushing ulcer can occur after acute ischemic stroke, but only a minority of strokes are associated with raised intracranial pressure and/or increased vagal tone. The 2005 Nobel Prize in Medicine honored the discovery that bacteria play key roles in the pathogenesis of peptic ulcer disease. Brain injury results in widespread changes in the gut microbiome in addition to gastrointestinal inflammation, including systemic upregulation of proinflammatory cytokines. Alterations in the gut microbiome in patients with severe traumatic brain injury include colonization with commensal flora associated with peptic ulceration. The brain-gut-microbiome axis integrates the central nervous system, the enteric nervous system, and the immune system.

They propose a novel hypothesis that neurogenic peptic ulcer may be associated with alterations in the gut microbiome, resulting in gastrointestinal inflammation leading to ulceration ¹⁾.

Omeprazole for Adults with peptic ulcers or gastroesophageal reflux disease (GERD) 20–40 mg PO daily. For Zollinger-Ellison syndrome: 20 mg PO q d to 120 mg PO TID (dose adjusted to keep basal acid output < 60 mEq/hr).

Side effects: N/V, H/A, diarrhea, abdominal pain, or rash in 1–5% of patients. Supplied: 10, 20 & 40 mg delayed-release capsules. Available OTC in 20.6 mg tablets as Prilosec OTC.

Misoprostol (Cytotec®), a prostaglandin, may be effective in mitigating NSAID-induced gastric erosion or peptic ulcer. Contraindicated in pregnancy. ℞ 200 mcg PO QID with food as long as the patient is on NSAIDs. If not tolerated, use 100 mcg. ✖ CAUTION: an abortifacient. Should not be given to pregnant women or women of childbearing potential