GAST and duodenal ulcer: Cysteamine (β-mercaptoethylamine) swiftly induces ulceration, escalates gastric acid secretion, diminishes somatostatin bioavailability [25], and elevates serum gastrin levels [26], thereby fostering increased gastric acid production and impeding defensive mechanisms like alkaline mucus secretion and bicarbonate levels in the proximal duodenum, ultimately culminating in duodenal ulcer formation [24].