21.6 : 消化性潰瘍疾患の薬：粘膜保護剤としてのスクラルファート

Recall that increased acid secretion in the gastric lumen disrupts mucosal defense mechanisms and weakens the mucus-bicarbonate barrier.

This enables pepsin to access epithelial cells and digest mucosal proteins, causing mucosal erosion and ulcer formation.

Mucosal protective or cytoprotective agents like sucralfate can inhibit this pepsin-mediated digestion of mucosal proteins.

Sucralfate is a complex of sulfated sucrose and aluminum hydroxide.

In acidic conditions, sucralfate dissociates into aluminum salt and negatively charged sucrose sulfate, which binds with the protein's positively charged groups at the ulcer site.

This creates an extensively cross-linked viscous, sticky polymer that binds to epithelial cells and forms a protective barrier over the sore, limiting acid and pepsin access and promoting ulcer healing.

Other cytoprotective effects of sucralfate include stimulation of prostaglandin production at the ulcerative site.

Prostaglandins promote the secretion of mucus and bicarbonate ions, which are essential components of the mucus-bicarbonate barrier.

These additional actions contribute to the overall healing and protection of the ulcerated area.