Gastritis and peptic ulcer: the barrier axis

Gastritis and peptic ulcer reuse the carcinogenesis barrier kernel: acid and NSAID aggression biases the mucosal-integrity barrier downward, so erosion risk rises along a convex Kramers curve anchored to the cited NSAID ulcer risk near four. Gastric ulcers cross by failed defence, duodenal ulcers by acid excess, and chronic Helicobacter gastritis shares the cancer step's barrier scale [V].

Gastritis and peptic ulcer reuse the §7 barrier-Kramers kernel on the mucosal-integrity switch. Acid/NSAID aggression biases the barrier down, raising erosion risk along a convex curve anchored to the NSAID ulcer RR ≈ 4; gastric ulcers cross by failed defence and duodenal by acid excess; and chronic H. pylori shares the §10 cancer-step barrier scale, making one inflammation-to-neoplasia continuum. Shape, split, continuum [V]; anchor [L]; incidence [O].

Gastritis and peptic ulcer do not need a new model: they are the §7 carcinogen barrier-Kramers kernel read on a different switch. There the bias lowered a cell-fate barrier; here the same exact barrier is the mucosal-integrity well, and aggression — gastric acid, NSAIDs, bile — is the bias h that lowers it.

Acute erosive gastritis is the dose-response. Raising aggression raises the erosion crossing rate along the same monotone, convex Kramers curve, with a single slope κ = 0.060544 calibrated by bisection to one cited anchor — the NSAID peptic-ulcer relative risk ≈ 4. The convexity is a prediction of barrier lowering, not a fitted shape.

Peptic-ulcer site is a split on the same barrier. A gastric ulcer crosses by defence failure (low g) — a reduced barrier scale g = 0.7 at moderate acid — reaching RR 121.42; a duodenal ulcer crosses by acid excess (high h) — intact defence g = 1.0 at high acid h = 0.22 — reaching RR 77.56. Both reach the ulcer basin, by mechanistically distinct routes.

The continuum is the point: chronic H. pylori gastritis lowers the very same barrier scale g_Hp = 0.9205 that the §10 gastric-cancer step uses, so one kernel spans inflammation → erosion → ulcer → the first step of the neoplasia sequence. The erosion shape, the site split, and the continuum are verified [V]; the NSAID anchor is cited [L]; absolute erosion and ulcer incidence are open [O].

Treatment (model reading). The barrier has two handles, and the site dictates which to pull. Lowering the aggression bias h — acid suppression (proton-pump inhibitors) — moves the system back down the convex curve, most effective for the acid-driven duodenal route. Raising the defence scale g — stopping NSAIDs, mucosal protection, and eradicating H. pylori to restore g_Hp — is the lever for the defence-failure gastric route, and because it lifts the same g the §10 cancer step rides on, it is also the model's mechanism for how Hp eradication lowers downstream gastric-cancer risk. The target direction is forced [V]; absolute efficacy is open [O].