Much of the divergence of theories concerning the etiology of gastric and duodenal ulcers may be more apparent than real. The experimental evidence in most of them agrees in one fundamental respect; e.g., the direct cause of ulcer is arterial obstruction. For example, the investigations of Payr,1 in which ulcers of the stomach followed the experimental production of endarteritis obliterans; the experiments of F. Rosenbach,2 in which ulcers followed prolonged vasoconstriction, and the researches of Honda,3 in which ulcers were produced by sterile emboli, represent fundamental principles of three theories considered divergent. Each of these, however, is but the expression of a method by which arterial obstruction may be produced.
From a histologic standpoint this theory of arterial obstruction has met considerable objection. Though all investigators admit the frequency of arterial obstructive changes in clinical ulcers, it is questioned whether these may not all be secondary and
SCHUTZ CB. THE ETIOLOGY OF GASTRIC AND DUODENAL ULCERS: A LARGE SECTION HISTOLOGIC STUDY OF LOCAL BLOOD VESSEL CHANGES IN POSTMORTEM SPECIMENS (PRELIMINARY REPORT). JAMA. 1931;96(26):2182–2185. doi:10.1001/jama.1931.02720520010003
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