The pathology of regional Ileitis
Identifieur interne : 012228 ( Main/Curation ); précédent : 012227; suivant : 012229The pathology of regional Ileitis
Auteurs : G. W. H. Schepers [Afrique du Sud]Source :
- The American Journal of Digestive Diseases [ 0002-9211 ] ; 1945-04-01.
Abstract
Conclusions: 1. The literature on Regional Ileitis as a clinico-pathological entity is reviewed and suggestions made as to what is required from future research. 2. A detailed study of the pathology, particularly the pathological histology is involved. 3. The disease has two components; namely: A. A primary phase, characterized by i. a stage of oedema of the submucosa and serosa with dilatation of submucosal lymphatics and hyperaemia of juxta-muscular adventitial blood vessels; ii. a stage of plasma cell infiltration of the submucosa and serosa; iii. diffuse fibrosis, with disappearance of the plasma cells, except where trapped; and iv. healing. B. A secondary phase, characterized by ulceration superimposed on any of these phases of the primary lesion, with corresponding modification of the pathological process. There are tendencies to early or late perforation; fistulation, and granuloma formation. 4. A critical analysis of possible aetiological factors suggests that the primary disturbance is due to either acute injury of the bowel wall by a metabolite, probably lipoid in character, or results from a neuropathic disturbance involving Auerbach’s and, or, Meissner’s plexuses, or mesenteric and coeliac ganglia. In nature the original neuropathic lesion is possibly a type of visceral herpes zoster. It is suggested that the chronic type of secondary ulceration only occurs when ganglionic lesions are not only irritative but destructive, and thus lead to denervation of the affected bowel wall.
Url:
DOI: 10.1007/BF02998555
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<front><div type="abstract" xml:lang="en">Conclusions: 1. The literature on Regional Ileitis as a clinico-pathological entity is reviewed and suggestions made as to what is required from future research. 2. A detailed study of the pathology, particularly the pathological histology is involved. 3. The disease has two components; namely: A. A primary phase, characterized by i. a stage of oedema of the submucosa and serosa with dilatation of submucosal lymphatics and hyperaemia of juxta-muscular adventitial blood vessels; ii. a stage of plasma cell infiltration of the submucosa and serosa; iii. diffuse fibrosis, with disappearance of the plasma cells, except where trapped; and iv. healing. B. A secondary phase, characterized by ulceration superimposed on any of these phases of the primary lesion, with corresponding modification of the pathological process. There are tendencies to early or late perforation; fistulation, and granuloma formation. 4. A critical analysis of possible aetiological factors suggests that the primary disturbance is due to either acute injury of the bowel wall by a metabolite, probably lipoid in character, or results from a neuropathic disturbance involving Auerbach’s and, or, Meissner’s plexuses, or mesenteric and coeliac ganglia. In nature the original neuropathic lesion is possibly a type of visceral herpes zoster. It is suggested that the chronic type of secondary ulceration only occurs when ganglionic lesions are not only irritative but destructive, and thus lead to denervation of the affected bowel wall.</div>
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