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An assessment of enteric nervous system and estroprogestinic receptors in obstructed defecation associated with rectal intussusception


Address for Correspondence
Professor Gabrio Bassotti, Clinica di Gastroenterologia ed Epatologia, Ospedale Santa Maria della Misericordia, Piazzale Menghini, 1, 06156 San Sisto (Perugia), Italy.
Tel: +39 075 578 4423; fax: +39 075 5847570;


Background  The pathophysiological basis of obstructed defecation (OD) is still incompletely understood. In particular, few or no data are available concerning the enteric nervous system (ENS) in this condition. We investigated ENS abnormalities in patients with OD, undergoing surgery, together with the presence of estrogen (α and β) and progesterone receptors, and compare the results with those obtained in controls.

Methods  Full-thickness rectal samples were obtained from 17 patients undergoing stapled transanal rectal resection for OD associated with rectal intussusception. Samples were analyzed by immunohistochemistry for enteric neurons, enteric glial cells, interstitial cells of Cajal (ICC), and for estrogen and progesterone receptors. Data were compared with those obtained in 10 controls.

Key Results  No differences between patients and controls were found for enteric neurons, whereas (compared with controls) OD patients displayed a significant decrease of enteric glial cells in both the submucous (= 0.0006) and the myenteric (< 0.0001) plexus. ICC were significantly increased in patients in the submucosal surface (< 0.0001) and the myenteric area (< 0.0001). Concerning estroprogestinic receptors, both were present on ICC in patients and controls. Estrogen receptors α and progesterone receptors were absent on enteric neurons and enteric glial cells in patients and controls, whereas estrogen receptors β were present in all controls and in 69% of patients’ enteric neurons (= 0.18) and in 12% of patients’ glial cells (= 0.0001).

Conclusions & Inferences  Patients with OD associated to rectal intussusception display abnormalities of the ENS and of estrogen receptors β.