Arash Babaei1, Sadaf Shad2, Benson T Massey2. 1. Division of Gastroenterology, Department of Medicine, National Jewish Health, Denver, Colorado. Electronic address: babaeia@njhealth.org. 2. Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Abstract
BACKGROUND & AIMS: In some patients, the type 3 achalasia (A3) motor pattern may be an effect of chronic use of high-dose opioids. No motor findings have been identified to differentiate opioid-induced A3 (OA3) from idiopathic A3 (IA3). We investigated whether OA3 could be distinguished from IA3 on the basis of differences in esophageal motor responses to amyl nitrite, cholecystokinin, or atropine. METHODS: We performed a retrospective study of patients who received pharmacologic provocation during esophageal high-resolution manometry from 2007 through 2017 at a tertiary referral center. We identified 26 patients with IA3 (9 women; mean age, 68 ± 13 years) and 24 patients with OA3 (15 women; mean age, 59 ± 10 years). We compared pressure topography metrics during deglutition and after administration of amyl nitrite, cholecystokinin, or atropine between patients with OA3 vs IA3. RESULTS: Amyl nitrite induced a similar relaxation response in both groups, but the rebound contraction of the lower esophageal sphincter during amyl nitrite recovery, and the paradoxical esophageal contraction during the first phase of cholecystokinin response, were both significantly attenuated in patients with OA3. The second phase of cholecystokinin response in patients with OA3 was 100% relaxation, when present, in contrast to only 26% of patients with IA3. There was no significant difference between groups in inhibition of lower esophageal sphincter tone or esophageal body contractility by cholinergic receptor blockade. CONCLUSIONS: Nearly half of patients with an A3 pattern of dysmotility are chronic, daily users of opioids with manometry patterns indistinguishable from those of patients with IA3. Patients with OA3 differ from patients with IA3 in responses to amyl nitrite and cholecystokinin. These findings might be used to identify patients with dysmotility resulting from opioid use.
BACKGROUND & AIMS: In some patients, the type 3 achalasia (A3) motor pattern may be an effect of chronic use of high-dose opioids. No motor findings have been identified to differentiate opioid-induced A3 (OA3) from idiopathic A3 (IA3). We investigated whether OA3 could be distinguished from IA3 on the basis of differences in esophageal motor responses to amyl nitrite, cholecystokinin, or atropine. METHODS: We performed a retrospective study of patients who received pharmacologic provocation during esophageal high-resolution manometry from 2007 through 2017 at a tertiary referral center. We identified 26 patients with IA3 (9 women; mean age, 68 ± 13 years) and 24 patients with OA3 (15 women; mean age, 59 ± 10 years). We compared pressure topography metrics during deglutition and after administration of amyl nitrite, cholecystokinin, or atropine between patients with OA3 vs IA3. RESULTS:Amyl nitrite induced a similar relaxation response in both groups, but the rebound contraction of the lower esophageal sphincter during amyl nitrite recovery, and the paradoxical esophageal contraction during the first phase of cholecystokinin response, were both significantly attenuated in patients with OA3. The second phase of cholecystokinin response in patients with OA3 was 100% relaxation, when present, in contrast to only 26% of patients with IA3. There was no significant difference between groups in inhibition of lower esophageal sphincter tone or esophageal body contractility by cholinergic receptor blockade. CONCLUSIONS: Nearly half of patients with an A3 pattern of dysmotility are chronic, daily users of opioids with manometry patterns indistinguishable from those of patients with IA3. Patients with OA3 differ from patients with IA3 in responses to amyl nitrite and cholecystokinin. These findings might be used to identify patients with dysmotility resulting from opioid use.
Authors: John E Pandolfino; Qing G Zhang; Sudip K Ghosh; Alexander Han; Christopher Boniquit; Peter J Kahrilas Journal: Gastroenterology Date: 2006-09-08 Impact factor: 22.682
Authors: P J Kahrilas; A J Bredenoord; M Fox; C P Gyawali; S Roman; A J P M Smout; J E Pandolfino Journal: Neurogastroenterol Motil Date: 2014-12-03 Impact factor: 3.598
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Authors: Rena Yadlapati; Peter J Kahrilas; Mark R Fox; Albert J Bredenoord; C Prakash Gyawali; Sabine Roman; Arash Babaei; Ravinder K Mittal; Nathalie Rommel; Edoardo Savarino; Daniel Sifrim; André Smout; Michael F Vaezi; Frank Zerbib; Junichi Akiyama; Shobna Bhatia; Serhat Bor; Dustin A Carlson; Joan W Chen; Daniel Cisternas; Charles Cock; Enrique Coss-Adame; Nicola de Bortoli; Claudia Defilippi; Ronnie Fass; Uday C Ghoshal; Sutep Gonlachanvit; Albis Hani; Geoffrey S Hebbard; Kee Wook Jung; Philip Katz; David A Katzka; Abraham Khan; Geoffrey Paul Kohn; Adriana Lazarescu; Johannes Lengliner; Sumeet K Mittal; Taher Omari; Moo In Park; Roberto Penagini; Daniel Pohl; Joel E Richter; Jordi Serra; Rami Sweis; Jan Tack; Roger P Tatum; Radu Tutuian; Marcelo F Vela; Reuben K Wong; Justin C Wu; Yinglian Xiao; John E Pandolfino Journal: Neurogastroenterol Motil Date: 2021-01 Impact factor: 3.598