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High-resolution Manometry Findings in Patients After Sclerotherapy for Esophageal Varices.
Journal of Neurogastroenterology and Motility 2016 April 31
BACKGROUND/AIMS: Endoscopic therapy for esophageal varices may lead to esophageal dysmotility. High-resolution manometry is probably the more adequate tool to measure esophageal motility in these patients. This study aimed to evaluate esophageal motility using high resolution manometry following eradication of esophageal varices by endoscopic sclerotherapy.
METHODS: We studied 21 patients (11 women, age 52 [45-59] years). All patients underwent eradication of esophageal varices with endoscopic sclerotherapy and subsequent high resolution manometry.
RESULTS: A significant percentage of defective lower esophageal sphincter (basal pressure 14.3 [8.0-20.0] mmHg; 43% hypertonic) and hypocontractility (distal esophageal amplitude 50 [31-64] mmHg; proximal esophageal amplitude 40 [31-61] mmHg; distal contractile integral 617 [403-920] mmHg·sec·cm; 48% ineffective) was noticed. Lower sphincter basal pressure and esophageal amplitude correlated inversely with the number of sessions (P < 0.001). No manometric parameter correlated with symptoms or interval between last endoscopy and manometry.
CONCLUSIONS: Esophageal motility after endoscopic sclerotherapy is characterized by: (1) defective lower sphincter and (2) defective and hypotensive peristalsis. Esophageal dysmotility is associated to an increased number of endoscopic sessions, but manometric parameters do not predict symptoms.
METHODS: We studied 21 patients (11 women, age 52 [45-59] years). All patients underwent eradication of esophageal varices with endoscopic sclerotherapy and subsequent high resolution manometry.
RESULTS: A significant percentage of defective lower esophageal sphincter (basal pressure 14.3 [8.0-20.0] mmHg; 43% hypertonic) and hypocontractility (distal esophageal amplitude 50 [31-64] mmHg; proximal esophageal amplitude 40 [31-61] mmHg; distal contractile integral 617 [403-920] mmHg·sec·cm; 48% ineffective) was noticed. Lower sphincter basal pressure and esophageal amplitude correlated inversely with the number of sessions (P < 0.001). No manometric parameter correlated with symptoms or interval between last endoscopy and manometry.
CONCLUSIONS: Esophageal motility after endoscopic sclerotherapy is characterized by: (1) defective lower sphincter and (2) defective and hypotensive peristalsis. Esophageal dysmotility is associated to an increased number of endoscopic sessions, but manometric parameters do not predict symptoms.
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