In conclusion, normal values were established. These values may prove clinically useful and could contribute to future studies with dysphagic patients.

No abstract

The pathophysiology of esophageal epiphrenic diverticula is still uncertain even though a concomitant motility disorder is found in the majority of patients in different series. High resolution manometry may allow detection of motor abnormalities in a higher number of patients with esophageal epiphrenic diverticula compared with conventional manometry. This study aims to evaluate the high resolution manometry findings in patients with esophageal epiphrenic diverticula. Nine individuals (mean age 63 ± 10 years, 4 females) with esophageal epiphrenic diverticula underwent high resolution manometry. A single diverticulum was observed in eight patients and multiple diverticula in one. Visual analysis of conventional tracings and color pressure plots for identification of segmental abnormalities was performed by two researchers experienced in high resolution manometry. Upper esophageal sphincter was normal in all patients. Esophageal body was abnormal in eight patients; lower esophageal sphincter was abnormal in seven patients. Named esophageal motility disorders were found in seven patients: achalasia in six, diffuse esophageal spasm in one. In one patient, a segmental hypercontractile zone was noticed with pressure of 196 mm Hg. High resolution manometry demonstrated motor abnormalities in all patients with esophageal epiphrenic diverticula.

The comparison between idiopathic achalasia (IA) and Chagas' disease esophagopathy (CDE) may evaluate if treatment options and their outcomes can be accepted universally. This study aims to compare IA and CDE at the light of high-resolution manometry. We studied 86 patients with achalasia: 45 patients with CDE (54% females, mean age 55 years) and 41 patients with IA (58% females, mean age 49 years). All patients underwent high-resolution manometry. Upper esophageal sphincter parameters were similar (basal pressure CDE = 72 ± 45 mmHg, IA = 82 ± 57 mmHg; residual pressure CDE = 9.9 ± 9.9 mmHg, IA = 9.8 ± 7.5 mmHg). In the body of the esophagus, the amplitude was higher in the IA group than the CDE group at 3 cm (CDE = 15 ± 14 mm Hg, IA = 42 ± 52 mmHg, P = 0.003) and 7 cm (CDE = 16 ± 15 mmHg, IA = 36 ± 57 mmHg, P = 0.04) above the lower esophageal sphincter (LES). The LES basal pressure (CDE = 17 ± 16 mmHg, IA = 40 ± 22 mmHg, P < 0.001) and residual pressure (CDE = 12 ± 11 mmHg, IA = 27 ± 13 mmHg, P < 0.001) were also higher in the IA group. Our results show that: (i) there is no difference in regards to the upper esophageal sphincter; (ii) higher pressures of the esophageal body are noticed in patients with IA; and (iii) basal and residual pressures of the LES are lower in patients with CDE. Our results did not show expressive manometric differences between IA and CDE. Some differences may be attributed to a more pronounced esophageal dilatation in patients with CDE.

PPGAP is present in a minority of patients after RYGB; this finding may explain part of the GERD control after RYGB and that the gastric fundus may play a role in the genesis of the PPGAP.

PPGAP is present in a minority of patients after Nissen fundoplication. This finding may explain part of the GERD control and that the gastric fundus may play a role in the genesis of the PPGAP.

No abstract

Gastric motility may play a role in the genesis of PPGAP in patients after RYGB. The contribution of gastric motility for the genesis of PPGAP is still elusive in other patients.