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Keywords:

  • Achalasia;
  • dilatation;
  • high-resolution manometry;
  • upper esophageal sphincter

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

Background

Pneumatic dilation of the lower esophageal sphincter (LES) in achalasia has an unappreciated effect on upper esophageal sphincter (UES) function. We studied UES pressure patterns at baseline and alterations in UES parameters resulting from therapy.

Methods

High-resolution manometry (HRM) tracings from 50 achalasia patients, seen at a tertiary center between January 2009 and July 2011, were reviewed. Manometric parameters studied were (i) LES: resting pressure (restP), 4-second integrated relaxation pressure (IRP4); (ii) UES: resting pressure (restP), minimal relaxation pressure (MRP), peak pressure (PP), relaxation interval (RI), intrabolus pressure (IBP), and deglutitive sphincter resistance (DSR). Mixed models analyses with LES and UES parameters as dependent variables and treatment stage as within-subject independent variable of interest were used. Correlations between treatment-induced changes in LES, UES, and esophageal body (EB) parameters were performed.

Key Results

Pre- and posttreatment HRM tracings were available from 50 patients (mean age 52.7 ± 18.6 years, 29 men). Upper esophageal sphincter parameters MRP (17.9 ± 1.2 vs 15.2 ± 0.9 mmHg; p = 0.02) and IBP (31.5 ± 1.5 vs 27.4 ± 1.2 mmHg; p = 0.009) were significantly reduced after initial balloon dilation and this effect was significant in type II achalasia (p = 0.002 and p = 0.0006). Peak pressure, RI, and DSR were not. The therapeutic effect on LES IRP4 correlated significantly with the change in UES MRP, statistically mediated by the change in EB deglutitive pressure (p = 0.004 and p = 0.0002).

Conclusions & Inferences

We present the first HRM study demonstrating that pneumatic dilation of the LES affects intraesophageal and UES pressures in patients with achalasia.

Key Messages
  • Pneumatic dilation of the LES affects intra-esophageal and UES pressures in patients with achalasia.
  • Purpose of the study was to investigate if deglutitive UES function differed in patients with achalasia compared to healthy controls and if deglutitive UES function was affected by treatment of EGJ hypertonicity using pneumatic dilation.
  • High resolution manometry tracings from 50 achalasia patients and 10 healthy controls were analyzed for UES, esophageal body and LES parameters using purpose built MATLAB and MMS software.
  • UES deglutitive parameters decreased significantly after treatment in type II achalasia patients. This effect was mediated by the change in intra-esophageal pressure secondary to the LES dilation.
Abbreviations
ANOVA

analysis of variance

DSR

deglutitive sphincter resistance

EB

esophageal body

EGJ

esophago-gastric junction

HRM

high-resolution manometry

IBP

intrabolus pressure

IRP4

4-second integrated relaxation pressure

LES

lower esophageal sphincter

MRP

minimal relaxation pressure

PI

pressure integral

PP

peak pressure

restP

resting pressure

RI

relaxation interval

UES

upper esophageal sphincter

Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

Achalasia is a primary esophageal motility disorder, characterized manometrically by aperistalsis of the esophagus and impaired esophago-gastric junction (EGJ) relaxation, in the absence of a structural abnormality.[1-3] The insidious loss of inhibitory nitrergic neurons in the myenteric plexus of the esophagus leads to hypertonicity of the lower esophageal sphincter (LES) causing retention of esophageal contents. This results clinically in dysphagia, chest pain, regurgitation, and eventually weight loss. Treatment aims at reducing LES pressure by means of pneumatic dilation or Heller myotomy, resulting in improved bolus flow across the EGJ and subsequent symptomatic benefit in patients.[4, 5]

Although the main pathophysiological findings have been attributed to smooth muscle dysfunction in the distal esophagus and the EGJ, the role of upper esophageal sphincter (UES) function in achalasia is unclear. Indications of abnormal functioning of the striated muscle, especially in the region of the UES, are mentioned in studies on achalasia[6-10] and a few cases on associated respiratory complications have been reported.[11, 12] Manometric assessment of the UES is useful but challenging and high-resolution manometry (HRM) allowed for further characterization of pharyngeal contraction and UES relaxation during swallowing.[13, 14]

We sought to systematically investigate whether deglutitive UES function in patients with achalasia differed from healthy controls and how this was affected by treatment of EGJ hypertonicity. The first comparison was between achalasia patients before treatment and healthy controls, and between achalasia subtypes. The second analysis was the effect of pneumatic dilation of the LES on UES deglutitive parameters in the whole group of achalasia patients, and by achalasia subtype. Finally, we assessed the associations between treatment-induced changes in LES and UES parameters and correlated each of these with the therapeutic changes in intraesophageal resting and UES pressures.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

Patients

All HRM studies of patients diagnosed with achalasia and treated at a tertiary reference center (University Hospital Leuven, Belgium) between January 2009 and July 2011 were reviewed. Medical records were analyzed for demographics, presenting symptoms and treatment. Diagnosis was based on clinical symptoms, esophageal motility pattern, endoscopic and/or radiographic studies. Only newly diagnosed patients whose initial treatment consisted of pneumatic dilation with consecutive manometric follow-up were considered for inclusion. High-resolution manometry studies of 10 healthy volunteers using the same manometric assembly were collected and studied as controls.

Manometry protocol

High-resolution manometry studies were performed at the time of diagnosis and after the dilation session using a 3.2 mm diameter perfusion catheter, which incorporated 22 2.0 cm-spaced pressure sensors. Studies were conducted in the semi-supine position after an overnight fasting period, with recording sites stretching from velopharynx to the stomach after transnasal placement and fixation of the manometric assembly. Manometric protocol included a resting period, followed by 10 water swallows of 5 mL each. Informed consent was obtained from each subject and the study was performed according to the Declaration of Helsinki.

Pneumatic dilation

Pneumatic dilation was performed as a series of graded dilations on one to three consecutive days, using Rigiflex balloons (Microvasive, Boston Scientific, Watertown, MA, USA) with increasing balloon diameter. Transoral placement of a flexible guide wire was followed by positioning of the dilator across the EGJ under fluoroscopic control.[15] During dilation, the balloon was inflated twice during 30 s at pressures of 5 and 7 psi and an additional 60 s at 10 psi. The first dilation was performed with a 3.0-cm balloon. In case of good manometric response (4-second integrated relaxation pressure [IRP4] ≤ 15 mmHg), a swallow of contrast (gastrograffin®) was administered. When there was good passage of the contrast, the patient was discharged. In case of high LES pressure or stasis on the swallow in spite of low LES pressure, an additional dilation with a 3.5-cm balloon was performed. All patients underwent a repeat manometry and a contrast swallow, similar as after a 3.0-cm balloon. None of the patients underwent further dilation.

HRM data analysis

Manometric criteria for achalasia

The diagnosis of achalasia was supported manometrically by a stepwise analysis according to the Chicago Classification for motility disorders.[16-18] Diagnostic criteria for classic (type I) achalasia were a mean IRP4 over 15 mmHg (upper limit of normal) in the absence of esophageal peristalsis. Type II achalasia (with esophageal compression) was recognized when panesophageal pressurization was also present with ≥20% of swallows. Type III achalasia was characterized by preserved fragments of distal peristalsis or premature (spastic) contractions with ≥20% of swallows.

LES parameters

High-resolution manometry tracings were recorded and analyzed using MMS Solar system software (Solar GI acquisition system, MMS, Enschede, The Netherlands). LES resting pressure (LES restP) was assessed at end-expiration after wet swallows using the LES markers in MMS software during a time frame of 10 s prior to UES swallow onset over the length of the LES from the upper to lower LES border. Impaired EGJ relaxation was calculated using the IRP4, a marker for deglutitive EGJ relaxation.[19, 20] Lower esophageal sphincter parameters were determined as the mean pressures for each series of 10 water swallows of 5 mL each.

UES parameters

Deglutitive UES function was analyzed with a purpose-designed MATLAB-based program (The Mathworks, Natick, MA, USA), which derived pharyngeal contractile and UES relaxation parameters using an established method for UES function, calculating the minimal relaxation pressure (MRP), pharyngeal peak pressure (PP), relaxation interval (RI), median intrabolus pressure (IBP), and deglutitive sphincter resistance (DSR, calculated IBP divided by the RI).[14] Upper esophageal sphincter resting pressures (UES restP) were calculated using the UES marker in MMS software during a time frame of 10 s prior to UES swallowing over the length of the UES from the upper to lower UES border. All pharyngeal and UES parameters were averaged for each series of 5 mL wet swallows.

Intraesophageal pressures

Intraesophageal pressures were analyzed by calculating a single pressure integral (PI) (mmHg s cm) over the length of the esophageal body (EB), ranging from the lower UES to upper LES border. This was done using MMS software and was calculated for the 10-second period preceding UES swallow onset and for the 1-second deglutitive period during UES relaxation. Both parameters were averaged for each series of swallows.

Statistical analysis

Manometric data were summarized using mean and standard error. p ≤ 0.05 were considered significant. Mean values of the UES and LES parameters were compared between achalasia patients before treatment and healthy controls using Student's t-tests and among the achalasia subtypes and the control group using one-way anova with post hoc tests and Bonferroni correction.

Mixed model analyses with each of the LES and UES manometric parameters as the dependent variable were applied. Treatment stage (pre- vs posttreatment) was the within-subject independent variable of interest and age, gender, achalasia subtype and the number of dilations were controlled for as between-subject independent variables. In addition, a treatment stage-by-achalasia subtype interaction effect was added to compute differences in treatment effect between achalasia subtypes.

Finally, Pearson correlation analysis was used to assess associations between treatment-induced changes in LES, UES, and EB parameters, which were affected by treatment according to the mixed models. In addition, mediation analysis was performed to test whether the relationship between treatment-induced changes in LES and UES parameters was indirect through changes in EB pressures.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

Patients

Of the 125 patients with achalasia seen between January 2009 and July 2011, 77 were newly diagnosed (mean age [SD] 54.9 ± 20.4 years, 43 men). Of these, 54 patients had pre- and posttreatment HRM studies available for analysis; four were excluded because of either Botulinum toxin injection (n = 2) or a previous dilation (n = 2), allowing total inclusion of 50 patients (mean age 52.7 ± 18.6 years, 29 men) and 10 controls (mean age 34.5 ± 6.6 years, three men) in this study. All patients were initially dilated with a 3.0-cm diameter balloon. In 23 patients (mean age 49.1 ± 16.7 years, 14 male), an additional dilation with a 3.5-cm balloon was needed and performed subsequently. Patient flow is summarized in Fig. 1.

image

Figure 1. Patient flow is summarized for this study.

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Classification of achalasia

The majority of the 77 newly diagnosed patients were classified as type II achalasia (n = 55), type I (n = 15), and type III achalasia (n = 7) was less common. Of the 50 patients with HRM tracings pre- and posttreatment, 38 were identified as type II, eight as type I and four as type III achalasia. An additional dilation was performed in five type I patients, 16 type II and two type III patients with insufficient manometric and/or radiographic response after the first dilation.

Manometric variables

Manometric variables at baseline differed significantly between the study population (n = 50) and control group (n = 10). Upper esophageal sphincter deglutitive parameters MRP (17.9 ± 1.2 vs 9.4 ± 1.7 mmHg, p = 0.003), IBP (31.5 ± 1.5 vs 17.0 ± 2.4 mmHg, p < 0.0001), and DSR (34.8 ± 2.2 vs 17.6 ± 1.8 mmHg/s, p = 0.001) were significantly increased in achalasia patients compared to controls. As expected, so was LES IRP4 (27.8 ± 1.6 vs 8.4 ± 1.1 mmHg, p < 0.0001). Differences between achalasia subtypes are depicted in Table 1.

Table 1. Mean values and SE for LES and UES parameters in achalasia subtypes before treatment and in healthy controls. Tests were performed using one-way anova with Bonferroni correction between achalasia subtypes and controls. Variables that significantly differed with controls are in bold and indicated as follows: ***p < 0.001, **p < 0.01, *p < 0.05
Achalasia subtypeType I (n = 8)Type II (n = 38)Type III (n = 4)Controls (n = 10)
  1. a

    p < 0.05 vs type 2.

  2. b

    p < 0.05 vs type 3.

LES restP (mmHg)43.3 ± 7.541.4 ± 3.1b 69.4 ± 12.1* 32.7 ± 4.0
LES IRP4 (s) 24.1 ± 4.1* 28.3 ± 2.0*** 29.8 ± 1.2** 8.4 ± 1.1
UES MRP (mmHg)11.3 ± 2.6a 19.4 ± 1.3** 16.8 ± 1.89.4 ± 1.7
UES IBP (mmHg)23.9 ± 4.3 32.9 ± 1.7*** 33.4 ± 1.7* 17.0 ± 2.4
UES DSR (mmHg/s)22.4 ± 3.0a 37.4 ± 2.6** 35.1 ± 3.717.6 ± 1.8

Treatment effect

Upper esophageal sphincter deglutitive parameters MRP and IBP were significantly reduced after initial pneumatic dilation (17.9 ± 1.2 vs 15.2 ± 0.9 mmHg; p = 0.02 and 31.5 ± 1.5 vs 27.4 ± 1.2 mmHg; p = 0.009) (n = 50); PP, RI, and DSR were not (Table 2 and Fig. 2). Lower esophageal sphincter parameters restP and IRP4 (43.9 ± 2.9 vs 25.9 ± 2.6 mmHg and 27.8 ± 1.6 vs 15.7 ± 1.7 mmHg; both p < 0.0001) also decreased as expected. Patient age, gender, achalasia subtype and number of dilations were controlled for in all analyses. Lower esophageal sphincter restP and IRP4 significantly decreased in patients who required an additional balloon dilation (40.5 ± 3.3 vs 25.1 ± 4.5 mmHg; p = 0.002 and also 27.8 ± 2.2 vs 16.5 ± 3.0 mmHg; p = 0.004 pretreatment vs postadditional treatment, respectively; n = 23). Upper esophageal sphincter parameters did not differ between after initial treatment and additional treatment stage.

Table 2. Mixed Models analysis of the LES and UES parameters that were significantly reduced after initial dilation (n = 50), with age, gender, achalasia subtype and number of dilations controlled for as between-subject independent variables. The treatment stage (pre- vs posttreatment) was the within-subject independent variable of interest
Dependent variableIndependent variableBeta coefficientSE p
  1. a

    Posttreatment stage was used as reference category.

  2. b

    Type III achalasia was used as reference category.

  3. c

    Male gender was used as the reference category.

  4. d

    Patients having two consecutive dilations were used as the reference category.

  5. e

    Bold values indicate statistical significance. Level significance was indicated as follows: ****p < 0.0001, ***p < 0.001, **p < 0.01, **p < 0.05.

LES restPIntercept 31.17 11.03 0.01*
Treatment stagea 18.04 2.42 <0.0001****
Age 0.34 0.12 0.01*
Genderc0.774.750.87
Achalasia typeb
Type I −22.22 10.14 0.03*
Type II −23.22 8.41 0.01*
Number of dilationsd3.934.580.40
LES IRP4Intercept 17.50 6.51 0.01*
Treatment stagea 12.12 1.83 <0.0001****
Age0.110.070.12
Genderc4.192.790.14
Achalasia typeb
Type I9.185.960.13
Type II6.944.950.17
Number of dilationsd5.502.690.05
UES MRPIntercept 10.01 4.38 0.03*
Treatment stagea 2.69 1.15 0.02*
Age0.060.050.26
Genderc1.821.880.34
Achalasia typeb
Type I1.644.020.69
Type II2.293.340.50
Number of dilationsd0.921.820.61
UES IBPIntercept 25.08 5.54 <0.0001*
Treatment stagea 4.11 1.51 0.01*
Age0.010.060.86
Genderc2.332.390.33
Achalasia typeb
Type I1.715.100.74
Type II0.264.230.95
Number of dilationsd0.562.300.81
image

Figure 2. The effect of initial treatment on upper esophageal sphincter parameters (A) minimal relaxation pressure and (B) intrabolus pressure in achalasia patients (n = 50) is shown. **p < 0.01, *p < 0.05. Tests were performed with Mixed Models analysis.

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To assess whether the treatment effect on UES variables differed between achalasia subtypes, a treatment stage-by-achalasia subtype interaction effect was added to the model. The interaction effect was significant for UES MRP (F2,44 = 5.91, p = 0.005) and IBP (F2,44 = 6.93, p = 0.002). There was a significant increase in UES parameters MRP and IBP after dilation in type I (11.3 ± 2.6 vs 16.8 ± 2.7 mmHg; p = 0.04 and 23.9 ± 4.3 vs 31.3 ± 3.5 mmHg; p = 0.03, respectively), but a decrease in both parameters after treatment in type II (19.4 ± 1.3 vs 15.0 ± 1.1 mmHg; p = 0.0006 and 32.9 ± 1.7 vs 26.6 ± 1.3 mmHg; p = 0.0002). However, only the effect in the type II achalasia subgroup remained significant after Bonferroni correction (p = 0.002 and p = 0.0006 for MRP and IBP; Fig. 3). It should be noted that the number of type I and type III patients was low.

image

Figure 3. Difference in treatment response between achalasia subtypes (type I [n = 8], type II [n = 38] and type III [n = 4]) for upper esophageal sphincter parameters (A) minimal relaxation pressure and (B) intrabolus pressure. ***p ≤ 0.001, **≤ 0.01. Mixed Models analysis with treatment stage-by-achalasia subtype interaction effect and Bonferroni correction were used.

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Intraesophageal pressure integrals (EB PI) before and during swallow were also significantly reduced after initial pneumatic dilation (767.2 ± 201.0 vs 173.4 ± 43.0 mmHg s cm; p = 0.003 and 31.0 ± 10.7 vs 6.9 ± 2.9 mmHg s cm; p = 0.01, respectively). To assess associations between treatment-induced changes in LES, UES and EB resting and deglutitive parameters, Pearson correlation analysis was used (Table 3 and Fig. 4). The therapeutic change in LES IRP4 (Δ IRP4) correlated significantly with the change in UES MRP (Δ MRP; r = 0.29, p = 0.04). This effect was statistically mediated by the change in intraesophageal deglutitive pressure, resulting from therapy (Δ EB PI; p = 0.004 and p = 0.0002; Fig. 5). No other correlations between changes in LES and UES parameters were significant.

Table 3. Pearson correlation analyses between changes (Δ pre- vs posttreatment) in LES and UES parameters and changes in EB resting and deglutitive pressure integrals. Correlation coefficients are given, with r and p values for each pair of bivariate associations
 Δ EB PI (mmHg s cm)
Before swallow
 Δ UES restP (mmHg)r = 0.15p = 0.29
 Δ LES restP (mmHg)r = 0.28p ≤ 0.05
During swallow
 Δ MRP (mmHg)r = 0.56p ≤ 0.0001
 Δ IBP (mmHg)r = 0.43p ≤ 0.002
 Δ LES IRP4 (mmHg)r = 0.40p = 0.004
image

Figure 4. High-resolution manometry clouse plot of an achalasia patient type II, with the 10-second window before swallow onset and 1-second window during upper esophageal sphincter (UES) relaxation indicated at the level of the UES, esophageal body (EB), and lower esophageal sphincter (LES). Manometric parameters assessed are indicated: UES resting pressure, UES deglutitive parameters minimal relaxation pressure and intrabolus pressure, EB pressure integral (PI), LES resting pressure and IRP4. Pearson correlation coefficients are given, with p values for each pair of bivariate associations between the therapeutic changes in these parameters. Variables that were significantly affected by treatment are indicated as follows: ****p ≤ 0.0001, **p ≤ 0.01, *p ≤ 0.05.

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image

Figure 5. Schematic representation of the mediation of therapeutic changes in upper esophageal sphincter (UES), esophageal body (EB), and lower esophageal sphincter (LES) function. This figure shows that the effect of dilation of the LES, resulting in a change of UES function is mediated by a change in intraesophageal pressure (defined as EB pressure integral, PI) during deglutition.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

The aim of this study was to determine whether UES pressure patterns in achalasia patients differed from healthy controls and how these parameters were affected by treatment of EGJ hypertonicity. The first finding of this study is that UES parameters MRP, IBP, and DSR were significantly increased before treatment in patients with achalasia compared to controls. The second observation is that UES parameters MRP and IBP decreased significantly after pneumatic dilation of the LES in achalasia patients. This treatment effect was statistically significant in the type II achalasia subgroup. Intraesophageal pressures were significantly diminished after initial treatment, and the therapeutic changes in the EB correlated with the changes in LES and UES parameters. We also found that the resulting change in UES MRP correlated with the therapeutic drop in LES IRP4, statistically mediated by the change in EB deglutitive pressure.

Little is understood about UES functioning during swallowing in achalasia patients. Dudnick et al.[6] compared 19 patients with achalasia and 14 controls and found increased deglutitive pressures and a reduced duration of UES relaxation. Zhang et al.[7] described repetitive contractions of the UES and upper EB in 67% of patients with achalasia and related this to increased intraesophageal and LES pressures. Yoneyama et al.[8] observed changes in UES deglutitive pressure in a series of 15 patients, following pneumatic dilation and addressed the association with LES hypertonicity.

These findings suggest that elevated UES relaxation pressures may be a secondary response to poor esophageal emptying and higher intraesophageal pressures. Moreover, the increase in UES deglutitive parameters has also been described for patients with distal esophageal spasm, who may also have impaired esophageal emptying and high intraesophageal pressures.[9] A neural feedback mechanism may exist between tension in the esophageal wall and UES relaxation, such that the UES acts as a dynamic barrier to prevent reflux and aspiration of esophageal content across the UES into the airway. UES pressure also decreases after rapid intraesophageal air infusion in healthy subjects whereas it increases in achalasia, trapping air inside and resulting in belching difficulty.[10] Furthermore, case reports on acute airway obstruction suggest an association between this unusual complication and UES dysfunction.[11, 12]

In this HRM study, UES deglutitive pressures were significantly increased before treatment compared to healthy controls. After pneumatic dilation of the LES, UES pressures decreased significantly and this change correlated with the decrease in intraesophageal deglutitive pressures. Most of the patients were also found to have type II achalasia, suggesting that diagnosis mostly occurred in an early stage of the disease. According to Pandolfino et al.[18] patients with type II achalasia had the best response to therapeutic interventions of the EGJ. Equally, the treatment effect on the UES parameters in our patient population was present in the type II achalasia subgroup. This finding suggests that decreasing intraesophageal pressures by diminishing EGJ hypertonicity and subsequent esophageal compression in type II achalasia patients results in less compensatory inhibition of UES relaxation.

A potential drawback of this study is its retrospective design and its limitation to patients seen at a single center. Because of the low incidence of the disorder and delineated time frame, our study had limited numbers of patients in each category and only short follow-up. Therefore, analyses on achalasia types I and III are subject to type 2 error. Strengths include the uniform dilation protocol, which aims at reaching symptomatic remission in a single dilation series and a single hospitalization, and the objective follow-up with HRM tracings using recently established manometric parameters. We did not consider blinding because the analysis was performed objectively using software with established high intra- and interrater reproducibility. Future prospective HRM studies with longer and symptomatic follow-up are therefore warranted, and larger healthy control groups for the establishment of normal ranges for these variables, which was not the aim of this study.

Our observations confirm that achalasia patients, in addition to altered distal esophageal motility, also present with motility changes in the proximal esophagus, including the UES. Increased deglutitive pressures in the UES upon swallowing may be a protective mechanism against reflux and aspiration of esophageal content in a highly pressurized EB. It is important to include UES and pharyngeal manometric analysis in esophageal HRM, so that potential UES dysfunction is not overlooked and correlated symptoms of airway obstruction are addressed appropriately. In conclusion, this study demonstrates that treatment of EGJ hypertonicity by means of pneumatic dilation of the LES relieves patients from higher intraesophageal pressures and restores UES relaxation accordingly, corresponding with a significant decrease in UES MRP and IBP posttreatment.

Funding

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

A Methusalem Grant from KU Leuven to Prof Dr J. Tack. M. Selleslagh and T. Vanuytsel are a doctoral research fellows and L. Van Oudenhove is a postdoctoral research fellow of the Research Foundation – Flanders (FWO – Vlaanderen) and a Research Professor KU Leuven, Special Research Fund (BOF).

Author Contribution

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References

LW made the analysis and interpretation of data, also made the statistical analysis, drafted the manuscript, and critically revised the manuscript; LO made the interpretation of data, statistical analysis, drafted the manuscript, and critically revised the manuscript; MS made critical revision of the manuscript for intellectual content; TV made critical revision of the manuscript for intellectual content; GB made critical revision of the manuscript for intellectual content; JT made interpretation of data, critical revision of the manuscript, provided technical, or material support, obtained funding, and supervised the study; TIO made interpretation of data, drafted the manuscript, and made critical revision of the manuscript for intellectual content; NR planned the study concept and design, made interpretation of data, statistical analysis, drafted the manuscript, critically revised the manuscript for intellectual content, and supervised the study.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Funding
  8. Disclosure
  9. Author Contribution
  10. References
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  • 6
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  • 7
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    Massey BT, Hogan WJ, Dodds WJ, Dantas RO. Alteration of the upper esophageal sphincter belch reflex in patients with achalasia. Gastroenterology 1992; 103: 15749.
  • 11
    Ali GN, Hunt DR, Jorgensen JO, DeCarle DJ, Cook IJ. Esophageal achalasia and coexistent upper esophageal sphincter relaxation disorder presenting with airway obstruction. Gastroenterology 1995; 109: 132832.
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    Souza MAN, Dantas RO. Crico-pharyngeal dysfunction in a patient with achalasia. J Clinical Gastroenterol 1998; 26: 2168.
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