* Dysphagia in patients with the joint hypermobility syndrome

[Guest guest]

Gut

2011;60:A181

doi:10.1136/gut.2011.239301.385

Posters

GI physiology

* Dysphagia in patients with the joint hypermobility

syndromehttp://gut.bmj.com/content/60/Suppl_1/A181.1.abstract?ct=ct

A Fikree *1,

Q Aziz1,

J Jafari1,

R Grahame2,

D Sifrim1+ Author Affiliations

1Neurogastroenterology, Blizard Institute of Cell

and Molecular Science, Barts and the London School of Medicine and Dentistry,

London, UK

2Rheumatology, University College Hospital,

London, UK

Abstract

Introduction

The Joint Hypermobility Syndrome (JHS) is a relatively frequent

inherited connective tissue disorder characterised by marked

joint hyperextensibility and

extra-articular manifestations. Recent work suggests that

gastrointestinal (GI) symptom prevalence

may be as high as 86%1 in these patients,

and that many of them have evidence of GI dysmotility.2 Dysphagia is a symptom

which is not uncommon in these patients, but which has never been formally

studied. In general terms,

dysphagia is either due to a structural

abnormality of the oesophagus or a motility problem.

Methods A

single-centre retrospective observational study was carried out to

characterise the cause of non-structural dysphagia in

patients with JHS. JHS patients who

were referred to the upper GI physiology unit and who complained of

dysphagia were identified.

Their HRM and 24-h pH-metry traces

were analysed to characterise oesophageal motility, presence of a hiatus

hernia, lower

oesophageal sphincter (LOS) pressure

and presence of gastro-oesophageal reflux (GOR).

Results 17

patients with JHS and dysphagia were referred by the rheumatologists to

our unit in 1 year: 76% female; age range: 12–58. None had evidence of a

structural cause for the dysphagia on either gastroscopy or barium

studies. 10 (59%) had an oesophageal dysmotility to account for their

dysphagia – out of these one had achalasia; the other 9 (53%) had

oesophageal hypomotility with 7 having frequent hypotensive peristalsis

and 2 having intermittent hypotensive peristalsis. 33% of those with

hypomotility had a normal Multiple Rapid Swallow test (MRS). 7 of the 17

patients (41%) had normal oesophageal motility and 6 of these had

reflux studies: 50% had GOR, 17% had a hypersensitive oesophagus and the

remaining 33% had normal studies. Only 2 patients (12%) had hiatus

hernias and both of these had oesophageal hypomotility and no GOR.

Conclusion

This is the first study of upper GI physiology in patients with JHS and

non-structural dysphagia. Oesophageal hypomotility

is common in these patients and

those patients with normal MRS are likely to show the best response to

prokinetics. 50% of

those with normal motility had

pathological GOR and would benefit from high dose proton pump inhibitor

therapy. The remainder

had normal studies, suggesting

hypersensitivity which may respond to treatment with neuromodulators

such as amitriptyline.

Only 12% of patients had a hiatus

hernia, which is in contrast to previous studies.3 Further prospective studies

are required to understand the pathophysiology and management options for

dysphagia in JHS.

  California Collegiate Shooting Sports 4-H All-Star Advisor to the most

awesome  kids of Amador County!