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PTH-049 Gastro-oesophageal mechanisms of recurrent postprandial vomiting in young patients with joint hypermobility syndrome and autonomic dysfunction
  1. J Jafari,
  2. E Yazaki,
  3. R Shimono,
  4. Q Aziz,
  5. D Sifrim
  1. GI Physiology Unit, Barts and the London School of Medicine and Dentistry, London, UK


Introduction We have recently demonstrated a high prevalence of functional GI disorders in patients with joint hypermobility syndrome.1 These patients frequently have autonomic nerves dysfunction and may present with recurrent vomiting, severe dyspepsia and constipation. We aimed to characterise the OGJ mechanisms underlying recurrent postprandial vomiting in a series of consecutive patients with joint hypermobility syndrome and/or autonomic dysfunction.

Methods Twelve patients (mean age=25.5 years, 9 females, 3 males) referred for gastro-oesophageal motility testing due to recurrent postprandial vomiting were studied during fasting and postprandial periods using combined high-resolution manometry-impedance. Eating disorders, neurologic and other organic gastrointestinal disorders were previously excluded. Median duration of postprandial vomiting was 17 months. Using Beighton Hypermobility Score, 7/12 patients were diagnosed with Joint Hypermobility Syndrome (JHS). In five of these patients we found autonomic dysfunction symptoms. Combined stationary HRM-impedance (Sandhill Scientific) was performed in semirecumbent position. The protocol included 10 single wet swallows, 2 multiple rapid swallows sequences, a semisolid standard meal followed by 30 min postprandial monitoring. Chicago Classification 2009 was used to classify oesophageal motility disorders.

Results Hiatus hernia was diagnosed in 4/12 patients. Normal oesophageal motility was observed in 6/12 patients and the remaining patients had intermittent hypotensive peristalsis. All patients vomited after the standard meal. Nausea preceding vomiting was present in only 5/12 patients. Aerophagia, objectively detected by impedance, was a major feature, found in 8/12 patients. However, only 4 patients had an impedance pattern of belching-liquid regurgitation. The majority of patients had objective abdominal straining (detected with HRM as abrupt, low amplitude, simultaneous increase in gastro-oesophageal pressure) followed by liquid intra-oesophageal retrograde flow with high proximal extent.

Conclusion JHS was present in a significant proportion of these young patients with recurrent postprandial vomiting. Aerophagia was a significant consistent finding in these patients. We hypothesise that patients with JHS and oesophago-gastro-intestinal involvement may perceive early postprandial mild gastric discomfort (probably due to liquid accumulation in the gastric cardiac region) and develop an aerophagic behaviour to alleviate their discomfort by belching. Subsequently, straining to belch is associated with vomiting.

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