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Functional Gastrointestinal Disorders and the Joint Hypermobility Syndrome
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Despite the fact that functional gastrointestinal disorders (FGID), such as irritable bowel syndrome, are common, our understanding of them is limited. The Joint Hypermobility Syndrome (JHS) is a common non-inflammatory connective tissue disorder which is thought to be associated with FGID although this has never been proven. Thus, further understanding of the link between JHS and GI symptoms is warranted. Our aim was to fully characterise the gastrointestinal (GI) manifestations of JHS, to determine if there is a true association between GI symptoms in JHS and FGID, and to determine the factors that are involved in this association. Using a cross-sectional design I demonstrate in the first study that patients with a known diagnosis of JHS who are referred from rheumatologists to gastroenterologists have significantly increased gastro-oesophageal symptoms, alternating bowel habit, bloating and abdominal pain compared to other patients referred to the GI clinics. Autonomic factors, and to a lesser extent, somatic hypersensitivity factors appear to mediate the association between JHS and gastro-oesophageal symptoms. In the second study, I demonstrate that healthy university students with JHS are more likely to experience postprandial dyspeptic symptoms compared to those without JHS. Although autonomic and somatic symptoms are increased in JHS their presence does not seem to confound the association with GI symptoms in this group of healthy individuals. In a case-control study of patients attending secondary care GI clinics, I demonstrate that JHS is overrepresented in patients with FGID and reflux disease but not in those with organic disease. Furthermore, the association with FGID is specifically with postprandial distress syndrome and this association is dependent on autonomic factors. In the final chapter, I confirm that abnormalities in GI physiology are common in JHS patients with GI symptoms attending a physiology unit. 60% of JHS patients with reflux symptoms have non-erosive pathological acid reflux, 56% with dysphagia have oesophageal hypomotility, and 87% with dyspeptic symptoms have gastroparesis. My studies suggest that there is overlap between JHS, gastro-oeosphageal symptoms, FGID and GI dysmotility. Understanding the mechanisms underlying GI involvement in JHS may further our understanding of FGID.
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