Gastrointestinal regulatory peptides in systemic sclerosis

Åkesson, Anita; Ekman, Rolf

doi:10.1002/art.1780360519

Cited by 27 publications

(6 citation statements)

References 18 publications

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“…Higher plasma VIP and motilin levels in SSc have been previously reported 38–41. VIP is known to inhibit gastric motility and elevated plasma levels of VIP have been reported in conditions related to gastric or intestinal dysmotility 42–45.…”

Section: Discussionmentioning

confidence: 76%

Gastric slow waves, gastrointestinal symptoms and peptides in systemic sclerosis patients

McNearney

Sallam

Hunnicutt

et al. 2009

Neurogastroenterology Motil

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Impaired gastric slow waves, frequent gastrointestinal (GI) symptoms and altered GI peptides have been reported in Scleroderma (SSc) patients. The aim of this study was to investigate the associations among these three important components in GI dysmotility. Seventeen fasted SSc patients underwent four channel surface electrogastrography, measuring % of normal gastric slow waves or dysrhythmia. Patients completed a questionnaire designed by us to assess demographics, upper and lower GI symptoms (symptom presence, frequency and impact on quality of life, QOL), by YES/NO, Likert Scales and Visual Analogue Scales 1-100 mm (called GI Dysmotility Questionnaire, GIDQ) and health-related QOL by SF-36. Fasting plasma vasoactive intestinal peptide (VIP) and motilin levels were measured by peptide immunoassays. There were significant correlations between percentages of gastric dysrhythmias (bradygastria or arrhythmia) and a number of major GI symptoms such as nausea, abdominal bloating and pain. The plasma level of VIP was correlated positively with % dysrhythmia but negatively with % normal slow waves. Motilin was positively correlated with slow wave coupling (coordination). No major differences were noted in the measured peptides or gastric slow waves between limited SSc and diffuse SSc. Correlations were noted between SF-36 domain scores and our GIDQ scores. In SSc patients, gastric dysrhythmias are correlated with certain GI symptoms. Correlations are also noted between plasma VIP/Motilin levels and gastric slow waves. Thus in SSc, gastric dysrhythmias may be predictive of development of certain dyspeptic symptoms. Plasma VIP may be involved in the development of dysrhythmias.

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Section: Discussionmentioning

confidence: 76%

Gastric slow waves, gastrointestinal symptoms and peptides in systemic sclerosis patients

McNearney

Sallam

Hunnicutt

et al. 2009

Neurogastroenterology Motil

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“…Some patients, however, have been noted to have severe GI dysmotility without evidence for cutaneous disease, increase in esophageal fibrosis or connective tissue, or other manifestations most often recognized as scleroderma (5,6). Moreover, previous studies (7)(8)(9) have proposed a neuropathic mechanism to account for the GI dysmotility seen in these patients.…”

Section: Introductionmentioning

confidence: 99%

Antimyenteric neuronal antibodies in scleroderma.

Howe¹,

Eaker²,

Sallustio³

et al. 1994

J. Clin. Invest.

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The pathogenesis of gastrointestinal (GI) dysmotility in scleroderma is incompletely understood, although previous studies have proposed a neuropathic mechanism. We studied patients with scleroderma as compared with other connective tissue disease patients and normal controls for the presence of circulating antibodies to myenteric neurons. Serial dilutions of sera were overlaid on rat intestine, doublelabeled with antineurofilament antibody as a myenteric plexus marker, and imaged using indirect immunofluorescence techniques. High titer sera ( -1:50) from 19 out of 41 scleroderma patients stained myenteric neurons, whereas none of 22 normals or 5 patients with idiopathic GI dysmotility were positive. Although 6 out of 20 SLE and 6 out of 10 mixed connective tissue disease patients' sera stained myenteric plexus neurons, when positive sera were absorbed with calf thymus extract to remove antinuclear antibody, 15 scleroderma sera, 0 SLE, and 2 mixed connective tissue disease patients retained positive staining of myenteric neurons. Western blotting using actin and neuronal intermediate filament preparations failed to show immunoreactivity with scleroderma sera containing antimyenteric neuronal antibodies. Paraneoplastic sera associated with GI dysmotility stained myenteric neurons in a different pattern than seen with scleroderma sera. A positive correlation between the presence of Raynaud's phenomenon and antimyenteric neuronal antibodies was observed in scleroderma patients. Our results indicate that IgG antibodies reacting with myenteric neurons are present in many patients with scleroderma. Although the neuronal antigen has not yet been identified, the presence of myenteric neuronal antibodies in patients with GI dysmotility and scleroderma suggests a neuropathic process. (J. Clin. Invest. 1994. 94:761-770.)

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“…Apart from the known fibrosis and myoelectric abnormalities, disturbances in the levels of gut regulatory peptides have been reported 13. Plasma concentrations of motilin, corticotropin releasing hormone, neuropeptide Y and peptide YY were all found to be significantly increased in scleroderma patients.…”

Section: Discussionmentioning

confidence: 99%