Barrett esophagus: prevalence of central adiposity, metabolic syndrome, and a proinflammatory state.
BACKGROUND
Obesity is a risk factor for esophageal adenocarcinoma, with a pathway through inflammation and metaplasia secondary to reflux the dominant hypothesis. The proinflammatory impact of adipocytokines associated with the metabolic syndrome of central adiposity may also be relevant. The objective of this study was to explore this profile in Barrett esophagus.


METHODS
Patients with specialized intestinal metaplasia were invited to attend the metabolic syndrome screening where they underwent anthropometry, segmental bioelectrical impedance analysis, and blood pressure measurement, and had blood taken for quantification of fasting lipids, insulin, glucose, C-reactive protein, and adipocytokines.


RESULTS
One hundred two patients were studied. Forty-six percent of Barrett patients had metabolic syndrome and 78% were centrally obese. Patients with metabolic syndrome were significantly more obese by body mass index, had a 9.4 cm greater waistline, were more hypertensive, and were insulin resistant with 25% having fasting hyperinsulinemia compared with Barrett patients without metabolic syndrome. Metabolic syndrome was associated with elevated C-reactive protein, leptin, and a trend toward decreased adiponectin levels. Sixty percent of patients with long-segment Barrett had metabolic syndrome, and 92% were centrally obese compared with 23.8% and 62%, respectively (P = 0.007 and 0.005) in short-segment Barrett. Long-segment Barrett was associated with hyperinsulinemia and significantly increased levels of interleukin-6 compared with short-segment Barrett.


CONCLUSIONS
The prevalence of metabolic syndrome in Barrett far exceeds population norms, and the syndrome was significantly associated with the length of specialized intestinal metaplasia. The data do suggest that the metabolic syndrome may be relevant to the continuum of metaplasia within the Barrett cohort.
Ryan
Aoife M
AM
Departments of Clinical Surgery, St. James's Hospital and Trinity College, Dublin, Ireland. ryana1@tcd.ie
Healy
Laura A
LA
Power
Derek G
DG
Byrne
Miriam
M
Murphy
Sinead
S
Byrne
Patrick J
PJ
Kelleher
Dermot
D
Reynolds
John V
JV
D052242:Adiponectin / Q000097:blood; D050154:Adiposity; D000704:Analysis of Variance; D000886:Anthropometry; D001471:Barrett Esophagus / Q000150:complications*; D001786:Blood Glucose / Q000032:analysis; D001795:Blood Pressure Determination; D002097:C-Reactive Protein / Q000032:analysis; D016009:Chi-Square Distribution; D016207:Cytokines / Q000097:blood; D017097:Electric Impedance; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications* / Q000453:epidemiology*; D008875:Middle Aged; D010641:Phenotype; D015995:Prevalence; D052243:Resistin / Q000097:blood
D052242:Adiponectin; D001786:Blood Glucose; D016207:Cytokines; D007328:Insulin; D020738:Leptin; D008055:Lipids; D052243:Resistin; D002097:C-Reactive Protein