ABSTRACT
BACKGROUND: Altered body composition is frequently observed in Crohn's disease (CD) patients. AIMS: To investigate the nutritional status, and the effect of different therapeutic regimes in adult CD patients. METHODS: Fat free mass (FFM) and BIA-derived phase angle (PhA) were assessed in 45 CD patients, 22 on conventional therapy (CT) and 23 on maintenance therapy with infliximab (MT). Nutritional status was also assessed in 12 CD patients before and following the induction protocol with infliximab. BIA data of CD patients were compared with those of 20 healthy asymptomatic volunteers. In CD patients C Reactive Protein (CRP) and albuminaemia dosage were obtained. RESULTS: The mean values of PhA and of FFM were significantly lower in CT patients when compared with control group and MT patients. Following infliximab treatment FFM increased, although not significantly, while mean phase angle value significantly increased from 4.6±0.3 to 6.2±0.4 (p<0.05). CRP was significantly lower in MT patients compared to that in CT patients. CONCLUSION: CD patients on conventional therapy showed a lower FFM and a lower mean phase angle score compared to those on infliximab therapy. Following infliximab treatment the mean phase angle score normalized. PhA is a reliable nutritional indicator in IBD patients and could be considered as an additional tool for assessing response to treatment.
Subject(s)
Crohn Disease/complications , Crohn Disease/drug therapy , Infliximab/therapeutic use , Malnutrition/etiology , Nutritional Status , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adult , Body Composition , Body Mass Index , Case-Control Studies , Electric Impedance , Female , Follow-Up Studies , Humans , Italy , Male , Middle Aged , Nutrition Assessment , Severity of Illness IndexABSTRACT
The confluence between the increased prevalence of gastro-esophageal reflux disease (GERD) and of obesity has generated great interest in the association between these two conditions. Several studies have addressed the potential relationship between GERD and obesity, but the exact mechanism by which obesity causes reflux disease still remains to be clearly defined. A commonly suggested pathogenetic pathway is the increased abdominal pressure which relaxes the lower esophageal sphincter, thus exposing the esophageal mucosal to gastric content. Apart from the mechanical pressure, visceral fat is metabolically active and it has been strongly associated with serum levels of adipo-cytokines including interleukin-6 and tumor necrosis factor α, which may play a role in GERD or consequent carcinogenesis. This summary is aimed to explore the potential mechanisms responsible for the association between GERD and obesity, and to better understand the possible role of weight loss as a therapeutic approach for GERD.
