In Inflammatory Bowel Disease (IBD), adipose tissue is postulated to be a source of pro-inflammatory cytokines and adipokines, which may affect disease outcomes. In patients with treatment refractory IBD, abdominal body composition is often characterized by excessive fat deposition and skeletal muscle deficits 1. The accumulation of hypertrophic mesenteric adipose tissue and the phenomenon of “creeping fat” in both the small and large bowel are recognized as unique characteristics of Crohn's Disease (CD). Several aspects of body composition have been investigated to assess outcomes in IBD including body mass index (BMI), visceral adipose tissue, subcutaneous adipose tissue, and muscle mass 2. BMI, as an anthropometric measure, is non-specific and not a reliable predictor of visceral or subcutaneous adiposity. Imaging modalities such as computed tomography (CT) or magnetic resonance imaging (MRI) have been used in studies to provide more accurate assessments of fat distribution. The aim of this study was to assess the role of adiposity, particularly visceral adipose tissue, in predicting clinical relapse in patients with IBD. This retrospective study evaluated anthropometric measures of adiposity, including abdominal body composition using routinely acquired CT scans of the abdomen from patients with a confirmed clinical, endoscopic, histological, and radiological diagnosis of IBD between 2014 and 2020 at the local tertiary IBD centre. The study was approved by the local ethics committee. Demographic variables included were age, sex, BMI, and smoking history. Clinical variables included IBD type, prior surgery, corticosteroid use, biologic therapy (specifically anti–tumor necrosis factor alpha TNF-α agents), anti-TNF drug levels, disease behavior (classified using Montreal and Vienna classifications), disease location (Montreal classification), disease duration, and disease complications. Abdominal body composition was assessed via CT measurements, including cross-sectional areas of total fat, subcutaneous fat, visceral fat, and skeletal muscle at the level of the third lumbar vertebra (L3) in the supine position. Image segmentation and measurement were performed using ImageJ/Fiji software (National Institutes of Health, Bethesda, MD, USA). Measurements were calculated by pixel count and expressed in square centimeters. Sarcopenia was defined as a skeletal muscle index (SMI), determined by CT imaging, two standard deviations below the mean for healthy young adults—specifically < 55 cm2/m2 in men and < 39 cm2/m2 in women. The primary outcome measure was clinical relapse within 12 months of current therapy. Clinical relapse was defined as an acute flare of symptoms and/or worsening biochemical markers and/or endoscopic recurrence requiring dose intensification of current therapy or surgical resection. Statistical analyses included Spearman's correlation between body composition parameters and binary logistic regression, adjusting for demographic, clinical, and treatment-related variables. A forward stepwise likelihood ratio method was used for regression modeling. Fifty-three patients with IBD and available imaging were included in the study. The mean age was 45.6 ± 14.4 years and over half were male (n = 31, 58.5%). The average BMI was 27 ± 6.1 kg/m2. Twenty patients (37.7%) were current smokers. The mean disease duration was 18.8 ± 10.8 years. Most patients had CD (n = 45; 85.0%). The majority had ileocolonic CD (n = 22; 41.5%), followed by ileal CD (n = 15; 28.3%), colonic CD (n = 7; 13.2%), left-sided Ulcerative Colitis (UC) (n = 6; 11.3%), and pancolitis (n = 2; 3.8%). Most patients (n = 50; 94.3%) were receiving biologic therapy, and 60% (n = 32) were on corticosteroids. Sarcopenia was identified in 58% of patients. IBD-related complications included colonic resection (n = 7; 13.2%), perianal or pericolic abscess (n = 6; 11.3%), and enterocutaneous fistula (n = 6; 11.3%). Within 12 months, 22 patients (41.5%) experienced clinical relapse. The mean age and BMI of patients who relapsed were 41.8 ± 16.2 years and 25.6 ± 4.4 kg/m2, respectively, compared to 48.4 ± 12.5 years and 28.16 ± 7.0 kg/m2 in those who remained in remission. Visceral fat area showed strong correlations with all other body composition parameters (subcutaneous fat area r = 0.717, skeletal muscle area r = 0.518, total fat area r = 0.861 and BMI r = 0.681) according to the Spearman's model (p < 0.001). In the multivariable logistic regression model, after adjusting for clinical variables (age, sex, smoking status, prior surgery, IBD type, corticosteroid use, biologic therapy, anti-TNF levels, disease behavior, location, and duration), visceral fat area was associated with clinical relapse, whereas BMI was not (p = 0.017 vs. p = 0.782) (Table 1). Although various anthropometric methods have been used to assess obesity and its association with adverse outcomes in IBD 3, conclusions regarding specific parameters have been inconsistent. The role of visceral adiposity in disease monitoring remains unclear due to heterogeneous evidence. Our findings suggest that visceral fat area is a significant predictor of clinical relapse in IBD, after adjusting for known clinical factors. Visceral adiposity is thought to be a prospective risk factor for increased disease activity in CD 4. A previous retrospective study found that increased visceral adiposity was associated with a shorter time to disease flare in IBD, particularly in CD compared to UC 5. Another study showed a strong correlation between visceral fat area and the development of complicated CD phenotypes, including strictures and fistulas 6. The mechanisms underlying these associations may include the production of pro-inflammatory cytokines—such as TNF-α, interleukin-6 (IL-6), and peroxisome proliferator-activated receptor gamma (PPAR-γ)—by visceral adipocytes 7. Additionally, bacterial translocation from the gut into mesenteric tissue in CD may trigger a chronic inflammatory response through exposure of mesenteric adipocytes to gut microbiota 8. The prevalence of obesity is rising globally, including among individuals with IBD. Contributing factors include dietary habits, physical inactivity due to extraintestinal manifestations (e.g., arthritis, spondyloarthropathy), and prolonged corticosteroid use. Furthermore, biologic agents such as TNF inhibitors may increase adiposity, potentially due to the reversal of appetite suppression through inhibition of TNF-α–mediated pathways 9. Limitations of this study include its relatively small sample size, retrospective design, and limited generalizability across diverse ethnic groups, as adipose distribution may vary by ethnicity. In conclusion, our findings suggest that visceral fat area plays an important role in the disease process of IBD and may be a more meaningful predictor of relapse than BMI. Further research is warranted to validate the utility of visceral fat area as a biomarker for predicting clinical outcomes in IBD. Open access publishing facilitated by Australian National University, as part of the Wiley - Australian National University agreement via the Council of Australasian University Librarians. The authors have nothing to report. Ethical approval has been obtained from the ACT Health Human Research Ethics Committee. Waiver of the requirement for consent was approved by the Ethics Committee. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.
Hasnol et al. (Sun,) studied this question.