P048 Bridging the Gap Between Body and Soul: A Pilot Study Examining Inflammation and Depression / Anxiety in Inflammatory Bowel Disease Patients
Mekori - Domachevsky, E..(1);Avinir, A.(2);Dar, S.(3);Haj, O.(1);Ben - Horin, S.(1);Gothelf, D.(4);Kopylov, U.(1);Taler, M.(3);
(1)Sheba Medical Center, Gastroenterology Department, Ramat Gan, Israel;(2)Sheba Medical Center, Child and Adolescent Psychiatry Clinic, Ramat Gan, Israel;(3)Sheba Medical Center, Laboratory of Pediatric Molecular Psychiatry, Ramat Gan, Israel;(4)Sheba Medical Center, Child and Adolescent Psychiatry Division, Ramat Gan, Israel;
Inflammatory bowel diseases (IBD) have a varied phenotype, among which are increased rates of emotional difficultiesthat were proven to worsen patients’ prognosis. Common to IBD and depression / anxiety is the postulated role of inflammation in their pathogenesis. The aim of this study was to examine whether inflammation per se is linked to depressive and anxious symptoms is a cohort of IBD patients (and is not merely an emotional response to a medical condition).
Fifty patients with Crohn’s disease (CD) and 30 with ulcerative colitis (UC) were recruited at the gastroenterology department, Sheba Medical Center. They completed a set of questionaries that measured depressive symptoms (BDI), state and trait anxiety symptoms (STAI), stress levels (PSS), IBD quality of life (IBDQ) and sleep quality (PSQI). After which blood samples were drawn and analyzed for C – reactive protein (CRP) and complete blood count. In addition, the ratios between several leukocyte sub-population (that were previously proven to be correlated with IBD as well as depression / anxiety) were calculated, and medical data was obtained from patients’ records. Finally, backwards linear regression was used to determine which factors are associated with the depressive and anxious symptoms.
For the Crohn’s group, predictive factors for depressive symptoms were gender (β = -0.17, p = 0.034), systemic symptoms (β = -0.59, p < 0.001), anxiety levels (β = 0.33, p < 0.001) and platelets to lymphocytes ratio (β = -0.33, p = 0.001). Predictive factors for anxiety were anxiety as a trait (β = 0.89, p < 0.001) and monocytes to lymphocytes ratio (β = 0.20, p = 0.010).
For the UC group, predictive factors for depressive symptoms were emotional functioning (β = -0.77, p < 0.001), systemic symptoms (β = 0.53, p = 0.025) and sleep quality (β = 0.52, p = 0.005). As for anxiety, predictive factors were gender (β = 0.21, p = 0.039), anxiety as a trait (β = 0.59, p < 0.001), depressive symptoms (β = 0.38, p = 0.004) and neutrophil to lymphocytes ratio (β = 0.25, p = 0.017). Intriguingly, CRP only had a single marginal contribution to depressive symptoms in the UC group (β = 0.20, p = 0.098).
Our results suggest that after controlling for demographics, disease activity, medication type and psychological factors inflammation by itself does play a role in the evolution of depression and anxiety in IBD patients. Furthermore, as the leukocytes’ ratios but not CRP had significant predictive values, we postulate that an imbalance between the innate and adaptive arms of the immune system mediates these phenomena, rather than an unspecified immune activation.