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Inflammatory bowel disease (IBD) is often comorbid with mood disorders and depressive symptoms. The aetiology of depressive symptoms in IBD, however, remains largely unknown. Consistent with the inflammatory hypothesis of depression, the aim of this study was to explore the prospective associations between inflammatory biomarkers and depressive symptoms in a cohort of IBD patients with and without a previous clinical diagnosis of mood disorder. IBD clinical activity was determined using the Harvey-Bradshaw Index for CD and the Partial Mayo score for UC; serum C-reactive protein (CRP) and faecal calprotectin (fCAL) were used as biomarkers of systemic and intestinal inflammation, respectively. Participants were administered the Hospital Anxiety and Depression Scale-depression (HADS-D) at baseline and 1-year follow-up. Eighty-four participants (50 ± 16 years; 75% UC and 25% CD) were included in the main analyses. Longitudinal moderated regression models showed that baseline CRP significantly predicted follow-up HADS-D scores among individuals with a previous mood disorder diagnosis (β = 0.843, p <.001), but not among individuals without (β = −0.013, p =.896), after controlling for baseline HADS-D scores, body mass index, IBD phenotype, sex, and perceived stress. Likely due to lower power, results on FCAL (n = 31) were not statistically significant. This study suggests that IBD patients with previous diagnosis of mood disorder may be at higher risk of inflammation-related depressive symptoms. • The aetiology of depressive symptoms in IBD remains elusive. • Enhanced innate immune response may drive depressive symptoms in IBD. • CRP longitudinally predicted depression only in those with a previous mood disorder. • Results on faecal calprotectin were underpowered and non-significant. [ABSTRACT FROM AUTHOR]

Summary Insomnia has been suggested as a potential modulator of systemic inflammation. However, few studies have examined the longitudinal association between insomnia and inflammation as well as the role of sex differences, despite accumulating evidence of the vulnerability of women to immune consequences of disturbed sleep. In this study, we tested the association between self‐reported insomnia symptoms and serum C‐reactive protein, a marker of systemic inflammation, at 1‐year follow‐up, in 54 outpatients with inflammatory bowel disease (52.81 ± 16.09, 40.7% women). Insomnia symptoms were measured using the Insomnia Severity Index. After controlling for baseline inflammation and health variables, longitudinal moderated regression analysis showed that baseline insomnia symptoms predicted C‐reactive protein levels at follow‐up in women (β = 0.416, p = 0.014), but not in men (β = −0.179, p = 0.212). Results were not influenced by sex differences in insomnia severity or C‐reactive protein levels. This study suggests insomnia symptoms may partially influence systemic inflammation in women with inflammatory bowel disease. Sex‐specific psychological, immune and neuroendocrine pathways linking sleep to inflammation should be further elucidated. [ABSTRACT FROM AUTHOR]

Innate immunity may influence the onset of affective symptoms and alter sleep patterns in chronic inflammatory conditions. Here, we tested the prospective associations between baseline serum C-reactive protein (CRP), albumin, and CRP/albumin ratio (CAR, i.e., an emerging biomarker of disease activity), and self-reported symptoms of anxiety, depression, and insomnia at 1-year follow up in paediatric inflammatory bowel disease (n = 17). After controlling for baseline values, CAR (ρ = 0.591, p = 0.026) predicted anxiety symptoms, while albumin predicted both anxiety (ρ = -0.687, p = 0.007) and insomnia symptoms (ρ = -0.648, p = 0.012). Current findings preliminarily suggest that inflammation may influence anxiety and sleep disturbance in paediatric IBD. [ABSTRACT FROM AUTHOR]