High rates of depression and anxiety have been reported among patients with inflammatory bowel disease (IBD). The bidirectional relationship between these two conditions, with each affecting the progression of the other, leads to a reduced quality of life. The aim of this study was to identify a miRNA-based pattern that may either be unique to IBD or associated with this complex phenotype. The levels of 179 miRNAs were assessed using qRT-PCR in the plasma of individuals primarily diagnosed with recurrent depressive disorder (SAD), IBD patients (IBD), IBD patients showing symptoms of stress, anxiety, and depression (IBD + SAD), and a control group. Four miRNAs were found to be specifically associated with IBD and more than 20 miRNAs with SAD. Notably, the levels of five miRNAs (miR-223-3p, miR-1260a, miR-320d, miR-423-5p, and miR-486-5p) differed in all the comparisons. miR-342-3p and miR-125a-5p were identified as possible biomarkers able to discriminate between IBD and IBD + SAD. The identification of this pattern of miRNA specific to IBD + SAD could be useful for monitoring disease activity and progression in IBD patients struggling with psychiatric symptoms, which can negatively impact adherence to follow-up care.

Borderline personality disorder (BPD) is characterized by emotion dysregulation, interpersonal dysfunction, and frequent non-suicidal self-injury (NSSI). Altered pain sensitivity in BPD has raised interest in the possible role of the endogenous opioid system, but only a few studies have explored β-endorphin, one of the major endogenous opioid peptides, in this disorder. Here we investigated serum β-endorphin levels in patients with BPD, their association with clinical features, and their longitudinal changes during psychotherapy. Forty-nine patients with BPD enrolled in the CLIMAMITHE randomized controlled trial and 25 age- and sex-matched unaffected controls were included. Serum β-endorphin concentrations were measured by ELISA at baseline in all participants and also after 6 and 12 months of treatment in patients receiving metacognitive interpersonal therapy or structured clinical management. Baseline β-endorphin levels did not differ between patients and controls and were not associated with symptom severity, interpersonal functioning, attachment style, psychotropic treatment, or NSSI. No overall longitudinal changes were observed during psychotherapy. However, responders showed a significant increase in β-endorphin levels from T0 to T12 (p = 0.016), whereas non-responders remained unchanged. Moreover, responders exhibited significantly lower baseline β-endorphin concentrations than non-responders (p = 0.001), and baseline levels showed potential discriminative value for treatment response (AUC = 0.806, p = 0.002) and correlated with changes in emotion dysregulation during treatment, measured through the DERS (r = 0.344, p = 0.040). In conclusion, these findings suggest that peripheral β-endorphin is unlikely to represent a trait biomarker of BPD but may be associated with response to psychotherapy, although its potential clinical relevance requires validation in larger independent cohorts.

Studies conducted in first-episode psychosis (FEP) patients have shown alterations in inflammation and metabolism. Our objective was to investigate potential treatment-related effects on these systems in Italian FEP patients undergoing either an experimental treatment consisting of a multi-element psychosocial intervention (EXP), including cognitive–behavioural therapy, or treatment as usual (TAU). A total of 191 FEP patients with first contact between April 2010 and March 2011 were clinically assessed at baseline and after 9 months of treatment, and the serum levels of 19 analytes were determined through single or multiplex enzyme-linked immunosorbent assays (ELISAs). A significant increase was observed in leptin levels and a significant decrease in Glucagon-Like Peptide-1 (GLP-1) levels during the treatment (time effect, p < 0.001 for both), with no significant interaction between time and treatment type. Although ghrelin levels changed significantly over time in the whole cohort (p = 0.008), a significant decrease was observed only in the EXP group (post hoc test: p = 0.001). None of the biomarkers measured at baseline showed a predictive effect on treatment efficacy, and no significant associations were identified between changes in clinical scores and changes in biomarker levels. These results suggest that early-phase psychosis treatments are associated with possible effects on metabolic regulation.