Background Alexithymic traits are quite prevalent in patients with inflammatory bowel diseases (IBD) and have been linked with a heightened psychological burden including anxiety, depression, somatization and obsessive-compulsive symptoms. However, there are limited data regarding the association of alexithymia with gastrointestinal symptom severity and disease activity. Methods The current study was conducted at the Division of Gastroenterology of the University Hospital of Patras, in Greece with the collaboration of the Department of Psychiatry. Adult IBD outpatients and healthy controls were enrolled to the study. Alexithymic traits were assessed with the Toronto Alexithymia Scale (TAS-20). Disease activity was assessed with the calculation of the Truelove-Witts Index for ulcerative colitis (UC) patients and the Harvey-Bradsaw Index for Crohn’s disease (CD) patients. Results 57 IBD patients and 50 healthy controls entered the study. 26 (45.6%) IBD patients reported clinically significant alexithymia traits. In addition, IBD patients faced increased difficulties in emotional expression (p=0.024) and reported increased overall alexithymic traits (p=0.033) compared to healthy controls. Moreover, we detected a borderline tendency of IBD patients to exhibit more disturbances in emotional recognition (p=0.067) compared to the control group. Difficulties in emotional recognition were significantly correlated with the presence of nausea (p=0.031), belly pain (p=0.015) and bloating (p=0.018), while overall alexithymic traits were strongly associated with the presence of nausea (p=0.008). Finally, increased disease activity was significantly associated with a higher total alexithymia score in Crohn’s disease (p=0.037) and ulcerative colitis (p=0.047) patients. Conclusion IBD patients report increased alexithymic traits which are associated with more severe gastrointestinal symptomatology and increased disease activity.

Single nucleotide polymorphisms (SNPs) in the vitamin D receptor (VDR) gene have been associated with chronic liver disease. We investigated the role of VDR SNPs on VDR protein levels and function in patients with chronic liver disease. VDR expression levels were determined in peripheral T lymphocytes (CD3+VDR+), monocytes (CD14+VDR+), and plasma from patients (n = 66) and healthy controls (n = 38). Genotyping of SNPs and the determination of expression of VDR/vitamin D-related genes were performed by using qPCR. The effect of FokI SNP on vitamin D-binding to VDR was investigated by molecular dynamics simulations. CD14+VDR+ cells were correlated with the MELD score. The ApaI SNP was associated with decreased CD3+VDR+ levels in cirrhotic patients and with higher liver stiffness in HCV patients. The BsmI and TaqI SNPs were associated with increased VDR plasma concentrations in cirrhotic patients and decreased CD14+VDR+ levels in HCV patients. The FokI SNP was associated with increased CD3+VDR+ levels in cirrhotic patients and controls. VDR polymorphisms were significantly related to the expression of genes critical for normal hepatocyte function and immune homeostasis. VDR expression levels were related to the clinical severity of liver disease. VDR SNPs may be related to the progression of chronic liver disease by affecting VDR expression levels.

Background Occludin and claudin-1 are integral components of tight junctions (TJs) that contribute to intestinal barrier integrity. The aim of this study was to prospectively evaluate the expression of occludin and claudin-1 in the intestinal mucosa of patients with Crohn’s disease (CD) undergoing treatment with tumor necrosis factor (TNF) inhibitors. Methods Clinical assessment, laboratory testing, and colonoscopy were performed on all participants prior to receiving anti-TNF therapy. Colonic or ileal biopsies were obtained from the affected intestinal areas. A follow-up exam and colonoscopy were performed at least 6 months after the start of anti-TNF therapy, and paired biopsies were obtained from the initially affected segments. The expression of the TJ proteins was evaluated by immunohistochemistry (IHC). Results In this prospective observational study, 21 consecutive patients with active CD [median age 32.5 years (IQR: 18.5-51), 66.7% male] and 10 healthy controls [36 years (IQR: 29-58), 60% male] were enrolled. Patients with CD received treatment with TNF inhibitors (infliximab, adalimumab, and certolizumab: 61.9%, 33.3%, and 4.8%, respectively), according to current guidelines, and a follow-up examination was conducted after a median period of 25 months (IQR: 9.5-66). Before treatment administration, patients with active CD exhibited an increased expression of both occludin [2 (IQR: 1.75-2.75) vs. 1.5 (IQR: 0-1.75); p = 0.032] and claudin-1 [2.5 (IQR: 2-3) vs. 1 (IQR: 0.75-2); p = 0.01] in comparison to healthy controls. In control mucosa, IHC staining for occludin and claudin-1 was weak to moderate, cytoplasmic, and membranous, confined to the surface epithelium, while staining in intestinal crypts was negative. On the other hand, an enhanced expression of both proteins in the enteric crypts and surface epithelium was demonstrated in CD patients upon initial examination. Treatment with TNF inhibitors resulted in a significant reduction of claudin-1 expression (p = 0.018) as well as a notable decline of occludin expression (p = 0.08). Occludin and claudin-1 immunostaining was restricted to the surface epithelium in post-treatment biopsies. In addition, the activity of the disease, as estimated by the Crohn’s Disease Activity Index (r = 0.476; p = 0.014) and C-reactive protein (r = 0.411; p = 0.039), was positively correlated with the expression of claudin-1 in the mucosa. Conclusion Active CD is plagued with a disruption of the expression and distribution of claudin-1 and occludin throughout the affected intestinal mucosa. Successful treatment with biological agents induces the restoration of intestinal barrier function, which is associated with an improvement in the patients' clinical condition.

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