A specific diet regimen is a promising way of managing inflammatory bowel disease (IBD), with the Mediterranean diet (MD) being a likely candidate due to its potential to modulate gut inflammation. Therefore, the aim of this study was to investigate nutritional habits and dietary attitudes of IBD patients, and to assess their adherence to the Mediterranean diet. The study enrolled 50 Crohn’s disease and 44 ulcerative colitis patients, with clinical and laboratory parameters taken. Dietary attitudes were examined, and adherence to MD was assessed using the Mediterranean Diet Service Score (MDSS). Average MDSS score was 6.0 (5.0–7.0), while only nine participants fulfilled criteria for Mediterranean diet adherence. Moreover, all of them were men (p = 0.021). Low percentage of adherence to recommended guidelines was observed for eating olive oil (25.5%), fresh fruit (14.9%), and vegetables (10.6%). Significant positive correlation was observed between total MDSS points and high-density lipoprotein (HDL) cholesterol levels (p = 0.002). The majority of the patients (86.2%) considered that a more controlled diet could reduce their IBD symptoms, while 17% visited a nutritionist for diet advice. The majority of patients (84%) would visit educational programs regarding nutrition. In conclusion, adherence to MD was very low, while IBD patients were willing to extend their nutritional knowledge if proper educational programs were organized.

Catestatin (CST) is an important peptide in the pathophysiology of chronic inflammatory disorders. However, clinical studies on inflammatory bowel disease (IBD) patients are lacking. Our goal was to investigate CST concentrations in IBD patients compared to healthy subjects. Additionally, we aimed to determine arterial stiffness parameters in relation to CST. This cross-sectional study compared 80 IBD patients (45 Crohn’s disease (CD) and 35 ulcerative colitis (UC) patients) with 75 control subjects. Serum CST levels were significantly higher in the IBD group compared to control subjects (11.29 ± 9.14 vs. 7.13 ± 6.08 ng/mL, p = 0.001) and in the UC group compared to CD patients (13.50 ± 9.58 vs. 9.03 ± 6.92 ng/mL, p = 0.021), irrespective of age and BMI. IBD patients exhibited significantly higher values of heart rate adjusted central augmentation index (cAIx-75) (14.88 ± 10.59 vs. 6.87 ± 9.50 %, p < 0.001) and pulse wave velocity (PWV) (8.06 ± 3.23 vs. 6.42 ± 1.47 m/s, p < 0.001) compared to control group. Furthermore, PWV was the only significant independent correlate of CST (B = 1.20, t = 4.15, p < 0.001), while CST, PWV, cAIx-75, high-sensitivity C-reactive protein and BMI were significant predictors of positive IBD status (1.089 (1.022–1.161), 1.515 (1.166–1.968), 1.060 (1.024–1.097), 1.458 (1.116–1.906), 0.793 (0.683–0.920), respectively). Serum CST levels were significantly higher in IBD patients compared to controls and an independent positive correlation of CST with PWV existed. Therefore, it is possible that CST could have a role in the complex pathophysiology of IBD and its cardiovascular complications.

As early commencement of inflammatory bowel disease (IBD) treatment has been shown to substantially improve outcomes, it is of utmost importance to make a timely diagnosis of this disease. Despite undisputed sensitivity of fecal calprotectin, the most widely accepted IBD biomarker, in discriminating between irritable bowel syndrome (IBS) and IBD, as well as recognized role in monitoring disease activity and response to therapy, perhaps the biggest setback of calprotectin use in IBD is lack of specificity. Therefore, an additional biomarker in IBD is warranted. B-cell activating factor (BAFF), a member of the tumor necrosis factor (TNF) superfamily, recently emerged as a viable candidate for this role. So far, overproduction of BAFF has been observed in various autoimmune diseases, most notably in systemic lupus erythematosus, where BAFF-inhibitor belimumab was approved for treatment. As BAFF levels were also shown to correlate with indices of IBD, in this review we aimed to summarize the current evidence with respect to the role of BAFF in diagnosis and assessing the activity of IBD, as well as putative therapeutic implications that may arise from exploring of this relation.

CD44 expressed in monocytes and lymphocytes seems to play a crucial role in gastrointestinal inflammation, such as the one occurring in the context of inflammatory bowel diseases. Differentially methylated genes are distinctly expressed across monocyte subpopulations related to the state of Crohn’s disease. Hence, the aim of this study was to detect CD44 expression in leukocyte subpopulations in relation to the type of IBD, therapy, and disease duration. Monocyte subpopulations CD14⁺⁺CD16⁻, CD14⁺⁺CD16⁺⁺, and CD14⁺CD16⁺ as well as other leukocytes were analyzed for their CD44 expression using flow cytometry in 46 patients with IBD and 48 healthy controls. Patients with Crohn’s disease treated with non-biological therapy (NBT) exhibited a lower percentage of anti-inflammatory CD14⁺CD16⁺⁺ monocytes, whereas NBT-treated patients with ulcerative colitis had lower expression of CD44 on CD14⁺CD44⁺ lymphocytes in comparison to controls, respectively. Conversely, patients with Crohn’s disease treated with biological therapy had a higher percentage of CD44⁺ granulocytes but lower expression of CD44 on anti-inflammatory monocytes compared to controls. Median fluorescence intensity (MFI) of CD44 on CD44⁺CD14⁺ lymphocytes was higher in ulcerative colitis patients treated with biological therapy compared to NBT. The percentage of classical CD14⁺⁺CD16⁻ monocytes was lower in the <9 years of IBD duration subgroup compared with the longer disease duration subgroup. The present study addresses the putative role of differentiation and regulation of leukocytes in tailoring IBD therapeutic regimes.

We aimed to provide insight into nutritional and clinical indicators of malnutrition risk and their influence on two-year mortality and re-hospitalization rate among patients hospitalized in internal clinic departments in the tertiary hospital in Croatia. Initially, data on 346 participants were obtained, while 218 of them where followed-up two years later. At baseline, the majority of participants were old and polymorbid (62.1% suffered from arterial hypertension, 29.5% from cancer, and 29.2% from diabetes). Even apparently presenting with satisfying anthropometric indices, 38.4% of them were at-risk for malnutrition when screened with the Nutritional Risk Screening-2002 (NRS-2002) questionnaire (NRS-2002 ≥ 3). More importantly, only 15.3% of all participants were prescribed an oral nutritional supplement during hospitalization. Those that were at-risk for malnutrition suffered significantly more often from cancer (54.9% vs. 20.6%; p < 0.001) and died more often in the follow-up period (42.7% vs. 23.5%; p < 0.003). Their anthropometric indices were generally normal and contradictory 46.3% were overweight and obese (body mass index (BMI) > 25 kg/m²). Only 36.6% of nutritionally endangered participants used an oral supplement in the follow-up period. NRS-2002 ≥ 3 correlated with anthropometric indices, glomerular filtration rate, age, and length of the initial hospital stay. Unlike other studies, NRS-2002 ≥ 3 was not an independent predictor of mortality and re-hospitalizations; other clinical, rather than nutritional parameters proved to be better predictors. Patients in our hospital are neither adequately nutritionally assessed nor managed. There is an urgent need to develop strategies to prevent, identify, and treat malnutrition in our hospital and post-discharge.

Inflammatory bowel disease (IBD; Crohn’s disease and ulcerative colitis) arises from convergent dysfunction of the epithelial barrier, mucosal immunity, and gut microbiome on a background of genetic susceptibility and environmental exposures. Diet is among the most modifiable of these exposures, yet much of the diet–microbiome research in IBD remains descriptive and poorly aligned with the molecular pathways linking food to mucosal effects. This comprehensive review reframes the field around functional dysbiosis, in which altered microbial metabolic capacity (rather than taxonomic shifts alone) drives disease-relevant biology. We trace how dietary substrates and additives are converted by gut microbes into bioactive metabolites (short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sulfur compounds, and polyphenol-derived molecules) and map these to host receptors and signaling pathways governing barrier function, mucus and antimicrobial peptide production, and Treg/Th17 balance. Defined dietary therapies (exclusive enteral nutrition, the Crohn’s disease exclusion diet plus partial enteral nutrition, and Mediterranean-style patterns) are reinterpreted as interventions that reshape microbial metabolic output, and candidate biomarkers for microbiome-informed precision nutrition are evaluated. Microbiota-derived metabolites provide the molecular interface between diet and mucosal immunity in IBD; personalized dietary algorithms remain a research goal, not a validated clinical tool, and diet is best framed as adjunctive to pharmacotherapy and dietitian care.