Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic conditions marked by persistent inflammation, impacting patients’ quality of life. This study assessed differences in coffee consumption between CD and UC patients and its potential effects on the subjective perception and objective changes in inflammation markers in these two categories of patients. Using questionnaires, coffee consumption patterns, and perceived symptom effects were evaluated. Biological samples were collected to measure the following inflammatory markers: leukocytes, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and fecal calprotectin (FC). Among 148 patients, 60% reported regular coffee consumption, with no significant difference between CD and UC patients. While 45.93% perceived no impact on symptoms, 48% of those reporting exacerbation continued their regular coffee consumption. FC values were significantly lower in coffee consumers than in non-consumers (p < 0.05), particularly in those consuming natural coffee (p < 0.001), and the case was observed for UC patients (p < 0.05). No significant differences were observed in other inflammatory markers, regardless of coffee type, frequency, or milk addition. This study highlights the commonality of coffee consumption among IBD patients and the association of lower FC levels with coffee consumption, especially in UC patients, suggesting that coffee may influence intestinal inflammatory responses.
Background and Objectives: Cholangiocarcinoma (CCA) is an aggressive tumor that originates in the biliary tract and is subdivided anatomically into intrahepatic (iCCA) and extrahepatic (perihilar-pCCA and distal-dCCA). Diagnosis remains challenging, particularly for extrahepatic forms (pCCA and dCCA). We aimed to assess the relation between systemic inflammatory markers—specifically lymphocyte-related ratios—and tumor characteristics in a Romanian cholangiocarcinoma cohort. Materials and Methods: We conducted an exploratory single-center study including adult patients with a confirmed CCA histopathological diagnosis. We excluded patients with an uncertain diagnosis or tumors of the ampulla of Vater or gallbladder. Demographic and clinical data were retrospectively collected from medical records. Results: Tumor localization was the strongest predictor of metastatic disease. The odd of metastasis was 7.3 times higher for iCCA than dCCA and 4.5 times higher for iCCA than pCCA. Although several evaluated inflammatory biomarkers showed statistically significant associations, their clinical relevance was limited. The odds ratios for these biomarkers were characterized by lower bounds near the null value and wide confidence intervals, reflecting considerable patient heterogeneity, model instability, and inconclusive effect sizes. Conclusions: Our findings suggest a potential biological link between systemic inflammation, metastatic spread, and tumor differentiation grade that deserves further investigation using more accurate systemic inflammation biomarkers than those routinely collected.