Evaluation of Gastrointestinal Inflammation and Barrier Dysfunction in Patients with Chronic Urticaria
Project no. 32507 · Status: Kapanmış · 2024
Summary
<p>Chronic urticaria (CU) is a heterogeneous clinical entity comprising different endotypes and triggers. The relationship between elevated serum histamine levels and intestinal inflammation or barrier dysfunction in patients with CU has not yet been clearly elucidated. In this study, serum markers of gastrointestinal (GI) epithelial barrier dysfunction (zonulin, IFABP), soluble CD14 (sCD14), diamine oxidase (DAO), lactic acid, and endotoxin were measured by ELISA in patients with CU and healthy controls. Calprotectin was assessed as a marker of GI inflammation, and serum histamine levels were also determined. In addition, several ratios were calculated as indicators of immunologic, metabolic, and epithelial barrier balance, and differences between groups were analyzed statistically.</p><p>No significant differences were detected between patient and control groups in terms of intestinal permeability markers (zonulin, I-FABP), microbial translocation (endotoxin), or innate immune activation markers (sCD14, calprotectin), suggesting that systemic epithelial barrier integrity is largely preserved in CU. In contrast, DAO and lactic acid levels were significantly higher in the patient group, while circulating histamine levels showed an increasing trend that did not reach statistical significance. In the controlled CU subgroup, the lactic acid/DAO ratio was significantly decreased. These findings support the presence of functional and microbiota-associated metabolic alterations accompanied by effective histamine degradation, even in the absence of overt barrier disruption or systemic histaminemia.</p><p>In the severe urticaria group, significantly elevated levels of sCD14, lactic acid/DAO, lactic acid/histamine, and histamine/DAO ratios suggest that both innate immune activation and metabolic reprogramming become more pronounced with increasing disease severity. In Anti-TPO–positive cases, significantly lower sCD14 levels indicate that CD14 reduction may reflect an autoimmune-related dysregulation of immune regulation rather than disease severity per se. Overall, the findings suggest that disease severity and the presence of autoimmunity cannot be explained through a single inflammatory axis; rather, distinct biological phenotypes may underlie CU.</p>