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Hilla University College Journal For Medical Science

Corresponding Author

Banaz Hussien Karim

Document Type

Original Study

Keywords

Ulcerative colitis, IL-17, CRP, Zinc, Th17, Inflammation

Abstract

Background: The chronic inflammatory bowel illness known as ulcerative colitis (UC) is characterized by dysregulated mucosal immunity. There is much more to learn about the relationship between interleukin-17 (IL-17), a key mediator in the Th17 pathway, and systemic inflammatory and metabolic indicators. Objectives: To examine the relationship between inflammatory (CRP), metabolic (FBS, HbA1c), and micronutrient (zinc) indicators and blood levels of IL-17 in individuals with UC, while excluding those with diabetes, autoimmune, hepatic, or renal disorders. Methods: In a case-control research, 90 participants were matched for age, sex, and BMI: 45 UC patients and 45 healthy controls. Measurements were made of zinc, HbA1c, FBS, CRP, and serum IL-17. Using Pearson correlation and independent t-tests, the data were examined. Results: IL-17 levels in UC patients were substantially greater than those in controls (63.85 ± 6.53 vs. 28.38 ± 4.94 pg/mL, p = 0.01). Moreover, CRP was significantly higher (31.29 ± 5.42 vs. 2.64 ± 0.28 mg/L, p = 0.01). IL-17 and CRP showed a high positive association in the UC group (r = 0.804, p < 0.01). On the other hand, zinc levels in UC patients were considerably lower (55.82 ± 3.32 vs. 89.18 ± 5.36 μg/dL, p = 0.001). The groups' FBS and HbA1c levels did not vary significantly from one another. Conclusion: Increased systemic release of IL-17 along with its robust positive association with CRP suggest a key role of IL-17 in active systemic and mucosal inflammation in UC, whereas low levels of zinc contribute to exaggerated Th17 responses. Importantly, these findings were robust even after excluding the patients who were both autoimmune positive and who had metabolic and systemic autoimmune comorbidities which also increased the reliability of these findings. In UC, zinc status in relation to IL-17 may be a focus for diagnosis and treatment.

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