Evaluation of Serum IL-36, Insulin Resistance and Correlated with Iron Overload Levels in Patients with Beta Thalassemia Major

Abstract

Background: Patients with chronic transfusion-dependent thalassemia major (β -TM) frequently exhibit iron overload, which may have an impact on insulin resistance and cell function. the cytokines interleukin (IL)-36 Their contributions to type 2 diabetes mellitus (T2DM) were poorly understood. Aim: This study was to assess the association between serum levels of IL-36, serum iron, and ferritin, as well as glucometabolic function and IL-36 levels in thalassemia major (β -TM) patients. Methods: The present case-control study was carried out in Department of Hematology and Transfusion Medicine, thalassemia Unit" at "AL-Zahra'a Teaching Hospital" in Najaf – Iraq, Throughout the period from January 2022 – June 2022 for as patient group treated by Iron chelators. Fasting serum glucose, fasting insulin, Serum iron, ferritin, insulin resistance index and IL-36 were assessed for 60 healthy control participants and 120 TM patients, Age range was 10-12 years. Results: Compared to controls, patients with β -TM had considerably higher serum levels of IL-36. According to correlation analysis, serum IL-36 was positively linked with age, BMI, ferritin, Fe, TS%, Insulin, S.FBG, and HOMO-IR, (r = (0.493**), (0.313**), (0.511**), (0.398**), (0.422**), (0.326**), (0.527**) and (0.440**) nonetheless, there was a significant negative correlation between serum IL-36 levels and TIBC ,UIBC ,Transferrin and HOMO- β (r = (-0.339**), (-0.431**), (-0.339**) and (-0.459**) respectively. the highest value of the AUCROC was found for serum IL-36 concentrations with a threshold value of 32.923 ng/mL (AUCROC = 0.737 [95% CI: 0.666 - 0.808; p<0.001]). The sensitivity and specificity for this variable were 0.675 and 0.683, respectively. Conclusions: Our research revealed that patients with β -TM had elevated serum levels of the inflammatory cytokine IL-36. Furthermore, to improper glucose metabolism, which is common in patients with β-TM who get chelation therapy and several transfusions and is connected to the reduced activity of HOMA-β cells (increased insulin resistance) and aberrant glucose metabolism (HOMA-IR).