Document Type : Original Article
Authors
1
Department of Clinical laboratory sciences, College of Pharmacy, University of AlKafeel, Iraq
2
Department of Biology, College of Education for Women, University of Shatrah, Thi-Qar, Iraq.
3
Babil Health Directorate, Marjan Teaching Hospital, Hilla, Babil, Iraq.
4
Department of Clinical Laboratory Sciences, College of Pharmacy, University of AlKafeel, Iraq.
Abstract
Background: Latent autoimmune diabetes in adults (LADA) is an adult-onset form of autoimmune diabetes characterised by islet autoantibodies. Circulating interleukin-17 (IL-17) in LADA, and its relation to autoantibody levels and human leukocyte antigen (HLA)-DQA1*03 carriage, have rarely been reported.
Objective: To describe serum IL-17 in patients with LADA compared with healthy controls and, within the LADA group, its relation to autoantibodies against glutamic acid decarboxylase 65 (GAD65), islet antigen-2 (IA-2) and zinc transporter 8 (ZnT8) and to HLA-DQA1*03 carrier status.
Methods: In this single-centre descriptive case-control study, 35 patients with LADA and 35 age- and sex-matched normoglycaemic controls were enrolled. Serum IL-17 and autoantibodies were measured by enzyme-linked immunosorbent assay, and HLA-DQA1*03 carriage by sequence-specific primer polymerase chain reaction.
Results: Median serum IL-17 was higher in patients than in controls (36.7 versus 14.6 pg/mL; p<0.001); as expected from the inclusion criteria, autoantibody levels were also higher (all p<0.001). HLA-DQA1*03 was carried by 82.9% of patients and 25.7% of controls (odds ratio 13.96, 95% confidence interval 4.37-44.57). Within the LADA group, IL-17 did not correlate with any autoantibody (all p>0.05) and was higher in HLA-DQA1*03-negative (n=6) than in HLA-DQA1*03-positive patients (n=29; p=0.034), a difference that did not survive correction for multiple comparisons.
Conclusion: Serum IL-17 was higher in patients with LADA than in healthy controls and was unrelated to autoantibody levels. Without diabetic comparator groups and clinical data, this difference cannot be attributed to autoimmunity rather than to hyperglycaemia, adiposity, metabolic inflammation or treatment. The findings are descriptive and require confirmation.
Keywords