Vitiligo is a pigmentation disorder of unknown aetiology, but it has been reported in association with other autoimmune diseases including type 1 diabetes mellitus (T1D). Vitiligo and T1D share a common theory of autoimmunity, but still an inflammatory link between them remains to be investigated. This study investigates the status and contribution of the inflammatory markers tumour necrosis factor-α (TNFα), interleukin (IL)-6 and IL-1 in patients with vitiligo, T1D and vitiligo-associated T1D (Vt-T1D). The data showed that sera from Vt-T1D patients (n = 21) had higher levels of TNFα, IL-6 and IL-1β compared with vitiligo patients (n = 39), T1D patients (n = 37) or controls (n = 42). Interestingly, serum levels of IL-6 were found to be significantly higher in Vt-T1D patients compared with the levels of TNFα and IL-1β. These data also showed that IL-6 was high in Vt patients as compared to the levels of TNFa and L-1β, whereas in T1D patients, IL-6 and TNFα were almost the same but were higher than IL-1β. In conclusion, this is the first study to show an inflammatory link between vitiligo and T1D. The data conclude that IL-6 plays an important role in the pathogenesis of Vt-T1D patients and is likely to gain favour as a therapeutic target in these patients.

Background: Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease with autoantibodies against glutamic-aciddecarboxylase (GAD)65, insulin and tyrosine phosphatase (TP) as a feature of disease. The correlations of these autoantibodies with disease severity remain to be explored. Here we investigate the status and contribution of autoantibodies against GAD65, insulin and TP in T1D patients and to explore whether these antibodies have a role in T1D progression and in T1D associated neuropathy. Methods: Sera from 57 T1D patients with varying levels of disease activities and 42 age-and sex-matched healthy controls were evaluated for anti-GAD65-antibodies, anti-insulin-antibodies and anti-TP-antibodies. Results: Serum analysis showed T1D patients contain 42% of anti-GAD65-antibodies, 76% of anti-insulin-antibodies and 34% of anti-TP-antibodies. Interestingly, not only was there an increased number of subjects positive for these antibodies, but also levels of these antibodies were significantly higher among T1D patients whose ages were >35 years as compared with younger T1D patients (age ≤35 years). In addition, significant correlation was observed between the levels of these antibodies and glycosylated haemoglobin (HbA 1c ). Furthermore, T1D neuropathic patients had higher levels of these antibodies compared with T1D patients without neuropathy. Conclusions: Our data support an association between these markers autoantibodies and severity of T1D. The stronger response observed in patients with uncontrolled T1D suggests that these antibodies may be useful biomarkers in evaluating the progress of T1D and in elucidating the mechanisms of disease pathogenesis.