Autoimmune Thyroid Disease Analysis

Autoimmune thyroid disease (ATD) is the most common autoimmune disease associated with type 1 diabetes. Therefore, a sound understanding of the disease process and how it impacts glycemia is important. ATD may present as Hashimoto thyroiditis (HT) or Grave’s disease. HT results in hypothyroidism and is the most common presentation, while Grave’s disease results in hyperthyroidism (Kakleas, Soldatou, Karachaliou, & Karavanaki, 2015).
Specific HLA types in patients with type 1 diabetes are associated with the development of hyperthyroidism and those are HLA DQA*0301, DQB1*0301, DQB1*0201. Likewise DQB1*0501 is associated with hypothyroidism. Interestingly enough, presence of DQB1*05 is correlated with protection from ATD development (Kakleas et al., 2011).
ATD is associated with production of autoantibodies against the thyroid gland, specifically thyroid gland proteins thyroglobulin (TG) and thyroid peroxidase (TPO). TPO is a glycosylated transmembrane protein responsible
Symptoms may include hyperglycemia, weight loss despite normal intake, palpitations, heat intolerance, thyroid enlargement, and ophthalmic changes (Kakleas et al, 2015). In a hyperthyroid state, glucose requirements are increased to support the increase in metabolism. This increased need for glucose results in endogenous glucose production mainly through stimulation of gluconeogenesis. However, studies also suggest that, in order to support gluconeogensesis, there is an increased rate of glycolysis and lactate formation relative to glucose oxidation the skeletal muscle. This effectively results in a decrease in glycogen synthesis, and an increase in glycogenolysis. These physiologic compensatory actions result in the hyperthyroid related hyperglycemia previously noted (Dimitriadis & Raptis, 2001). Additionally, the half-life of insulin is reduced contributing to hyperglycemia (Hage, Zantout, & Azar,