Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 44 P257 | DOI: 10.1530/endoabs.44.P257

SFEBES2016 Poster Presentations Thyroid (26 abstracts)

Vitamin D supplementation in Graves’ disease and risk of relapse

Suhel Ashraff , Caroline Addison , Vasilieos Tsatlidis & Salman Razvi

Queen Elizabeth Hospital, Gateshead, UK.

Background: Graves’ disease (GD) is an auto-immune condition where the thyroid gland produces excess hormones due to stimulation of the TSH receptor. Treatments for GD have largely remained unchanged for over 60 years. The commonest treatment strategy is to use anti-thyroid drugs (ATD) which has limited efficacy and may have serious side-effects. Newer therapies are required that will supplement existing therapies and impact on the underlying immune mechanisms of GD. Vitamin D (D) is a potent immune modulator and its deficiency/insufficiency has been linked with several other auto-immune conditions such as type 1 diabetes and multiple sclerosis. We therefore assessed if supplementation with D in patients with GD and D insufficiency/deficiency impacts on risk of relapse at 12 months.

Methods: All consecutive patients with GD and D insufficiency/deficiency (25-OH-D <50 nmol/l) were treated with D3 20,000 IU weekly for the duration of ATD therapy. After ATD cessation regular thyroid function monitoring was performed up to 12 months to assess relapse. Patients with sufficient D levels (≥ 50 nmol/l) were used as controls.

Results: Amongst patients with GD treated with ATD for 12–18 months, those who were also treated with D for co-existing D insufficiency/deficiency (n=71) had lower relapse rate at 12 months post ATD cessation, compared to those that did not have D therapy (n=71); 19.7 vs 32.4%, P=0.02. In addition, TSH receptor antibody (TRAb) levels were lower in the D treated group at ATD cessation than in those with no D treatment (1.7 vs 3.1 U/l, P=0.04). No patient with D treatment had hypercalcemia at the time of ATD cessation. ΔTRab was significantly correlated with ΔD (Pearson’s correlation=−0.22, P=0.04). In further linear modelling after accounting for baseline D levels, ΔTRab continued to be significantly associated with ΔD levels (standardised beta co-efficient −0.36, P=0.02). Moreover, this relationship continued to show a significant negative association when other clinical variables that are recognised to have an impact on TBII levels such as age, gender and smoking status were included in the model.

Conclusions: D insufficiency/deficiency may have a permissive role in the immune dysfunction underlying many cases of GD and that manipulating D levels could provide significant benefit in reducing autoimmune function and the risk of relapse in a safe and cost-effective manner. Prospective randomised controlled trials of the adjuvant effects of D, alongside routine ATD therapy, on recurrence of GD are required to confirm this data.

Volume 44

Society for Endocrinology BES 2016

Brighton, UK
07 Nov 2016 - 09 Nov 2016

Society for Endocrinology 

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