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Vitamin D, Thyroid Autoimmunity and Cancer: An Interplay of Different Factors.

ABSTRACT: Background and Aims:In spite of large volume of data linking Vitamin D with cardiovascular morbidity, autoimmunity, cancer, and virtually every organ system, Vitamin D and thyroid is a lesser-known aspect of Vitamin D in clinical practice. This article intends to highlight the current literature on the impact of Vitamin D status and supplementation on thyroid autoimmunity and cancer. Methods:References for this review were identified through searches of PubMed for articles published to from 1950 to August 2019 using the terms "thyroid" [MeSH Terms] AND "Vitamin D" [MeSH Terms] OR "thyroid" [All Fields] AND "Vitamin D" [All Fields]. Results:Significant inverse correlation was documented between anti-thyroid peroxidase antibody (TPOAb) and serum 25-hydroxy-Vitamin D (25OHD). TPOAb positivity is more prevalent in Vitamin D deficient individuals. A large volume of medical literature is available from observational studies linking Vitamin D with thyroid autoimmunity. Data from interventional studies documenting beneficial effects of Vitamin D on thyroid autoimmunity is also available, but lesser than that from observational studies. Short-term high dose oral Vitamin D supplementation reduces TPOAb titers. Certain Vitamin D receptor (VDR) gene polymorphism have been linked to increased occurrence of autoimmune thyroid disorders (AITD). Vitamin D deficiency, decreased circulating calcitriol has been linked to increased thyroid cancer. Certain VDR gene polymorphisms have been linked with increased as well as decreased occurrence of thyroid cancer. Data is scant on use of Vitamin D and its analogues for treating thyroid cancer. Conclusion:In spite of large volume of medical literature from observational studies linking Vitamin D with thyroid autoimmunity and cancer, meaningful concrete clinical data on impact of Vitamin D supplementation on hard clinical end points in these disorders is lacking, and should be the primary area of research in the next decade.

SUBMITTER: Dutta D

PROVIDER: S-EPMC6873262 | biostudies-literature | 2019 Sep-Oct

REPOSITORIES: biostudies-literature

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Vitamin D, Thyroid Autoimmunity and Cancer: An Interplay of Different Factors.

Dutta Deep D Sharma Meha M Aggarwal Sameer S Mohindra Ritin R Bhattacharya Saptarshi S Kalra Sanjay S

Indian journal of endocrinology and metabolism 20190901 5

<h4>Background and aims</h4>In spite of large volume of data linking Vitamin D with cardiovascular morbidity, autoimmunity, cancer, and virtually every organ system, Vitamin D and thyroid is a lesser-known aspect of Vitamin D in clinical practice. This article intends to highlight the current literature on the impact of Vitamin D status and supplementation on thyroid autoimmunity and cancer.<h4>Methods</h4>References for this review were identified through searches of PubMed for articles publish ...[more]

PMID: 31803589

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Project description:Background:Environmental and genetic factors possibly trigger thyroid autoimmunity. Studies on perinatal risk factors for childhood thyroid autoimmunity are sparse. Objectives:The aim was to investigate if perinatal factors, family history of autoimmune diseases, and HLA-DQ genotypes contribute to thyroid autoimmunity in the Diabetes Prediction in Skåne (DiPiS) study. Methods:Samples from 1,874 ten-year-old children were analyzed for autoantibodies to thyroid peroxidase (TPOAb), thyroglobulin (TGAb), and HLA-DQ genotypes. Information on perinatal events and family history of autoimmunity was gathered prospectively in questionnaires. Results:Thyroid autoimmunity was found in 6.9% of the children (TPOAb 4.4%, TGAb 5.8%, both autoantibodies 3.3%) and was overrepresented in girls. Prematurity was positively related to TGAb (OR: 2.4, p = 0.003, pc = 0.021). Autoimmune diseases in the family increased the risk of thyroid autoimmunity: TPOAb (OR: 2.2, p = 0.012), any autoantibody (OR: 1.7, p = 0.04), and both autoantibodies (OR: 2.2, p = 0.024). A first-degree relative (FDR) with thyroid disease increased the risk for TPOAb (OR: 2.4, p = 0.03) and both autoantibodies (OR: 2.6, p = 0.03), a FDR or sibling with celiac disease increased the risk for both autoantibodies (OR: 3.7, p = 0.03, and OR: 4.8, p = 0.003), a FDR or sibling with diabetes increased the risk for thyroid autoantibody (OR: 3.0, p = 0.01, and OR: 5.4, p = 0.032), and a father with rheumatic disease increased the risk for TPOAb (OR: 15.2, p = 0.017), TGAb (OR: 11.3, p = 0.029), any autoantibody (OR: 9.6, p = 0.038), and both autoantibodies (OR: 20, p = 0.01). Conclusions:Thyroid autoimmunity was found in 6.9% of the 10-year-old children who were being followed for their risk of type 1 diabetes. No relation to perinatal factors was found, with the exception of a possible association between prematurity and TGAb. Family history of autoimmune diseases increased the risk of thyroid autoimmunity.

Project description:Thyroid autoimmunity involves loss of tolerance to thyroid proteins in genetically susceptible individuals in association with environmental factors. In central tolerance, intrathymic autoantigen presentation deletes immature T cells with high affinity for autoantigen-derived peptides. Regulatory T cells provide an alternative mechanism to silence autoimmune T cells in the periphery. The TSH receptor (TSHR), thyroid peroxidase (TPO), and thyroglobulin (Tg) have unusual properties ("immunogenicity") that contribute to breaking tolerance, including size, abundance, membrane association, glycosylation, and polymorphisms. Insight into loss of tolerance to thyroid proteins comes from spontaneous and induced animal models: 1) intrathymic expression controls self-tolerance to the TSHR, not TPO or Tg; 2) regulatory T cells are not involved in TSHR self-tolerance and instead control the balance between Graves' disease and thyroiditis; 3) breaking TSHR tolerance involves contributions from major histocompatibility complex molecules (humans and induced mouse models), TSHR polymorphism(s) (humans), and alternative splicing (mice); 4) loss of tolerance to Tg before TPO indicates that greater Tg immunogenicity vs TPO dominates central tolerance expectations; 5) tolerance is induced by thyroid autoantigen administration before autoimmunity is established; 6) interferon-α therapy for hepatitis C infection enhances thyroid autoimmunity in patients with intact immunity; Graves' disease developing after T-cell depletion reflects reconstitution autoimmunity; and 7) most environmental factors (including excess iodine) "reveal," but do not induce, thyroid autoimmunity. Micro-organisms likely exert their effects via bystander stimulation. Finally, no single mechanism explains the loss of tolerance to thyroid proteins. The goal of inducing self-tolerance to prevent autoimmune thyroid disease will require accurate prediction of at-risk individuals together with an antigen-specific, not blanket, therapeutic approach.

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Dataset Information

Vitamin D, Thyroid Autoimmunity and Cancer: An Interplay of Different Factors.

Publications

Vitamin D, Thyroid Autoimmunity and Cancer: An Interplay of Different Factors.

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