Abstract
Thyroid-related pathologies, especially subclinical and clinical hypothyroidism, are commonly described in clinical practice. While illnesses related to aberrant thyroid hormone homeostasis are the most prevalent endocrinological conditions diagnosed, important aspects related to thyroid hormone physiology are often overlooked. Further, the only known physiological purpose of iodine is its requirement for the synthesis of thyroxine (T4) and triiodothyronine (T3). However, although it can be applied as curative agent in the management of thyrotoxicosis, the halogen is often prescribed and used inappropriately with significant, but preventable clinical consequences. In an attempt to kindle a better understanding of aspects related to aberrant thyroid hormone regulation, iodine metabolism, and the clinical management of thyroid related pathology, the current paper provides a physiological and clinical overview of said constructs from a hypothyroid perspective.
Highlights
What begins as a rapidly changing process of concentrating iodide already by the 11th week of gestation, quickly matures to become one of the most important endocrine systems in the human body
It is understandable that while D1 is located in the major peripheral organs that drive the basal metabolism, i.e. liver, kidneys and thyroid gland, D2 is expressed in organs or body systems that may be susceptible to severe pathological processes following excessive T3 exposure, i.e. the central nervous system (CNS), heart, placenta, skeletal muscle and brown adipose tissue (BAT)
It is undeniable that the clinical heterogeneity of thyroidal pathology is considerable, and much more complicated than what can be divulged in this paper, the examples provided in Table 1 provide useful and insightful perspectives on the general diagnostic directions flagged by laboratory findings
Summary
What begins as a rapidly changing process of concentrating iodide already by the 11th week of gestation, quickly matures to become one of the most important endocrine systems in the human body. As explained in paragraphs 1.1–1.3, the body is able to respond to iodine deficiency by 1) increasing the synthesis ratio of T3:T4, 2) increasing TSH release and bolstering the actions of thyroid peroxidase (TPO) and the sodium-iodide symporter (NIS), 3) upregulating the expression of iodothyronine deiodinase type 2 (D2), while downregulating the activity of D1 and D3, 4) increasing the extent of dissociation between thyroid binding globulin (TBG) and T3/T4, and 5) reducing the clearance rate of both T3 and T4 While such mechanisms can be deployed to sustain a relatively euthyroid state in conditions of iodine deficiency, the same cannot be stated in case of iodine excess.
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