Thyroiditis, which literally means thyroid inflammation, is a term that includes different conditions with some sort of controversy in nomenclature even among thyroid disorders expert endocrinologists. Thyroiditis disorders can be classified in several ways, based on different etiology—whether known or suspected—different pathology, or different clinical presentation. They include painful conditions as subacute thyroiditis (SAT) and suppurative thyroiditis and painless conditions in which the primary manifestations are thyroid dysfunction or enlargement (goiter) in the absence of clinically evident manifestations of acute inflammation.
Thyroid hormones are key regulators of metabolism and development and are known to have pleiotropic effects in many different organs. The thyroid gland synthesises and releases triiodothyronine (T3) and thyroxine (T4), which represent the only iodine-containing hormones in vertebrates. T4 is the main product of thyroid secretion and local deiodination in peripheral tissues produces T3, the biologically active thyroid hormone. T3 and T4 are bound to thyroglobulin, providing a matrix for their synthesis and a vehicle for their subsequent storage in the thyroid. More than 99% of the circulating T3 and T4 is protein bound, mainly to T4-binding globulin and to a lesser extent to transthyretin and albumin. Thyroid hormones can rapidly be released from these proteins, this process facilitating their entry into cells. The production of thyroid hormones is controlled by serum thyrotrophin (TSH) synthesised by the anterior pituitary gland in response to TSH-releasing hormone (TRH), which is secreted by the hypothalamus. Unbound or free T3 and T4 (fT3 and fT4 respectively) exert a negative feedback on the synthesis and release of TSH and TRH in order to maintain circulating thyroid hormone levels within the required range.
Thyroid disease is common, affecting around 2% of women and 0.2% of men in the UK. Our understanding of the effects of thyroid hormones under physiological circumstances, as well as in pathological conditions, has increased dramatically during the last two centuries and it has become clear that overt thyroid dysfunction is associated with significant morbidity and mortality. Both hypo-and hyperthyroidism and their treatments have been linked with increased risk from cardiovascular disease and the adverse effects of thyrotoxicosis in terms of osteoporosis risk are well established. Although the evidence suggests that successful treatment of overt thyroid dysfunction significantly improves overall survival, the issue of treating mild or subclinical hyper- and hypothyroidism remains controversial. Furthermore, the now well-established effects of thyroid hormones on neurodevelopment have sparked a whole new debate regarding the need to screen pregnant women for thyroid function abnormalities. This review describes the current evidence of the effects of thyroid hormone on the cardiovascular, skeletal and neurological systems, as well as the influence of thyroid diseases and their treatments on the development of malignancy. Furthermore we will describe some recent developments in our understanding of the relationship between thyroid status and health.