Thyrotoxicosis is the clinical spectrum due to increased activity of the thyroid hormones. The causes of thyrotoxicosis include those due to hyperfunctioning thyroid gland (hyperthyroidism) commonly due to Graves’s disease, toxic adenoma and toxic MNG, and those without hyperfunctioning thyroid gland which may be due to silent thyroiditis, subacute thyroiditis, and ingestion of excess thyroid hormone or drugs like amiodarone. It is extremely important to identify the aetiology, as the clinical presentation is more or less common, but the treatment and prognosis differs 1.
Thyrotoxicosis has multiple etiologies, manifestations, and potential therapies. Appropriate treatment requires an accurate diagnosis and is influenced by coexisting medical conditions and patient preference.
The term thyrotoxicosis is a clinical state resulting from increased thyroid hormone action. It may be due to from excess thyroid hormone synthesis and its releasefor which the term hyperthyroidism is applicable. Thyrotoxicosis can also result from unregulated excess release of stored thyroid hormones without increased production resulting from a destructive process in the thyroid 1, 2.
The exogenous source either iatrogenic or factitious may also cause the thyrotoxicosis syndrome. Subclinical hyperthyroidism is considered when there is mild increase in peripheral thyroid hormone levels, although it is within normal laboratory reference range but it is considered excess for that individual. As a result hypothalamus-pituitary axis through negative feedback mechanism results in suppressed or abnormally low thyrotrophic hor mone (TSH). Thus it can be called as a biochemical hyperthroidism rather than a clinical term. Subclinical hyperthyroidism may be symptomatic or asymptomatic with adverse effects in either case 3. In the United States
subclinical hypothyroidism (3-10 %) is more common followed by subclinical hyperthyroidism (0.7%) and clinical hyperthyroidism (0.5 %). Increased peripheral thyroid levels do not result in thyrotoxicosis syndrome if biologic activity of thyroid hormones is reduced such as in thyroid hormone resistance 4.
Thyrotoxicosis syndrome has many diverse etiologies 1. When due to excess thyroid hormone effect if patient is clinically symptomatic or has biochemical findings diagnostic measures should be directed at finding the specific etiology, since management and therapy will depend on the etiology. In the United States Graves’ hyperthyroidism is the most common cause of hyperthyroidism followed by toxic multinodular goiter and toxic adenomas . In older individuals and in geographic areas with historical iodine deficiency nodular toxic goiter is more common 5. Subclinical hyperthyroidism is also caused by inappropriate excess thyroxine (T4) therapy or T4 suppressive therapies for follicular cell-derived thyroid cancer.
The first step is to obtain a radioactive iodine uptake of thyroid after establishing the diagnosis of thyrotoxicosis syndrome, if not contraindicated because of pregnancy or lactation. .Graves’ hyperthyroidism and very rarely TSH-producing pituitary adenoma is consistent with high radioactive iodine uptake (RAIU) in iodine-sufficient areas . Occasionally In toxic nodular goiter uptake is normal and sometimes low but may have mildly elevated uptake occasionally 6. In Graves’ disease degree of elevated uptake is usually proportional to the severity of Graves’ disease; subclinical cases may have normal uptake. Silent thyroiditis, subacute thyroiditis, postpartum thyroiditis, iodine-induced hyperthyroidism, drug-induced hyperthyroidism, or any cause of hyperthyroidism after iodine contrast studies or excess exogenous iodine consumption is consistent with very low and near zero RAIU. Mild or sub clinical hyperthyroidism of Graves’ disease or nodular toxic goiter can be associated with normal RAI uptake.
Stimulation of TSH receptors by TSH receptor antibodies (TRAB) is the pathogenesis of hyperthyroidism associated with Graves’ disease 7. Pathogenesis of extra-thyroidal manifestations such as ophthalmopathy and dermopathy is less clear. Interaction of TRAB with TSH receptors in non-thyroidal tissues is important in the pathogenic process 7, 8.
American Thyroid Association (ATA)/American Association of Clinical Endocrinologists (AACE) has given recent extensive guidelines for management of various types of thyrotoxic conditions.
By measuring the functional status of the gland ,thyroid scintigraphy has an important role in determining various causes of clinical and subclinical thyrotoxicosis 2,3. Ultrasonography which is simple and extremely useful but a 100% confirmation of cause may not be possible because there is overlap in USG features of Grave’s and thyroidits . The ultrasonography with assessment of vascularity using colour flow Doppler has been described in literature which shows high diagnostic accuracy 4.
Hence the present observational study was done at our tertiary care hospital to assess the clinical, biochemical and imaging profiles of patients with thyrotoxicosis in armed forces personnel & their dependents