Abstract
Background: Subclinical hypothyroidism is characterized by normal circulating thyroid hormone levels with super-normal TSH concentrations in absence of clinical manifestations. In majority of subjects, an etiologic factor is often identified. Moreover, therapy with levothyroxine normalizes serum TSH concentration while maintaining normal thyroid hormone concentrations. However, the exact pathophysiology of these thyroid hormone alterations is not well defined. Objective: Major steps in synthesis i.e. iodine uptake and the release of thyroid hormones in response to SC TSH administration were assessed in subjects with subclinical hypothyroidism. Methods: 10 men and 5 women with subclinical hypothyroidism, ages 42 - 76 years and 10 euthyroid men (39 - 70 years) participated. 24 hr 131Iodine thyroid uptake and serum T3, T4 and TSH concentrations were determined prior to and after SC administration of recombinant human TSH, 0.9 mg for two consecutive days. Comparisons were conducted for 24 hour uptake values as well as serum T3, T4 and TSH levels obtained prior to and after TSH administration. Results: In subjects with subclinical hypothyroidism 24 hour 131I thyroidal uptakes were normal (10% - 30%). However, the mean value was significantly lower, (p 3 and T4 concentrations in subjects with subclinical hypothyroidism were not significantly different in comparison to normal subjects. Serum TSH concentrations were supernormal and therefore were significantly higher in subjects with subclinical hypothyroidism in comparison to normal subjects and rose markedly in both groups following TSH administration with no significant difference among groups. Serum T4 and T3 rose significantly from PreTSH levels in both groups (p 131I Thyroid uptake is inhibited prior to as well as following SC TSH administration in comparison to normal subjects with maintenance of normal hormone release.
Highlights
Major steps in synthesis i.e. iodine uptake and the release of thyroid hormones in response to SC TSH administration were assessed in subjects with subclinical hypothyroidism
It is well documented that the major aberration of a single step in thyroid hormone synthesis or release results in clinical hypothyroidism, whereas, a minor inhibition of any of these individual steps induces a goiter without a clinical hypothyroidism [20,21,22,23,24]
In all subjects with subclinical hypothyroidism 24 hour 131I thyroidal uptakes were within the normal range [10% 30%] as defined previously by the local nuclear medicine department
Summary
Subclinical hypothyroidism is a syndrome characterized by normal circulating thyroid hormone levels with simultaneous supra-normal TSH concentrations frequently in absence of clinical manifestations of hypothyroidism [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18]. Objective: Major steps in synthesis i.e. iodine uptake and the release of thyroid hormones in response to SC TSH administration were assessed in subjects with subclinical hypothyroidism. Serum TSH concentrations were supernormal and were significantly higher in subjects with subclinical hypothyroidism in comparison to normal subjects and rose markedly in both groups following TSH administration with no significant difference among groups. Conclusion: In subjects with subclinical hypothyroidism secondary to Hashimoto’s thyroiditis, 24 hour 131I Thyroid uptake is inhibited prior to as well as following SC TSH administration in comparison to normal subjects with maintenance of normal hormone release
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