Author(s)

Udaya M. Kabadi

Endocrine Section, Medical Service, Veterans Affairs Medical Center, Des Moines, Iowa, University of Iowa, Iowa City, USA.

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 < 0.05) as compared to euthyroid volunteers. 24 hr uptakes rose following TSH administration in both groups. However, the rise was significant (p < 0.01) only in normal subjects. Furthermore, both the mean absolute uptake and the mean % rise following TSH administration were markedly significantly lower in subjects with subclinical hypothyroidism in comparison to normal subjects. Serum T₃ 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 < 0.05). However, the rises were not significantly different between 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.

Subclinical Hypothyroidism; 131I Thyroid Uptake; Thyroid Hormone Release

U. M. Kabadi, "Inhibited 131I Uptake but Normal Release of Thyroid Hormone by Thyroid Gland in Response to TSH Administration in Subclinical Hypothyroidism," Open Journal of Endocrine and Metabolic Diseases, Vol. 2 No. 4, 2012, pp. 98-101. doi: 10.4236/ojemd.2012.24015.