TY - JOUR
T1 - Radioimmunoassay for 3, 5-diiodothyronine and evidence for dependence on conversion from 3, 5, 3'- triiodothyr onine
AU - Pangaro, Louis
AU - Burman, Kenneth D.
AU - Wartofsky, Leonard
AU - Cahnmann, Hans J.
AU - Smallridge, Robert C.
AU - O'brian, John T.
AU - Wright, Frances D.
AU - Latham, Keith
PY - 1980/6
Y1 - 1980/6
N2 - The present report describes a RIA for 3, 5-diiodothyronine (3, 5T2) which uses inner ring-labeled 3, 5-[125I]T2 as the ligand and has a lower limit of detectability of 0.5 ng/dl. Cross-reaction was 0.14% with T;t, less than 0.001% with T4, 1.2% with 3, 3', 5-triiodothyroacetic acid, and 6.1% with 3, 5-diiodothyroacetic acid. Cross-reaction with T3 began when T3 levels were elevated to 500 ng/dl. No cross-reaction was detectable for iodothyronines within their physiological ranges. Intraassay variation ranged from 2.2-7.8%, and interassay variation ranged from 12.7-14%. The mean (±SE) serum 3, 5T2 concentration in 70 normal subjects was 4.3 ± 0.2 ng/dl. The mean (±SE) 3, 5T2 in 14 hyperthyroid patients was increased to 18.4 ± 2.3 ng/dl (P < 0.001), and all but 1 patient had an elevated level. In 10 hypothyroid patients the mean (±SE) 3, 5T2 level was decreased to 1.4 ± 0.3 ng/dl (P < 0.001). In 4 patients, levels overlapped with the normal range. In 4 hypothyroid subjects treated with L-T4, 3, 5T2 levels were normal, suggesting that the majority of 3, 5T2 originates from extrathyroidal conversion from T3. Studies in fasting obese subjects demonstrated that serum 3, 5T2 (mean ± SE) levels fell from 3.4 ± 0.3 to 2.5 ± 0.7 ng/dl during fasting. This fall was significant (P < 0.001) and in parallel with the fall in T3 levels of 182 ± 20 to 126 ± 12 ng/dl. In fasting subjects given 100 μg oral L-T3/day T3 levels rose from 138 ±11 to 362 ± 26 ng/dl. 3, 5T2 levels (corrected for cross-reaction and for contamination of oral T3 with 3, 5T2) rose from 2.2 ± 0.7 to 6.4 ± 1.0 ng/dl. In fasting subjects given 25 μg oral L-T3/day, T3 levels fell from 165 ± 5.1 to 139 ± 6.9 ng/dl. Corrected 3, 5T2 levels changed from 3.7 ± 0.4 to 2.5 ± 0.3 ng/dl. Neither change was significant. In summary, 3, 5T2 circulates in the serum of normal subjects, is increased in hyperthyroidism, and is decreased in hypothyroidism. Serum 3, 5T2 level depends on and is probably derived from circulating T3. In the clinical protocol employed, fasting does not seem to inhibit deiodination of T3 to 3, 5T2 as it does of T4 to T3.
AB - The present report describes a RIA for 3, 5-diiodothyronine (3, 5T2) which uses inner ring-labeled 3, 5-[125I]T2 as the ligand and has a lower limit of detectability of 0.5 ng/dl. Cross-reaction was 0.14% with T;t, less than 0.001% with T4, 1.2% with 3, 3', 5-triiodothyroacetic acid, and 6.1% with 3, 5-diiodothyroacetic acid. Cross-reaction with T3 began when T3 levels were elevated to 500 ng/dl. No cross-reaction was detectable for iodothyronines within their physiological ranges. Intraassay variation ranged from 2.2-7.8%, and interassay variation ranged from 12.7-14%. The mean (±SE) serum 3, 5T2 concentration in 70 normal subjects was 4.3 ± 0.2 ng/dl. The mean (±SE) 3, 5T2 in 14 hyperthyroid patients was increased to 18.4 ± 2.3 ng/dl (P < 0.001), and all but 1 patient had an elevated level. In 10 hypothyroid patients the mean (±SE) 3, 5T2 level was decreased to 1.4 ± 0.3 ng/dl (P < 0.001). In 4 patients, levels overlapped with the normal range. In 4 hypothyroid subjects treated with L-T4, 3, 5T2 levels were normal, suggesting that the majority of 3, 5T2 originates from extrathyroidal conversion from T3. Studies in fasting obese subjects demonstrated that serum 3, 5T2 (mean ± SE) levels fell from 3.4 ± 0.3 to 2.5 ± 0.7 ng/dl during fasting. This fall was significant (P < 0.001) and in parallel with the fall in T3 levels of 182 ± 20 to 126 ± 12 ng/dl. In fasting subjects given 100 μg oral L-T3/day T3 levels rose from 138 ±11 to 362 ± 26 ng/dl. 3, 5T2 levels (corrected for cross-reaction and for contamination of oral T3 with 3, 5T2) rose from 2.2 ± 0.7 to 6.4 ± 1.0 ng/dl. In fasting subjects given 25 μg oral L-T3/day, T3 levels fell from 165 ± 5.1 to 139 ± 6.9 ng/dl. Corrected 3, 5T2 levels changed from 3.7 ± 0.4 to 2.5 ± 0.3 ng/dl. Neither change was significant. In summary, 3, 5T2 circulates in the serum of normal subjects, is increased in hyperthyroidism, and is decreased in hypothyroidism. Serum 3, 5T2 level depends on and is probably derived from circulating T3. In the clinical protocol employed, fasting does not seem to inhibit deiodination of T3 to 3, 5T2 as it does of T4 to T3.
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U2 - 10.1210/jcem-50-6-1075
DO - 10.1210/jcem-50-6-1075
M3 - Article
C2 - 7372786
AN - SCOPUS:0018946239
SN - 0021-972X
VL - 50
SP - 1075
EP - 1081
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 6
ER -