Radiothyroxine Turnover Studies in Myxedema, Thyrotoxicosis, and Hypermetabolism Without Endocrine Disease

Sterling, Kenneth; Chodos, Robert B.

doi:10.1172/jci103333

Cited by 158 publications

(79 citation statements)

References 11 publications

(6 reference statements)

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“…of 6.87 ± 1.23 days and a 98% confidence limit (mean ± 2 S.D.) of 4.41-9.33 days [8][9][10][11][12]. Furthermore, Kallner [13] estimated the serum T4 levels after intake of 3000 µg of L-T4 in patients who were classified into two groups (Suppressible and Nonsuppressible) based on the T3 suppression test.…”

Section: Discussionmentioning

confidence: 99%

Thyroxine (T4) Metabolism in an Athyreotic Patient Who Had Taken a Large Amount of T4 at One Time.

et al. 1998

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Abstract. As we had an opportunity to take blood samples from a totally thyroidectomized patient who had attempted suicide by taking 2,000 tg of Levothyroxine (L-T4), the serum levels of thyroid hormones were sequentially measured to investigate the metabolism of circulating thyroid hormones in an athyreotic human. The serum concentrations of most thyroid hormones reached a peak on the second day, but the serum T3 level showed a peak one day later. The maximum concentrations of T4 (315 µg/l), FT4 (48.8 ng/l) and rT3 (0.80 µg/l) were very high, while the peak T3 level (1.92 jug/l) did not exceed the upper limit of the normal range. The serum T4 and rT3 levels returned to their normal range 13-17 days after the suicide attempt. The TSH level was suppressed rapidly and reached its nadir (0.044 mU/I) on the 6th day. During this period, the T112 and MCR of serum T4 were 10.4 days and 0.64 1/day, respectively, which values were almost equivalent to those observed during 15 days after discontinuation of the maintenance L-T4 therapy. In summary, the oral intake of a large amount of L-T4 at one time does not induce a proportional increase in the T3 level in an athyreotic person. The MCR of serum T4 is decreased and the T112 of serum T4 is prolonged, probably due to the lack of intrathyroidal deiodination. These findings support the conclusion that the D1 activity in the thyroid is one of the major determinants in the metabolic clearance of serum T4. Wenzel et al. [5] reported that the maximum concentration of serum T3 after oral intake of an excessive dose (3000 ,ug) of Levothyroxine (L-T4) at one time did not exceed the upper limit of normal range in normal subjects.Nevertheless, the contribution of the thyroid to systemic T4 metabolism is not clear and the precise consequence has not been well documented in reference to the high T3 level in patients with hyperthyroid Graves' disease. In order to evaluate the effect of the thyroid on the metabolism of circulating thyroid hormones, we examined the metabolism of thyroid hormones in an athyreotic patient who had taken an excessive dose of L-T4 at one time.

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Section: Discussionmentioning

confidence: 99%

Thyroxine (T4) Metabolism in an Athyreotic Patient Who Had Taken a Large Amount of T4 at One Time.

et al. 1998

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“…The half-life of thyroid hormones is as long as 6.7 ± 0.7 days in normal subjects and 4.4 ± 1.1 days in patients with hyperthyroidism [182]. Therefore, thyroid function takes a long time to recover from thyroid storm after thyroid hormone production has been suppressed by anti-thyroid medications.…”

Section: • Commentsmentioning

confidence: 99%

2016 Guidelines for the management of thyroid storm from The Japan Thyroid Association and Japan Endocrine Society (First edition)

et al. 2016

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“…The rate of hormonal degradation is increased in thyrotoxicosis and decreased in hypothyroidism (Sterling & Chodos, 1956). It is also low in some poikilotherms which do not respond calorigerlically to the administration of T4 (Galton & Ingbar, 1962).…”

Section: Hormonal Deiodination and Control Of Actionmentioning

confidence: 99%

The Action of Thyroid Hormone

Bernal

Refetoff

1977

Clinical Endocrinology

104

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SUMMARYThyroid hormone affects both developmental and metabolic processes. It has a relatively specific effect on the synthesis of a number of enzymes and other proteins. The fundamental cellular mechanism of action seems to be at the level of genetic regulation. It involves interaction with nuclear receptors, leading to an activation of the protein synthesizing machinery. How binding to receptors is coupled to genetic activation is completely unknown. At least part of the metabolic effects of thyroid hormone could be mediated through an interaction with mitochondria and cell membrane, and with some enzymatic systems such as adenylcyclase.

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Radiothyroxine Turnover Studies in Myxedema, Thyrotoxicosis, and Hypermetabolism Without Endocrine Disease

Cited by 158 publications

References 11 publications

Thyroxine (T4) Metabolism in an Athyreotic Patient Who Had Taken a Large Amount of T4 at One Time.

Thyroxine (T4) Metabolism in an Athyreotic Patient Who Had Taken a Large Amount of T4 at One Time.

2016 Guidelines for the management of thyroid storm from The Japan Thyroid Association and Japan Endocrine Society (First edition)

The Action of Thyroid Hormone

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