Differentiation of Thyrotoxicosis Induced by Thyroid Destruction From Graves' Disease

Amino, Nobuyuki; Miyai, Kiyoshi; Azukizawa, M; Yabu, Yukiko; Fujie, Tomiko; Onishi, Toshio; Kumahara, Yuichi

doi:10.1016/s0140-6736(78)92943-4

Cited by 72 publications

(29 citation statements)

References 19 publications

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“…Many studies have reported T 3 and T 4 levels in patients diagnosed with all types of thyrotoxicosis combined (20) or in a few (4,21,22,23) or even up to four nosological subtypes of thyrotoxicosis (24). In this study, comparing ten nosological types of thyrotoxicosis, GD patients presented the highest T 3 level and T 3 :T 4 ratio, which is in accordance with other studies (4,22,23,25).…”

Section: Serum T 3 and T 4 In Subtypes Of Thyrotoxicosissupporting

confidence: 92%

Determinants of serum T4 and T3 at the time of diagnosis in nosological types of thyrotoxicosis: a population-based study

Carlé

Knudsen

Pedersen

et al. 2013

European Journal of Endocrinology

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Section: Serum T 3 and T 4 In Subtypes Of Thyrotoxicosissupporting

confidence: 92%

Determinants of serum T4 and T3 at the time of diagnosis in nosological types of thyrotoxicosis: a population-based study

Carlé

Knudsen

Pedersen

et al. 2013

European Journal of Endocrinology

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“…Possible mechanisms of the increase in this ratio in Graves' disease include the increased T3 production in the thyroid [23] by enhanced thyroid type 1 deiodinase (D1) activity which is caused by increased T3 and anti-thyrotropin receptor antibodies [24] and the enhanced T3 production from T4 in the liver and kidneys caused by the increased T3 [25], but the T3/T4 ratio remains within the normal range in thyrotoxicosis induced by temporary thyroid destruction [26]. The failure of the ratio to increase is probably due to the minimal or erratic release of thyroid hormones [26], since the serum half-life of T3 is much shorter than that of T4. In the present case, the T3/T4 ratio did not increase, indeed, it was lower than normal despite the marked increase in T4.…”

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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“…Low serum TSH levels are observed in overt hyperthyroidism, treated Graves' disease, euthyroid Graves' disease [1], subclinical hyperthyroidism [2], destructive thyroiditis [3], and thyrotoxicosis of extrathyroidal origin (thyrotoxicosis factitia [4], metastatic thyroid carcinoma [5], struma ovarii [6,7]), central hypothyroidism [8], nonthyroidal illness [9] and aging [10]. Usually it is not difficult to determine the cause of low serum TSH levels.…”

mentioning

confidence: 99%

Immeasurably Low and Non-TRH-stimulatable TSH Associated with Normal I-123 Uptake in Two Goitrous Euthyroid Patients: Possible Existence of Other Thyroid-hormone Regulated Thyroid Stimulators other than TSH

et al. 2005

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Abstract. We described two euthyroid patients with normally functioning goiters, but with persistently undetectable and non-stimulatable TSH levels. Subject 1 was a 64-year-old woman with a large diffuse goiter who has been clinically and biochemically euthyroid without any medication for at least 19 years. Subject 2 was a 31-year-old woman with a small diffuse goiter who has been euthyroid for 4 years. Both patients had persistently undetectable levels of serum TSH, TSH receptor antibodies (TRAb) and thyroid stimulating antibodies (TSAb). Their basal TSH levels were very low and their T 3 responses to TRH were very diminished or absent. In contrast, the basal levels of the other pituitary hormones and their responses to LHRH, GRH and CRH stimulation were all within normal limits in both patients. MRI images of pituitary glands, 123 I thyroid uptake, and thyroid scans were normal. Ectopic thyroids were not detected on 99m TcO 4 -and 123 I total body scans. Factors interfering with the measurement of TSH were excluded by recovery studies. In subject 1 a T 3 -suppression test was positive and a perchlorate discharge test was negative. In subject 2 a T 3 -suppression test was negative. Euthyroid Graves' disease, subclinical hyperthyroidism, destructive thyroiditis, thyrotoxicosis of extrathyroid origin, central hypothyroidism, and nonthyroidal illness were all ruled out by these observations. These results suggest that an unknown factor, such as thyrostimulin, but not TSH or TSAb, stimulates the thyroid and maintains euthyroidism, and may have a role in the regulation of the hypothalamus-pituitary-thyroid axis. Usually it is not difficult to determine the cause of low serum TSH levels. We report here two unusual euthyroid patients with goiters and persistently undetectable TSH levels. We consider the clinical significance of the association of goiter with long-term undetectable TSH and normal thyroid hormone levels and the possible implications for the hypothalamus-pituitary-thyroid axis. Since the cause of the low TSH could not be determined after extensive evaluation, it is suggested that there are factors in addition to TSH that contribute to the control of the thyroid gland.

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Differentiation of Thyrotoxicosis Induced by Thyroid Destruction From Graves' Disease

Cited by 72 publications

References 19 publications

Determinants of serum T4 and T3 at the time of diagnosis in nosological types of thyrotoxicosis: a population-based study

Determinants of serum T4 and T3 at the time of diagnosis in nosological types of thyrotoxicosis: a population-based study

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

Immeasurably Low and Non-TRH-stimulatable TSH Associated with Normal I-123 Uptake in Two Goitrous Euthyroid Patients: Possible Existence of Other Thyroid-hormone Regulated Thyroid Stimulators other than TSH

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