Abstract:Ten patients with hyperthyroidism due to Graves' disease were treated with sodium ipodate (1 g daily) in addition to propranolol (P) plus propylthiouracil (PTU; 100 mg every 8 h) and were compared with a control group of 8 patients treated with P and PTU. Patients on P and PTU had a mean (+/- SEM) basal free T3 index of 387 +/- 59 (normal, 70--160) compared with that of 409 +/- 47 (P greater than 0.05) in the sodium ipodate group. The respective basal free T4 index values (normal, 4.5-10.9) were 21.3 +/- 2.8 f… Show more
“…Ipodate or similar compounds have been found useful for short-term therapy of hyperthyroidism (16,17) and for special indications (18) but less effective for prolonged therapy (19). In our study, PTU plus ipodate gave the most profound decrease in serum T 3 with a decrease in the T 3 /T 4 % in serum to around one third of the initial value.…”
Context: Graves' hyperthyroidism and multinodular toxic goiter lead to high serum T 3 compared with serum T 4 . The source of this high T 3 has not been clarified.
Objective:Our objective was to assess the role of iodothyronine deiodinase type 1 (D1) and type 2 (D2) for T 3 production and to estimate the sources of T 3 in hyperthyroidism.
Design and Setting:The study was a prospective, randomized, open-labeled study in a secondary care setting.
Patients and Methods:Consecutive patients with hyperthyroidism caused by Graves' disease or by multinodular toxic goiter were randomized to be treated with high-dose propylthiouracil (PTU) to block D1, PTU plus KI, or PTU plus sodium ipodate to additionally block D2. T 3 and T 4 were measured in serum, and we estimated the sources of T 3 .Results: PTU reduced the T 3 /T 4 in serum to 47.7 Ϯ 2.5% (mean Ϯ SEM) of the initial value on d 4 of therapy in patients with Graves' disease. The addition of KI to PTU led to a greater fall in T 3 and T 4 , but the balance was unaltered. After PTU plus ipodate, T 3 /T 4 on d 4 was lower, 34.1 Ϯ 1.2% of the initial value. Similar variations were observed in patients with multinodular toxic goiter. Thus, the major source of the excess T 3 was D1-catalyzed T 4 deiodination, with a minor role for D2. It was estimated that the majority of this D1-catalyzed T 3 production takes place in the hyperactive thyroid gland.
Conclusion:Although thyroidal T 3 contributes only around 20% of total T 3 production in normal individuals, this is much higher in patients with a hyperactive thyroid, ranging up to two thirds. The major part is produced from T 4 deiodinated in the thyroid.
“…Ipodate or similar compounds have been found useful for short-term therapy of hyperthyroidism (16,17) and for special indications (18) but less effective for prolonged therapy (19). In our study, PTU plus ipodate gave the most profound decrease in serum T 3 with a decrease in the T 3 /T 4 % in serum to around one third of the initial value.…”
Context: Graves' hyperthyroidism and multinodular toxic goiter lead to high serum T 3 compared with serum T 4 . The source of this high T 3 has not been clarified.
Objective:Our objective was to assess the role of iodothyronine deiodinase type 1 (D1) and type 2 (D2) for T 3 production and to estimate the sources of T 3 in hyperthyroidism.
Design and Setting:The study was a prospective, randomized, open-labeled study in a secondary care setting.
Patients and Methods:Consecutive patients with hyperthyroidism caused by Graves' disease or by multinodular toxic goiter were randomized to be treated with high-dose propylthiouracil (PTU) to block D1, PTU plus KI, or PTU plus sodium ipodate to additionally block D2. T 3 and T 4 were measured in serum, and we estimated the sources of T 3 .Results: PTU reduced the T 3 /T 4 in serum to 47.7 Ϯ 2.5% (mean Ϯ SEM) of the initial value on d 4 of therapy in patients with Graves' disease. The addition of KI to PTU led to a greater fall in T 3 and T 4 , but the balance was unaltered. After PTU plus ipodate, T 3 /T 4 on d 4 was lower, 34.1 Ϯ 1.2% of the initial value. Similar variations were observed in patients with multinodular toxic goiter. Thus, the major source of the excess T 3 was D1-catalyzed T 4 deiodination, with a minor role for D2. It was estimated that the majority of this D1-catalyzed T 3 production takes place in the hyperactive thyroid gland.
Conclusion:Although thyroidal T 3 contributes only around 20% of total T 3 production in normal individuals, this is much higher in patients with a hyperactive thyroid, ranging up to two thirds. The major part is produced from T 4 deiodinated in the thyroid.
“…Basal and TRH-stimulated thyrotropin (TSH) values have been shown to increase or remain unchanged (2,(14)(15)(16)(22)(23)(24)(25)(26). In hyperthyroid subjects with Graves' disease, where there is increased expression of 59-MDI, T 4 levels decrease or remain unchanged (10,(27)(28)(29)(30)(31). In subacute thyroiditis, where there is uncontrolled release of thyroid hormones, and in euthyroid and hypothyroid subjects, serum T 4 levels increase or remain unchanged (2,12,15,16,25,26,32,33).…”
Section: Effects On Thyroid Hormone Physiologymentioning
Oral iodinated radiographic contrast agents such as ipodate and iopanoic acid form an important part of the armamentarium used to treat hyperthyroidism. They rapidly and dramatically reduce serum triiodothyronine (T3) levels by inhibiting conversion of thyroxine (T4) to T3 in the periphery and by blocking secretion from the thyroid. Potential risks from the large iodine load resulting from their use limit their widespread applicability. In addition, they are ineffective when used alone on a long-term basis. However, these agents may be especially useful in treating thyrotoxic patients preoperatively, in neonatal Graves' disease, in massive levothyroxine ingestion, and when other conventional antithyroid drugs are unsuccessful or contraindicated.
“…Thirdly, as 500 mg of SI contains 308 mg iodine, large amounts of iodine are released during its metabolism, resulting in the inhibition of the organifica tion of iodine (Wolff-Chaikoff effect) [5] and of thyroid hormone release [6], Furthermore, SI seems to inhibit the hormonal secretion of the thyroid also by a direct effect which is independent of the inhibition induced by iodine [3,7,8]. It has been shown that during treatment with SI plasma T4 values decrease by 20-31 % in thyro toxic Graves' patients [1,[9][10][11][12][13], but remain unchanged or even rise in healthy adults [1,14,15]; on the other hand, plasma T3 values decrease by 67-76% in thyro toxic Graves' patients and by 25-55% in healthy adults [1,[9][10][11][12][13][14][15].…”
Sodium ipodate (SI) is an oral cholecystographic agent that also affects thyroid hormone metabolism. It inhibits the peripheral T4 to T3 conversion and the thyroidal hormone release. We investigated the safety and efficacy of SI (500 mg daily during 5 days) in the preparation for subtotal thyroidectomy of 7 Graves’ hyperthyroid patients in whom treatment with thionamides was unsuccessful due to allergy or noncompliance. Plasma T3 levels (mean ± SD) decreased from 4.90 ± 1.80 nmol/l on day 0 to 1.70 ± 0.30 nmol/l on day 4 of treatment. Thyroidectomy performed on day 5 of treatment was uneventful. In comparison with 14 Graves’ hyperthyroid patients who underwent thyroidectomy during the same period after conventional preparation with thionamides and potassium iodide, the therapeutic outcome 1 year postoperatively was similar in both groups. However, in the mildly hypothyroid patients prepared with SI, the plasma thyroid-stimulating hormone level was transiently higher 3 and 6 months postoperatively. It is concluded (1) that SI is a safe and efficacious drug in the preparation of Graves’ hyperthyroid patients for thyroidectomy; (2) the therapeutic outcome 12 months postoperatively is similar in SI and in conventionally prepared Graves’ hyperthyroid patients, and (3) postoperative mild or subclinical hypothyroidism is more pronounced in SI than in conventionally prepared patients.
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