A Comparison of the Effect of Desiccated Thyroid and Sodium Levothyroxine on the Serum Protein-Bound Iodine

Sturnick, Melvin I.; Lesses, Mark Falcon

doi:10.1056/nejm196103232641207

Cited by 18 publications

(6 citation statements)

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“…Until recently, it has been assumed that adequate replacement therapy with L-thyroxine would require doses sufficient to establish values for serum T4 concentration above the normal range, since the metabolic contribution normally provided by Ts was presumed to be lacking (23)(24)(25)(26)(27). With the demonstration of peripheral T4 to Ts conversion, however, the rationale for this approach no longer seemed valid, provided that the rate of production of Ta was physiologically significant.…”

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confidence: 99%

“…The few available data of other workers also supports the conclusion that 0.3 mg of L-thyroxine daily may often be an excessive replacement dose. Most authors emphasize the difficulty of selecting between 0.2 mg daily and 0.3 mg daily on the basis of subjective findings alone (26,27,(36)(37)(38); however, when objective criteria such as BMR have been assessed, doses of 0.2 mg daily frequently seem sufficient (36,39). The most telling evidence, however, is the recent finding of Cotton,Gorham,and Mayberry (40) that in patients with hypothyroidism doses of 0.2 mg daily usually suffice to restore serum thyroid-stimulating hormone (TSH) concentration to normal.…”

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confidence: 99%

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Effects of Replacement Doses of Sodium-L-Thyroxine on the Peripheral Metabolism of Thyroxine and Triiodothyronine in Man

Braverman¹,

Vagenakis²,

Downs³

et al. 1973

J. Clin. Invest.

101

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A B S T R A C T Studies of the effect of L-thyroxine administration (0.3 mg daily for 7-9 wk) on the peripheral metabolism of "'I-labeled triiodothyronine (Ta) and "IIlabeled thyroxine (T4) and on the concentration and binding of T4 and Ts in serum were carried out in 11 euthyroid female subjects. Administration of L-thyroxine led to consistent increases in serum Ta concentration (137 vs. 197 ng/100 ml), Ta distribution space (39.3 vs. 51.7 liters), Ta clearance rate (22.9 vs. 30.6 liters/ day) and absolute Ts disposal rate (30 vs. 58 Ag/day), but no change in apparent fractional turnover rate (60.3 vs. 60.6%/day). The proportion and absolute concentration of free Ta also increased during L-thyroxine administration. Increases in serum total T4 concentration (7.3 vs. 12.8 ,g/100 ml) and in both the proportion and absolute concentration of free thyroxine also occurred. In five of the subjects, the kinetics of peripheral T4 turnover were simultaneously determined and a consistent increase in fractional turnover rate (9.7 vs. 14.2%/day), clearance rate (0.84 vs. 1.37 liters/day), and absolute disposal rate (64.2 vs. 185.0 Ag/day) occurred during L-thyroxine administration. Despite these increases in the serum concentration and daily disposal rate of both To and Ta, the patients were not clinically thyrotoxic. However, basal metabolic rate (BMR) values were marginally elevated and, as in frank thyrotoxicosis,

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confidence: 99%

Effects of Replacement Doses of Sodium-L-Thyroxine on the Peripheral Metabolism of Thyroxine and Triiodothyronine in Man

Braverman¹,

Vagenakis²,

Downs³

et al. 1973

J. Clin. Invest.

101

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“…However, in the present study, it was noteworthy that 3 of 10 patients had still elevated TSH concentrations in serum, despite the administration of T4 for approximately 3 months, although the doses were slightly less than the dosis (2.25 pg/kg body weight) recommended by the previous report (Stock et al, 1974). It has been suggested that adequate replacement therapy with L-T4 would require doses sufficient to establish values for a serum T4 concentration above the normol range (Sturnick and Lesses, 1961;Lavietes and Epstein, 1964). Moreover, the amount of T3 generated by the conversion of T4 to T3 was found to contribute to approximately 70% of the daily T3 production in normal subjects and, therefore, the 30% of the T3 production was assumed to be secreted directly from the thyroid (Inada et al, 1975).…”

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confidence: 99%

Effect of 3,5,3'L-triiodothyronine administration on serum thyroid hormone levels in hypothyroid patients maintained on constant doses of thyroxine.

et al. 1980

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“…However, PBI was limited in terms of monitoring a response to treatment as the “ concentration of the PBI associated with restoration of a normal metabolic state depends upon the particular thyroid hormone employed ” (76). For example, LT3 was reported as correcting BMR without much increase in PBI (77), whereas LT4 increased PBI sometimes to above the upper limit of the normal range (78), and combination LT4 + LT3 and desiccated thyroid had the advantage of normalizing PBI (79).…”

Section: Need For Thyroid Replacement Established Treatment Strategimentioning

confidence: 99%

The Swinging Pendulum in Treatment for Hypothyroidism: From (and Toward?) Combination Therapy

McAninch

Bianco

2019

Front. Endocrinol.

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Thyroid hormone replacement for hypothyroidism can be achieved via several approaches utilizing different preparations of thyroid hormones, T3, and/or T4. “Combination therapy” involves administration of both T3 and T4, and was technically the first treatment for hypothyroidism. It was lauded as a cure for the morbidity and mortality associated with myxedema, the most severe presentation of overt hypothyroidism. In the late nineteenth and the early Twentieth centuries, combination therapy per se could consist of thyroid gland transplant, or more commonly, consumption of desiccated animal thyroid, thyroid extract, or thyroglobulin. Combination therapy remained the mainstay of therapy for decades despite development of synthetic formulations of T4 and T3, because it was efficacious and cost effective. However, concerns emerged about the consistency and potency of desiccated thyroid hormone after cases were reported detailing either continued hypothyroidism or iatrogenic thyrotoxicosis. Development of the TSH radioimmunoassay and discovery of conversion of T4-to-T3 in humans led to a major transition in clinical practices away from combination therapy, to adoption of levothyroxine “monotherapy” as the standard of care. Levothyroxine monotherapy has a favorable safety profile and can effectively normalize the serum TSH, the most sensitive marker of hypothyroidism. Whether levothyroxine monotherapy restores thyroid hormone signaling within all tissues remains controversial. Evidence of persistent signs and symptoms of hypothyroidism during levothyroxine monotherapy at doses that normalize serum TSH is mounting. Hence, in the last decade there has been acknowledgment by all thyroid professional societies that there may be a role for the use of combination therapy; this represents a significant shift in the clinical practice guidelines. Further bolstering this trend are the recent findings that the Thr92AlaD2 polymorphism may reduce thyroid hormone signaling, resulting in localized and systemic hypothyroidism. This strengthens the hypothesis that treatment options could be personalized, taking into consideration genotypes and comorbidities. The development of long-acting formulations of liothyronine and continued advancements in development of thyroid regenerative therapy, may propel the field closer to adoption of a physiologic thyroid hormone replacement regimen with combination therapy.

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A Comparison of the Effect of Desiccated Thyroid and Sodium Levothyroxine on the Serum Protein-Bound Iodine

Cited by 18 publications

References 4 publications

Effects of Replacement Doses of Sodium-L-Thyroxine on the Peripheral Metabolism of Thyroxine and Triiodothyronine in Man

Effects of Replacement Doses of Sodium-L-Thyroxine on the Peripheral Metabolism of Thyroxine and Triiodothyronine in Man

Effect of 3,5,3'L-triiodothyronine administration on serum thyroid hormone levels in hypothyroid patients maintained on constant doses of thyroxine.

The Swinging Pendulum in Treatment for Hypothyroidism: From (and Toward?) Combination Therapy

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