Salicylates and Thyroid Function. II. The Effect on the Thyroid-Pituitary Interrelation

Wolff, J.; Austen, Frank K.

doi:10.1172/jci103704

Cited by 46 publications

(16 citation statements)

References 35 publications

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“…An indirect action, presumably via the pituitary or higher centers, similar to that of thyroxine is suggested. The localization of this indirect inhibition and the implication of a decrease in available thyrotropin form the subject of the following report (46 3. The serum protein bound iodine concentration was reduced from a mean of 5.5 to 3.8 micrograms per 100 ml.…”

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confidence: 99%

Salicylates and Thyroid Function. I. Depression of Thyroid Function

Austen¹,

Rubini²,

Meroney³

et al. 1958

J. Clin. Invest.

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Section: Com Mentmentioning

confidence: 99%

Salicylates and Thyroid Function. I. Depression of Thyroid Function

Austen¹,

Rubini²,

Meroney³

et al. 1958

J. Clin. Invest.

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“…(Submitted for publication February 6, 1961; accepted April 6, 1961) A number of compounds such as 2,4-dinitrophenol,' salicylate, tetrachlorothyronine, and diphenylhydantoin have been shown to lower the protein-bound iodine level of the blood (1)(2)(3)(4)(5). In the case of DNP and salicylate, it was concluded that they acted in part via an inhibition of the pitutary TSH mechanism and partly by an accelerated loss of T4 from the circulation (2,6). A likely site of action was, therefore, expected to involve binding of T4 to serum proteins.…”

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Thyroxine Displacement From Serum Proteins and Depression of Serum Protein-Bound Iodine by Certain Drugs

Wolff¹,

Standaert²,

Rall³

1961

J. Clin. Invest.

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A number of compounds such as 2,4-dinitrophenol,' salicylate, tetrachlorothyronine, and diphenylhydantoin have been shown to lower the protein-bound iodine level of the blood (1-5). In the case of DNP and salicylate, it was concluded that they acted in part via an inhibition of the pitutary TSH mechanism and partly by an accelerated loss of T4 from the circulation (2, 6). A likely site of action was, therefore, expected to involve binding of T4 to serum proteins.The ability of various analogs of thyroxine to bind to proteins of serum has been extensively studied with electrophoretic techniques. At least three serum proteins and perhaps four have been described which bind thyroxine (7). Less direct methods of studying this binding of the thyroid hormones consist of measurement of the "uptake" of triiodothyronine by erythrocytes (8) and the rate of dialysis of T4 through a cellophane membrane (9). By these techniques several compounds have been found that appear to alter the binding of T4 to serum proteins when studied by these techniques but if whole serum is used, the effect cannot be localized to specific proteins. Thus it has been suggested from dialysis studies that salicylates and DNP act by inhibiting T4 binding to serum proteins. Electrophoretic studies in barbital buffer of sera containing salicylate failed to show any influence on the distribution of T4 between TBG and albumin, nor was there any change in the T4 binding capacity measured under these conditions (2). Since then it has been shown that barbital buffer inhibits T4 binding to prealbumin (10) and Ingbar has stated that 1 The following abbreviations have been used: DNP = 2,4-dinitrophenol; PBI = protein-bound iodine, T4 = thyroxine; TBG = thyroxine-binding globulin of the interalpha zone in paper electrophoresis; TBPA = thyroxinebinding prealbumin; TCT=DL-tetrachlorothyronine; TSH =thyroid-stimulating hormone.salicylate could interfere with T4 binding in electrophoretic systems in buffers other than barbital (11). It was therefore desired to examine T4 binding in the presence of these four agents in a system where prealbumin binding of T4 could be observed. Furthermore, the possible correlation between the effect of inhibition of thyroxine binding to TBPA and to TBG by various drugs with the in vivo effect of these drugs on the PBI was studied. METHODSA single batch of pooled normal human serum obtained from the Baxter Laboratories was used in all the studies. Butanol solutions of thyroxine were evaporated to dryness in vacuo prior to the addition of serum. The mixtures were incubated at 4°C for at least 24 hours before use and were kept in the cold until used.Electrophoresis in 0.12 M ammonium carbonate buffer, pH 8.4, was performed at room temperature on 3.75 X 49 cm strips of Whatman no. 3 MM filter paper. The edges of the strips were coated with a thin border of paraffin. The strips were saturated with buffer and suspended horizontally between two plastic clamps in a closed system. The strips were equilibrated for at least 1 hour before the ...

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“…21 Wolff and his associates 22 present detailed data to demonstrate an "extrathyroidal hypermetabolic" effect of sodium salicylate. That the hypoglycemia following salicylate administration is not solely a result of increased utilization by an induced hypermetabolic state is suggested by the work of Reid.…”

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confidence: 99%