THE EFFECTS OF PHENYLBUTAZONE ON THYROID FUNCTION

1973 ◽  
Vol 72 (2) ◽  
pp. 257-264 ◽  
Author(s):  
M. O. Abiodun ◽  
R. Bird ◽  
C. W. H. Havard ◽  
N. K. Sood

ABSTRACT It is known that phenylbutazone suppresses the thyroidal uptake of radioactive iodine and the serum level of protein-bound iodine (PBI) during the first week of treatment, with a return to normal values after 2 weeks of continuous treatment. Up till now the initial suppression of thyroid function has been presumed due to inhibition of TSH secretion. In the present study, total serum thyroxine and percentage dialysable thyroxine have been measured and the serum absolute free thyroxine concentration calculated in 12 patients before starting treatment with phenylbutazone orally, after 4 days of treatment and again after 14 days. Serum TSH was assayed in 10 of these patients before, and on the 4th day of treatment. Sera were assayed for TSH after 14 days on the drug in 6 patients. On the 4th day of treatment, the levels of total thyroxine had fallen but the levels of free thyroxine remained unchanged. TSH levels were also unaltered. By the 14th day of treatment, free thyroxine levels had fallen significantly below pre-treatment values but no significant rise in TSH could be demonstrated in the 6 patients studied. At no time was there a fall in TSH levels and we conclude that suppression of some thyroid function tests during the first week of treatment with phenylbutazone is due to direct inhibition of the gland by the drug.

1976 ◽  
Vol 22 (10) ◽  
pp. 1562-1566
Author(s):  
R W Pain ◽  
B M Duncan

Abstract Clinicians experience difficulty in correctly interpreting the results of in vitro thyroid function tests in the presence of abnormalities of thyrobinding proteins or when results are borderline. This difficulty has been largely resolved in our laboratory by three innovations. First, the borderline areas for each of three routine tests of thyroid function (total thyroxine, thyrobinding index, and free thyroxine index) were accurately determined. Second, the results from this routine profile of three tests were displayed pictorially so as to produce patterns characteristic of various diagnostic situations, including euthyroidism in the presence of abnormalities of thyrobinding proteins. Third, interpretive comments and, in the case of borderline patterns, suggested further testing procedures were added to the report. Clinicians find the reporting system helpful and respond when additional tests are suggested. The system, operated manually at first, was later computerized.


2021 ◽  
Vol 184 (5) ◽  
pp. 699-709
Author(s):  
Irene Campi ◽  
Ilaria Bulgarelli ◽  
Antonella Dubini ◽  
Giovanni Battista Perego ◽  
Elena Tortorici ◽  
...  

Objective Alterations in thyroid function tests (TFTs) have been recorded during SARS-CoV-2 infection as associated to either a destructive thyroiditis or a non-thyroidal illness. Methods We studied 144 consecutive COVID-19 patients admitted to a single center in intensive or subintensive care units. Those with previous thyroid dysfunctions or taking interfering drugs were excluded. Differently from previous reports, TSH, FT3, FT4, thyroglobulin (Tg), anti-Tg autoantibodies (TgAb) were measured at baseline and every 3–7 days. C-reacting protein (CRP), cortisol and IL-6 were also assayed. Results The majority of patients had a normal TSH at admission, usually with normal FT4 and FT3. Low TSH levels were found either at admission or during hospitalization in 39% of patients, associated with low FT3 in half of the cases. FT4 and Tg levels were normal, and TgAb-negative. TSH and FT3 were invariably restored at the time of discharge in survivors, whereas were permanently low in most deceased cases, but only FT3 levels were predictors of mortality. Cortisol, CRP and IL-6 levels were higher in patients with low TSH and FT3 levels. Conclusions Almost half of our COVID-19 patients without interfering drugs had normal TFTs both at admission and during follow-up. In this series, the transient finding of low TSH with normal FT4 and low FT3 levels, inversely correlated with CRP, cortisol and IL-6 and associated with normal Tg levels, is likely due to the cytokine storm induced by SARS-Cov-2 with a direct or mediated impact on TSH secretion and deiodinase activity, and likely not to a destructive thyroiditis.


Author(s):  
Nicholas Woodhouse ◽  
Fatima Bahowairath ◽  
Omayma Elshafie

Summary A 55-year-old female was referred with abnormal thyroid function tests (TFTs); the free thyroxine level (FT4) was undetectable <3.3 pmol/L (normal: 7.9–14.4), while her FT3, TSH and urinary iodine levels were normal. She was clinically euthyroid with a large soft lobulated goitre that had been present for more than thirty years. She received an injection of recombinant human TSH (rhTSH) following which there was a progressive rise of the FT3 and TSH levels to 23 pmol/L and >100 mIU/L respectively at 24 h, The FT4 however remained undetectable throughout. Being on thyroxine 100 µg/day for one month, her FT4 level increased to 15 pmol/L and TSH fell to 0.08 mIU/L. Four years earlier at another hospital, her FT4 level had been low (6.8 pmol/L) with a normal TSH and a raised Tc-99 uptake of 20% (normal<4%). We checked the TFTs and Tc-99 scans in 3 of her children; one was completely normal and 2 had euthyroid with soft lobulated goitres. Their Tc-99 scan uptakes were raised at 17% and 15%, with normal TFTs apart from a low FT4 7.2 pmol/L in the son with the largest thyroid nodule. This is a previously unreported form of dyshormonogenesis in which, with time, patients gradually lose their ability to synthesize thyroxine (T4) but not triiodothyroxine (T3). Learning points: This is a previously unreported form of dyshormonogenetic goitre. This goitre progressively loses its ability to synthesize T4 but not T3. The inability to synthesize T4 was demonstrated by giving rhTSH.


1984 ◽  
Vol 105 (4) ◽  
pp. 477-481 ◽  
Author(s):  
Hitoshi Suzuki ◽  
Noriko Yamazaki ◽  
Yoshinobu Suzuki ◽  
Masaki Hiraiwa ◽  
Shin-ichi Shimoda ◽  
...  

Abstract. To evaluate the effect of anticonvulsants on serum levels of free thyroxine (FT4) and thyroxinebinding globulin (TBG), 32 patients with epilepsy receiving long-term anticonvulsant treatment (mean duration 81.8 ± 8.9 months) were employed in the present study. The serum levels of total thyroxine (TT4), total triiodothyronine (TT3), T3 resin uptake (T3U) and thyrotrophin (TSH) were also measured. Free thyroxine index (FT4I) was calculated from TT4 and T3U. Mean levels of these thyroid function tests were as follows: 5.52 ± 1.51 μg/dl (TT4), 1.16 ± 0.32 ng/dl (FT4), 101.5 ± 16.2 ng/dl (TT3), 27.5 ± 2.6% (T3U), 19.64 ± 3.97 μg/ml (TBG), 1.50 ± 0.36 (FT4I) and 2.21 ± 0.18 μU/ml (TSH). These values except for T3U and TSH were significantly lower than normal values (P < 0.01). Using correlation analysis, a significant dose-dependency (daily doses) was found between diphenylhydantoin (DPH) and TT4, FT4 and TBG. Other anticonvulsants (bartiturates, carbamazepine, primidone) or duration of treatment were not significantly correlated with thyroid function tests. Therefore serum levels of DPH were also measured in 19 out of 32 patients receiving anticonvulsant treatment. Significant negative correlation was found between serum levels of DPH and FT4 (r = −0.65) and DPH and TBG (r = −0.61).


Author(s):  
Jim Stockigt

The assessment of thyroid function by laboratory testing began in about 1934 with the measurement of oxygen consumption or basal metabolic rate. Twenty years later measurement of protein-bound iodine became the standard technique and after a further 20 years this assay was superseded by radioimmunoassays of thyroxine (T4) and triiodothyronine (T3). Radioimmunoassays for thyroid-stimulating hormone (TSH) were reported from 1965, but early techniques could not distinguish normal values from the suppressed levels found in thyrotoxicosis. Until about 1990 this distinction was made by the administration of intravenous thyrotropin-releasing hormone (TRH), which fails to increase TSH to measurable levels in thyrotoxicosis, while producing a clear 5- to 15-fold increase in serum TSH in euthyroid subjects with normal pituitary function. Immunometric TSH assays now allow the suppressed serum TSH levels of thyrotoxicosis to be clearly distinguished from normal. This fundamental advance has coincided with the development of ingenious techniques to estimate the minute fraction of total serum T4 that circulates in the unbound state, but even the best free T4 methods offer only a marginal diagnostic advantage over the measurement of total T4, e.g. when the concentration of thyroxine-binding globulin (TBG) is abnormal. Current enthusiasm for free T4 and T3 estimation needs to be tempered by an understanding of the method-dependent limitations of these techniques, particularly in situations where assessment of thyroid function is most difficult (see below).


1971 ◽  
Vol 10 (04) ◽  
pp. 299-304
Author(s):  
József Takó ◽  
János Fischer ◽  
Jusztina Juhász ◽  
Ilona Sztraka ◽  
István Kapus ◽  
...  

SummaryThe results of thyroid function tests have been compared with data on the thyroxine-binding capacity of plasma proteins in hyper-, hypo- and euthyroid cases, the latter including women taking oral contraceptives (Infecundin). It was found that there exists a significant correlation of exponential nature between the in vitro red blood cell 125I-triiodothyronine uptake (RCU) and the free thyroxine-binding capacity of the thyroxine-inding globulin (TBG).


2021 ◽  
pp. 73-76
Author(s):  
Vasudev Sankhla ◽  
Aman Deep

Thyroid function tests are one of the most common endocrine panels in general practice because a good understanding of when to order them, indications for treatment are important for the optimal treatment of thyroid dysfunction. Thyroid-stimulating hormone (TSH) should be the rst test to be performed on any patient with suspected thyroid dysfunction and in follow-up of individuals on treatment. It is useful as a rst-line test because even small changes in thyroid function are sufcient to cause a signicant increase in TSH secretion. Thyroxine levels may be assessed in a patient with hyperthyroidism, to determine the severity of hyperthyroxinemia. Antithyroid peroxidase measurements should be considered while evaluating patients with subclinical hypothyroidism and can facilitate the identication of autoimmune thyroiditis during the evaluation of nodular thyroid disease. The measurement of TSH receptor antibody must be considered when conrmation of Graves’ disease is needed and radioactive iodine uptake cannot be done.


Author(s):  
Jayne A. Franklyn

Subclinical hypothyroidism is defined biochemically as the association of a raised serum thyroid-stimulating hormone (TSH) concentration with normal circulating concentrations of free thyroxine (T4) and free triiodothyronine (T3). The term subclinical hypothyroidism implies that patients should be asymptomatic, although symptoms are difficult to assess, especially in patients in whom thyroid function tests have been checked because of nonspecific complaints such as tiredness. An expert panel has recently classified individuals with subclinical hypothyroidism into two groups (1): (1) those with mildly elevated serum TSH (typically TSH in the range 4.5–10.0 mU/l) and (2) those with more marked TSH elevation (serum TSH >10.0 mU/l).


2010 ◽  
Vol 56 (6) ◽  
pp. 912-920 ◽  
Author(s):  
L. M. Thienpont ◽  
K. Van Uytfanghe ◽  
G. Beastall ◽  
J. D. Faix ◽  
T. Ieiri ◽  
...  

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