scholarly journals Measurement of the Plasma Free Thyroxine Level as a Test of Thyroid Function

BMJ ◽  
1966 ◽  
Vol 2 (5515) ◽  
pp. 668-670 ◽  
Author(s):  
M. Wellby ◽  
M. W. O'Halloran
Keyword(s):  
Thyroid Function ◽  
Free Thyroxine ◽  
Thyroxine Level ◽  
Free Thyroxine Level

scholarly journals Euthyroid athyroxinemia – a novel endocrine syndrome

2017 ◽  
Vol 2017 ◽  
Author(s):  
Nicholas Woodhouse ◽  
Fatima Bahowairath ◽  
Omayma Elshafie
Keyword(s):  
Thyroid Nodule ◽  
Thyroid Function ◽  
Urinary Iodine ◽  
Free Thyroxine ◽  
List Type ◽  
Thyroid Function Tests ◽  
Thyroxine Level ◽  
Learning Points ◽  
Free Thyroxine Level ◽  
Tsh Levels

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.

scholarly journals Low serum free thyroxine level in a girl with McCune-Albright syndrome

2015 ◽  
Vol 2015 (jan05 1) ◽  
pp. bcr2014206497-bcr2014206497 ◽  
Author(s):  
M. Roosimaa ◽  
A. Pajuvali ◽  
A. Peet ◽  
V. Tillmann
Keyword(s):  
Free Thyroxine ◽  
Mccune Albright Syndrome ◽  
Serum Free ◽  
Thyroxine Level ◽  
Albright Syndrome ◽  
Free Thyroxine Level ◽  
Mccune Albright ◽  
Low Serum ◽  
Serum Free Thyroxine

Association between bisphenol A and abnormal free thyroxine level in men

Endocrine ◽  
2013 ◽  
Vol 44 (2) ◽  
pp. 441-447 ◽  
Author(s):  
Chutintorn Sriphrapradang ◽  
La-or Chailurkit ◽  
Wichai Aekplakorn ◽  
Boonsong Ongphiphadhanakul
Keyword(s):  
Bisphenol A ◽  
Free Thyroxine ◽  
Thyroxine Level ◽  
Free Thyroxine Level

scholarly journals Understanding the Pathogenesis of Gestational Hypothyroidism

2021 ◽  
Vol 12 ◽  
Author(s):  
Oshini Mallawa Kankanamalage ◽  
Qiongjie Zhou ◽  
Xiaotian Li
Keyword(s):  
Thyroid Function ◽  
Fetal Loss ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Premature Delivery ◽  
Overt Hypothyroidism ◽  
Thyroglobulin Level ◽  
Vulnerable Individual ◽  
Levothyroxine Treatment ◽  
Free Thyroxine Level

Pregnancy is a complex state with many endocrinological challenges to a woman’s physiology. Gestational Hypothyroidism (GHT) is an emerging condition where insufficiency of the thyroid gland has developed during pregnancy in a previously euthyroid woman. It is different to overt hypothyroidism, where marked elevation of thyroid-stimulating hormone with corresponding reduction in free thyroxine levels, is well known to cause detrimental effects to both the mother and the baby. During the past couple of decades, it has been shown that GHT is associated with multiple adverse maternal and fetal outcomes such as miscarriage, pre-eclampsia, placental abruption, fetal loss, premature delivery, neurocognitive and neurobehavioral development. However, three randomized controlled trials and a prospective cohort study performed within the last decade, show that there is no neurodevelopmental improvement in the offspring of mothers who received levothyroxine treatment for GHT. Thus, the benefit of initiating treatment for GHT is highly debated within the clinical community as there may also be risks associated with over-treatment. In addition, regulatory mechanisms that could possibly lead to GHT during pregnancy are not well elucidated. This review aims to unravel pregnancy induced physiological challenges that could provide basis for the development of GHT. During pregnancy, there is increased renal clearance of iodine leading to low iodine state. Also, an elevated estrogen level leading to an increase in circulating thyroglobulin level and a decrease in free thyroxine level. Moreover, placenta secretes compounds such as human chorionic gonadotropin (hCG), placental growth factor (PIGF) and soluble FMS-like tyrosine kinase-1 (s-Flt1) that could affect the thyroid function. In turn, the passage of thyroid hormones and iodine to the fetus is highly regulated within the placental barrier. Together, these mechanisms are hypothesized to contribute to the development of intolerance of thyroid function leading to GHT in a vulnerable individual.

scholarly journals THYROTOXIC PERIODIC PARALYSIS IN A COMPETITIVE BODYBUILDER WITH THYROTOXICOSIS FACTITIA

2020 ◽  
Vol 6 (5) ◽  
pp. e252-e256
Author(s):  
Amy J. Patel ◽  
Stephanie Tejera ◽  
Stanislaw P. Klek ◽  
Gary D. Rothberger
Keyword(s):  
Thyroid Hormone ◽  
Muscle Weakness ◽  
Potassium Level ◽  
Periodic Paralysis ◽  
Free Thyroxine ◽  
Thyroid Peroxidase ◽  
Fluid Restriction ◽  
Thyrotoxic Periodic Paralysis ◽  
Thyroxine Level ◽  
Free Thyroxine Level

Objective: We report a case of thyrotoxic periodic paralysis (TPP) in a bodybuilder who developed paralysis secondary to thyrotoxicosis factitia after taking a supplement containing thyroid hormone. Interestingly, the patient had no intrinsic thyroid disease. Prompt recognition of thyrotoxicosis is critical to avoid progression of paralysis and subsequent complications. Methods: We discuss a 27-year-old body builder who presented after a 3-day bodybuilding competition with sudden upper and lower extremity paralysis. He admitted to taking anabolic steroids, a supplement containing an unknown amount of thyroid hormone for 2 weeks, and furosemide 40 mg twice daily with near-complete fluid restriction for 3 days. Results: Laboratory results showed a thyroid-stimulating hormone (TSH) level of <0.010 μIU/mL (normal, 0.3 to 5.8 μIU/mL), normal total triiodothyronine level, elevated free thyroxine level of 3.6 ng/dL (normal, 0.8 to 1.9 ng/dL), and potassium level of 1.9 mEq/L (normal, 3.7 to 5.2 mEq/L). Thyroid peroxidase antibody, thyroid-stimulating immunoglobulin, and thyroglobulin antibody levels were normal. Thyroid uptake was 1% (normal, 8 to 25%) after administration of I-123 and thyroglobulin level was 9 ng/mL (normal, 1.4 to 29.2 ng/mL). The patient was treated with normal saline infusion, magnesium supplementation and a total of 230 mEq of potassium within 12 hours of hospitalization. Muscle weakness resolved within this time period and potassium level normalized. By the third day of hospitalization free thyroxine level also normalized and TSH improved to 0.1 mIU/L. Conclusion: TPP is a rare complication of thyrotoxicosis that should be considered in bodybuilders who are presenting with acute muscle weakness.

scholarly journals Alternative Sequences of Thyrotropin and Free Thyroxine Assays for Routine Thyroid Function Testing

1998 ◽  
Vol 158 (3) ◽  
pp. 266 ◽  
Author(s):  
Robert A. Nordyke ◽  
Thomas S. Reppun ◽  
Lynn D. Madanay ◽  
Joseph C. Woods ◽  
Alan P. Goldstein ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Free Thyroxine ◽  
Thyroid Function Testing ◽  
Function Testing
Sign in / Sign up

Export Citation Format

Share Document