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Endocrine Abstracts (2023) 94 P397 | DOI: 10.1530/endoabs.94.P397

SFEBES2023 Poster Presentations Thyroid (63 abstracts)

Is it euthyroid sick syndrome or central hypothyroidism?

Hla Myat Mon & Praveena Vankayalapati

Chelsea and Westminster Hospital NHS Foundation Trust, London, United Kingdom

73-year-old gentleman presented to AEC with 3-week history of shortness of breath, cough with sputum production, generalised weakness and loss of appetite. He was found to have iron deficiency anaemia and hyponatraemia (120mmol/l). He had history of type2 diabetes, and hypertension. On workup for hyponatremia, both free T3 and free T4 are reduced with suppressed TSH 0.01 uIU/ml. TSH receptor antibody was negative. He was started on levothyroxine 50mg on suspicion of secondary hypothyroidism. On further workup, CT imagings and biopsy confirmed Diffuse Large B Cell Lymphoma (non-germinal centre type). MRI(pituitary) demonstrated normal pituitary gland with no evidence of altered enhancement confirming no lymphoma infiltration. Pituitary biochemical profile showed normal ACTH, IGF and prolactin levels with low free testosterone and high LH and FSH, suggesting primary hypogonadism, likely age-related. Given the above pituitary profile and MRI(pituitary) findings, he was clinically diagnosed as severe euthyroid sick syndrome. There are many proposed mechanisms regarding the pathogenesis of euthyroid sick syndrome. One cause suggested is that presence of thyroid-binding hormone inhibitors in the serum and different body tissues inhibits the binding of the thyroid hormone to the thyroid-binding protein. The euthyroid sick syndrome is also caused by cytokines such as interleukin 1, interleukin 6, tumour necrosis factor-alpha, and interferon-beta affecting the hypothalamus and pituitary glands, thus inhibiting TSH, thyroid-releasing hormone (TRH), thyroglobulin (TG), T3, and the thyroid-binding globulins (TBG) production. Cytokines were also thought to reduce the activity of type 1 deiodinase and decrease the binding capacity of the T3 nuclear receptors. Another mechanism suggested that expression of thyroid hormone receptors(THRs) and their coactivators are diminished in acute illness.

Conclusion: Biochemical pictures of severe sick euthyroid syndrome can resemble secondary hypothyroidism. Differentiating features would be associated severe non-thyroidal illness and raised cortisol.

Volume 94

Society for Endocrinology BES 2023

Glasgow, UK
13 Nov 2023 - 15 Nov 2023

Society for Endocrinology 

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