Abstract
Background
Thyroid hormone synthesis is a complex process in the human body. Although the thyroid gland is essential for thyroid hormone synthesis, skeletal muscles also have crucial roles in thyroid hormone metabolism due to the deiodinase activities of the muscle cells. Hypothyroidism-related myopathy is a well-known entity. However, systemic effects of acute myopathies, such as rhabdomyolysis, on thyroid hormone metabolism have not to date been fully clarified.
Methods
Fifty-three earthquake victims were evaluated retrospectively. We investigated the thyroid function tests (TFTs) among patients with creatine kinase (CK) levels higher than 10.000 U/L at admission. Fifteen patients had CK levels higher than 10.000 U/L and 12 of them had data of TFTs, including thyroid stimulating hormone (TSH), free T4 (FT4), and free T3 (FT3) during hospitalization. These patients were evaluated.
Results
TSH levels were increased in all seven patients who required HD due to severe crush syndrome. Decreased FT4 levels were detected in 71.4% of them. None of the five non-HD patients had increased TSH levels or reduced FT4 levels. During follow-up, all patients survived. Renal and thyroid functions were normalized during follow-up without thyroxin replacement in patients with no prior history of hypothyroidism. Moreover, TFTs were normalized in two patients with history of hypothyroidism under thyroxine treatment without dose adjustments.
Conclusions
In severe forms of crush syndrome, temporary hypothyroidism might be seen. The exact mechanism underlying this entity is not well-known. Further clinical and experimental trials should be conducted to illuminate the mechanism of disrupted thyroid hormonogenesis in crush syndrome victims.
Similar content being viewed by others
Data availability
The data that support the findings of this study are available from the corresponding author upon reasonable request.
References
Salvatore D, Simonides WS, Dentice M, Zavacki AM, Larsen PR (2014) Thyroid hormones and skeletal muscle–new insights and potential implications. Nat Rev Endocrinol 10(4):206–214. https://doi.org/10.1038/nrendo.2013.238
Sindoni A, Rodolico C, Pappalardo MA, Portaro S, Benvenga S (2016) Hypothyroid myopathy: a peculiar clinical presentation of thyroid failure. Review of the literature. Rev Endocr Metab Disord 17(4):499–519. https://doi.org/10.1007/s11154-016-9357-0
KDIGO AKI Work Group (2012) KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2:1–138
Lee S, Farwell AP (2016) Euthyroid sick syndrome. Compr Physiol 6(2):1071–80. https://doi.org/10.1002/cphy.c150017
Favresse J, Burlacu MC, Maiter D, Gruson D (2018) Interferences with thyroid function immunoassays: clinical implications and detection algorithm. Endocr Rev 39(5):830–850. https://doi.org/10.1210/er.2018-00119
Davis PJ, Yoshida K, Schoenl M (1980) Interaction of thyroid hormone and hemoglobin. I. Nature of the interaction and effect of hemoglobin on thyroid hormone radioimmunoassay. J Lab Clin Med 95(5):714–24
Kiessling WR (1981) Correlation between serum myoglobin and thyroid status in myasthenia gravis. J Neurol Neurosurg Psychiatry 44(12):1159–1161. https://doi.org/10.1136/jnnp.44.12.1159
Sheng Y, Ma D, Zhou Q, Wang L, Sun M, Wang S, Qi H, Liu J, Ding G, Duan Y (2019) Association of thyroid function with sarcopenia in elderly Chinese euthyroid subjects. Aging Clin Exp Res 31(8):1113–1120. https://doi.org/10.1007/s40520-018-1057-z
Amato AA, Santos GM, Neves Fde A (2008) Thyroid hormone action in chronic kidney disease. Curr Opin Endocrinol Diabetes Obes 15(5):459–465. https://doi.org/10.1097/MED.0b013e32830eb85e
Iitaka M, Kawasaki S, Sakurai S, Hara Y, Kuriyama R, Yamanaka K, Kitahama S, Miura S, Kawakami Y, Katayama S (1998) Serum substances that interfere with thyroid hormone assays in patients with chronic renal failure. Clin Endocrinol (Oxf) 48(6):739–746. https://doi.org/10.1046/j.1365-2265.1998.00419.x
Iglesias P, Olea T, Vega-Cabrera C, Heras M, Bajo MA, del Peso G, Arias MJ, Selgas R, Díez JJ (2013) Thyroid function tests in acute kidney injury. J Nephrol 26(1):164–172. https://doi.org/10.5301/jn.5000106
Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, Rivkees SA, Samuels M, Sosa JA, Stan MN, Walter MA (2016) American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid 26(10):1343–1421. https://doi.org/10.1089/thy.2016.0229
Pelusi C, Gasparini DI, Bianchi N, Pasquali R (2016) Endocrine dysfunction in hereditary hemochromatosis. J Endocrinol Invest 39(8):837–847. https://doi.org/10.1007/s40618-016-0451-7
Miyoshi K, Kawai H, Iwasa M, Kusaka K, Yonezawa M, Shishiba Y (1983) The presence of myoglobin in human thyroid tissue. J Clin Endocrinol Metab 56(6):1301–1305. https://doi.org/10.1210/jcem-56-6-1301
Miyoshi K, Ohshima I, Ohto Y, Matsuoka M, Kawai H (1974) Theoretical analysis of creatine kinase isozyme patterns in various human tissues and myopathic skeletal muscles. Tokushima J Exp Med 21(00):75–78
Weinstein IR, Fairchild ES, Davis PJ, Davis FB, Schoenl M, LaMantia RS (1983) Identification and properties of myocardial myoglobin as a binder of iodothyronines. Biochem Med 29(1):85–95. https://doi.org/10.1016/0006-2944(83)90057-1
Ardalan MR, Ghabili K, Mirnour R, Shoja MM (2011) Hypothyroidism-induced rhabdomyolysis and renal failure. Ren Fail 33(5):553–554. https://doi.org/10.3109/0886022X.2011.569109
Altay M, Duranay M, Ceri M (2005) Rhabdomyolysis due to hypothyroidism. Nephrol Dial Transplant 20(4):847–848. https://doi.org/10.1093/ndt/gfh745
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Consent for publication
Informed consent was obtained from the 12 patients.
Conflict of interest
The authors declare no competing interests.
Additional information
Publisher's note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Supplementary Information
Below is the link to the electronic supplementary material.
Rights and permissions
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
About this article
Cite this article
Dirim, A.B., Sezer, G.E., Uzun, E. et al. Temporary hypothyroidism in severe crush syndrome: a potential novel entity. Hormones 22, 603–609 (2023). https://doi.org/10.1007/s42000-023-00475-1
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s42000-023-00475-1