Vol 72, No 2 (2021)
Original paper
Published online: 2021-01-21

open access

Page views 1122
Article views/downloads 707
Get Citation

Connect on Social Media

Connect on Social Media

Low incidence of focal lesions in the thyroid glands of patients with hereditary haemochromatosis — a single-centre study from Poland

Katarzyna J. Banaszkiewicz1, Katarzyna Sikorska12, Damian Panas3, Łukasz Obołończyk4, Krzysztof Sworczak4
Pubmed: 33619709
Endokrynol Pol 2021;72(2):126-132.

Abstract

Introduction: Hereditary haemochromatosis (HH) is a disease characterised by the excessive absorption of iron and its deposition in various organs. Late complications of this disease include cirrhosis, hepatocellular carcinoma, and endocrine disorders. Data from the literature on thyroid disorders in patients with HH are inconsistent and ambiguous, and no research has been done to determine the relationship between excessive accumulation of iron and the thyroid morphology. Therefore, the aim of this study was to characterise thyroid function and ultrasound images in patients with clinically overt hereditary haemochromatosis.

Material and methods: We studied 40 patients who were diagnosed with hereditary haemochromatosis with one of the mutations of the HFE gene and iron deposits in liver in specimen from liver biopsies (graded G2 to G4) or in MRI. To assess thyroid function, ultrasound examinations of the thyroid gland were performed and serum TSH concentrations were measured.

Results: We showed in our study that patients with HH have been diagnosed with thyroid focal lesions statistically less frequent than in the control group. We did not reveal any statistically significant difference in TSH concentration between patients with HH and the general population. However, patients with more severe iron deposits in liver showed lower TSH concentration.

Conclusions: Our results indicate lower incidence of focal lesions in thyroid gland in a group of patients with clinically overt hereditary haemochromatosis. 

Article available in PDF format

View PDF Download PDF file

References

  1. Sikorska K, Bielawski KP, Romanowski T, et al. [Hereditary hemochromatosis: the most frequent inherited human disease]. Postepy Hig Med Dosw (Online). 2006; 60: 667–676.
  2. Distante S, Robson KJH, Graham-Campbell J, et al. The origin and spread of the HFE-C282Y haemochromatosis mutation. Hum Genet. 2004; 115(4): 269–279.
  3. Feder JN, Gnirke A, Thomas W, et al. novel MCH class I-likr gene is mutated in patients with hereditary haemochromatosis. Nat Genet. 1996; 13: 399–408.
  4. Aranda N, Viteri FE, Montserrat C, et al. Effects of C282Y, H63D, and S65C HFE gene mutations, diet, and life-style factors on iron status in a general Mediterranean population from Tarragona, Spain. Ann Hematol. 2010; 89(8): 767–773.
  5. Pietrangelo A. Iron and the liver. Liver Int. 2016; 36 Suppl 1: 116–123.
  6. Niederau C, Fischer R, Pürschel A, et al. Long-term survival in patients with hereditary hemochromatosis. Gastroenterology. 1996; 110(4): 1107–1119.
  7. Banaszkiewicz K, Sikorska K, Dorniak K, et al. Primary adrenal insufficiency and hemochromatosis - Cause and effect relationship or a coincidence? Ann Endocrinol (Paris). 2019; 80(1): 64–67.
  8. Banaszkiewicz K, Sikorska K, Sworczak K. Endocrine disorders in patients with hereditary hemochromatosis. Eur J Translat Clin Med. 2019; 1(2): 72–76.
  9. Muckenthaler MU, Rivella S, Hentze MW, et al. A Red Carpet for Iron Metabolism. Cell. 2017; 168(3): 344–361.
  10. Nemeth E, Tuttle MS, Powelson J, et al. Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization. Science. 2004; 306(5704): 2090–2093.
  11. Rasenack J. Diagnostic and therapy of chronic liver and biliary diseases. Revised ed. Falk Foundation, Freiburg 2016: 1–58.
  12. Wood JC. Guidelines for quantifying iron overload. Hematology Am Soc Hematol Educ Program. 2014; 2014(1): 210–215.
  13. Noma S, Konishi J, Morikawa M, et al. MR imaging of thyroid hemochromatosis. J Comput Assist Tomogr. 1988; 12(4): 623–625.
  14. Adams PC. Epidemiology and diagnostic testing for hemochromatosis and iron overload. Int J Lab Hematol. 2015; 37 Suppl 1: 25–30.
  15. Niederau C, Fischer R, Sonnenberg A, et al. Survival and causes of death in cirrhotic and in noncirrhotic patients with primary hemochromatosis. N Engl J Med. 1985; 313(20): 1256–1262.
  16. Edwards CQ, Kelly TM, Ellwein G, et al. Thyroid disease in hemochromatosis. Increased incidence in homozygous men. Arch Intern Med. 1983; 143(10): 1890–1893.
  17. Murphy MS, Walsh CH. Thyroid function in haemochromatosis. Ir J Med Sci. 2004; 173(1): 27–29.
  18. European Association For The Study of The Liver. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol 2015. 2010; 53(1): 3–22.
  19. Sikorska K, Stalke P, Jaskiewicz K, et al. Could iron deposits in hepatocytes serve as a prognostic marker of HFE gene mutations? Hepatogastroenterology. 2008; 55(84): 1024–1028.
  20. Główny Urząd Statystyczny. Stan zdrowia ludności Polski w 2004 roku. GUS, Warszawa 2016: 100–121.
  21. Ruchała M, Szczepanek E. Thyroid nodular disease. Fam Med Primary Care Rev. 2008; 10(4): 1383–1392.
  22. Just MJ. Prevalence of thyroid diseases in the population of the town Piekary Slaskie in the years 2006-2011 on the basis of the implementation prevention program. Pol Merkur Lekarski. 2019; 47(282): 212–216.
  23. Maldonado-Araque C, Valdés S, Lago-Sampedro A, et al. Iron deficiency is associated with Hypothyroxinemia and Hypotriiodothyroninemia in the Spanish general adult population: Di@bet.es study. Sci Rep. 2018; 8(1): 6571.
  24. Azizi F, Mirmiran P, Sheikholeslam R, et al. The relation between serum ferritin and goiter, urinary iodine and thyroid hormone concentration. Int J Vitam Nutr Res. 2002; 72(5): 296–299.
  25. St Germain DL, Galton VA. The deiodinase family of selenoproteins. Thyroid. 1997; 7(4): 655–668.
  26. Zimmermann MB. The influence of iron status on iodine utilization and thyroid function. Annu Rev Nutr. 2006; 26: 367–389.
  27. Zimmermann M, Adou P, Torresani T, et al. Persistence of goiter despite oral iodine supplementation in goitrous children with iron deficiency anemia in Côte d'Ivoire. Am J Clin Nutr. 2000; 71(1): 88–93.
  28. Hernik A, Szczepanek-Parulska E, Filipowicz D, et al. The hepcidin concentration decreases in hypothyroid patients with Hashimoto's thyroiditis following restoration of euthyroidism. Sci Rep. 2019; 9(1): 16222.
  29. Campisi A, Bonfanti R, Raciti G, et al. Gene Silencing of Transferrin-1 Receptor as a Potential Therapeutic Target for Human Follicular and Anaplastic Thyroid Cancer. Mol Ther Oncolytics. 2020; 16: 197–206.