ECE2010 Poster Presentations Thyroid (122 abstracts)
Thyroid hormones regulate the production of complement mannan-binding lectin regardless of the MBL2 genotype: a cohort study of 95 patients with autoimmune thyroid disorders.
Eliska Potlukova 1 , Jan Jiskra 1 , Tomas Freiberger 2 , Zdenka Limanova 1 , Dana Zivorova 3 , Karin Malickova 3 , Drahomira Springer 3 , Lucie Grodecka 2 , Marie Antosova 1 , Zdenek Telicka 1 , Sattu Sinikka Pesickova 4 & Marten Trendelenburg 5
1Third Department of Medicine, General University Hospital and First Faculty of Medicine, Charles University, Prague, Czech Republic; 2Molecular Genetics Laboratory, Centre for Cardiovascular Surgery and Transplantation, Brno, Czech Republic; 3Laboratory of Clinical Allergology and Immunology, Institute of Clinical Biochemistry and Laboratory Diagnostics, General Teaching Hospital and 1st Faculty of Medicine, Charles University, Prague, Czech Republic; 4Clinic of Nephrology, General Teaching Hospital and 1st Faculty of Medicine, Charles University, Prague, Czech Republic; 5Laboratory of Clinical Immunology, Department of Biomedicine, University Hospital Basel, Basel, Switzerland.
Introduction: Complement mannan-binding lectin (MBL) deficiency is associated with increased susceptibility to infections and autoimmune diseases. Previous studies suggested that the production of MBL is stimulated by thyroid hormones. The aim of our study was to investigate this association in patients with autoimmune thyroid diseases (AITD).
Methods: Serum levels of MBL and parameters of the thyroid function were determined in 62 patients with Hashimoto’s thyroiditis, 33 with Graves’ disease and 47 blood donors. Follow-up measurements were performed after 6 to 24 months. MBL2 genotypes were determined using multiplex PCR and compared to 359 healthy Czech individuals.
Results: Serum levels of MBL tightly correlated with thyroid hormones, leading to strongly increased MBL levels in hyperthyroidism and decreased levels in hypothyroidism. With normalisation of the thyroid function during follow-up, MBL levels decreased or increased respectively. The observed correlations weren’t due to MBL polymorphisms since the frequency of MBL2 polymorphisms in AITD patients was not different from the general population.
Conclusion: AITD are not associated with MBL polymorphisms. However, the MBL production is strongly dependent upon the thyroid function, regardless of the genotype.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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