The production of mannan-binding lectin is dependent upon thyroid hormones regardless of the genotype: a cohort study of 95 patients with autoimmune thyroid disorders
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
20356797
DOI
10.1016/j.clim.2010.02.015
PII: S1521-6616(10)00074-4
Knihovny.cz E-resources
- MeSH
- C-Reactive Protein metabolism MeSH
- Adult MeSH
- Genotype MeSH
- Graves Disease blood MeSH
- Hashimoto Disease blood MeSH
- Thyroid Hormones blood MeSH
- Mannose-Binding Lectin blood genetics MeSH
- Middle Aged MeSH
- Humans MeSH
- Young Adult MeSH
- Polymorphism, Genetic genetics MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Thyrotropin blood MeSH
- Thyroxine blood MeSH
- Triiodothyronine blood MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Young Adult MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic MeSH
- Names of Substances
- C-Reactive Protein MeSH
- Thyroid Hormones MeSH
- Mannose-Binding Lectin MeSH
- MBL2 protein, human MeSH Browser
- Thyrotropin MeSH
- Thyroxine MeSH
- Triiodothyronine MeSH
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). 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. Serum levels of MBL tightly correlated with thyroid hormones, leading to strongly increased MBL levels in hyperthyroidism and decreased levels in hypothyroidism. With normalization of the thyroid function during follow-up, MBL levels decreased or increased respectively. The observed correlations were not due to MBL polymorphisms since the frequency of MBL2 polymorphisms in AITD patients was not different from the general population. We conclude that AITD are not associated with MBL polymorphisms. However, the MBL production is strongly dependent on thyroid function, regardless of the genotype.
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