Thyroid hormone increases mannan-binding lectin levels

被引:25
作者
Riis, ALD [1 ]
Hansen, TK
Thiel, S
Gravholt, CH
Gjedde, S
Gormsen, LC
Jorgensen, JOL
Weeke, J
Moller, N
机构
[1] Aarhus Univ Hosp, Med Dept M, Immunoendocrine Res Unit, DK-8000 Aarhus, Denmark
[2] Aarhus Univ Hosp, Dept Med C, DK-8000 Aarhus, Denmark
[3] Aarhus Univ, Inst Clin Med, DK-8000 Aarhus, Denmark
[4] Aarhus Univ, Dept Med Microbiol & Immunol, DK-8000 Aarhus, Denmark
关键词
D O I
10.1530/eje.1.02013
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Recent studies have indicated the existence of causal links between the endocrine and immune systems and cardiovascular disease. Mannan-binding lectin (MBL), a protein of the innate immune system, may constitute a connection between these fields. Methods: To test whether thyroid hormone regulates MBL levels, we studied eight patients with Graves' hyperthyroidism before and after methimazole therapy, eight healthy subjects before and after short-term experimental hyperthyroidism, and eight hypothyroid patients with chronic autoimmune thyroiditis before and after L-thyroxine substitution. Results: In all hyperthyroid patients, MBL levels were increased - median (range), 1886 ng/ml (1478-7344) - before treatment and decreased to 954 ng/ml (312-3222) after treatment (P = 0.01, paired comparison: Wilcoxon's signed ranks test). The healthy subjects had MBL levels of 1081 ng/ml (312-1578). Administration of thyroid hormones to these persons induced mild hyperthyroidism and increased MBL levels significantly to 1714 ng/ml (356-2488) (P = 0.01). Two of the eight hypothyroid patients had undefectably low levels of MBL both before and after L-thyroxine substitution. The other six hypothyroid patients had decreased levels of MBL of 145 ng/ml (20-457) compared with 979 ng/ml (214-1533) after L-thyroxine substitution (P = 0.03. paired comparison: Wilcoxon's signed ranks test). Conclusion: Our data show that thyroid hormone increases levels of MBL. MBL is part of the inflammatory complement system, and this modulation of complement activation may play a role in the pathogenesis of a number of key components of thyroid diseases.
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收藏
页码:643 / 649
页数:7
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