Thyroid hormones and complement parameters in hereditary angioedema with C1-inhibitor deficiency

Thyroid hormones and complement parameters in hereditary angioedema with C1-inhibitor deficiency: Thyroid hormones control and up-regulate the synthesis of many plasma proteins.

Abstract

Background

Thyroid hormones control and up-regulate the synthesis of many plasma proteins.

Objective

To explore possible associations between thyroid hormone and complement levels in patients with hereditary angioedema resulting from the deficiency of the C1-inhibitor (C1-INH-HAE).

Methods

In this case-control study, serum thyrotropin, free triiodothyronine (FT₃), and free thyroxine (FT₄) levels, anti–thyroid peroxidase and antithyroglobulin antibody titers, and C1-INH concentrations were measured in 117 euthyroid patients with C1-INH-HAE and compared with their clinical properties. The control group comprised 150 healthy, age- and sex-matched, euthyroid individuals.

Results

The thyrotropin and antithyroglobulin levels were similar between the patients and the controls. Significantly lower FT₃ (P < .001) and FT₄ (P = .002) levels, as well as higher anti–thyroid peroxidase titers (P < .001), were seen in the patients with C1-INH-HAE. The proportion of patients with reduced C1-INH activity was greater among those with below-median FT₄ levels than among those with above-median values (P = .02). Patients who experienced more edematous attacks per year had lower FT₄ levels (within the normal range) than those afflicted by fewer episodes (P = .01). The FT₃ and FT₄ levels were significantly higher in patients undergoing long-term danazol therapy than in those who did not receive this drug (P = .01 and P = .02, respectively). The proportion of patients with FT₄ levels in the below-median range was higher in the subset with increased d-dimer concentration (P = .009).

Conclusion

Minor variations of the thyroid hormone levels (within the reference range) can influence the function of C1-INH in C1-INH-HAE. Our findings suggest a role for the endocrine system in the pathophysiology of C1-INH-HAE.

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