title: The role of complement in the pathogenesis of postpartum thyroiditis: ultrasound echogenicity and the degree of complement-induced thyroid damage.
abstract: Postpartum thyroiditis (PPT) is a transient autoimmune thyroiditis occurring during the postpartum year that is characterized by circulating antithyroid antibodies, abnormal thyroid ultrasound echotexture, and episodes of hyperthyroidism, hypothyroidism, or both. In this study we examined the relationship between lymphocytic thyroiditis, as indicated by echotexture changes, and complement-activating thyroid autoantibodies. Thyroid ultrasound echotexture, thyroid function, and bioactive (complement-activating) thyroid peroxidase (TPO) antibodies have been measured in a group of 63 TPO antibody-positive women during the postpartum year. When the maximum bioactive TPO antibody activity recorded was compared with echogenicity and thyroid status, there was a correlation between hypoechogenicity, elevated antibody activity, and abnormal thyroid status (r = 0.72, p < 0.001). However, 7 cases showed severe ultrasound changes in the absence of any thyroid dysfunction (3 of these cases showed normal bioactive antibody activity), while 4 (all hyperthyroid PPT) showed thyroid dysfunction in the absence of any ultrasound changes. Within the euthyroid ultrasound normal group, bioactive TPO antibody activity remained low throughout the postpartum year. Antibody activity in the hypoechogenic euthyroid women was significantly elevated (p < 0.001) compared with the echo normal group, but was indistinguishable from the activity curve obtained in women whose PPT included a hypothyroid phase. The determination of echotexture by thyroid ultrasonography gives a useful, noninvasive measure of the degree of thyroiditis in these women. However, as a significant number of cases with severe changes in echotexture remained euthyroid, we conclude that the development of thyroid dysfunction is not an inevitable consequence of lymphocytic thyroiditis during the postpartum and suggests that other factors must also be involved in progression to overt thyroid dysfunction.
authors.affiliation: Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff, Wales.
authors.forename: A B
authors.initials: AB
authors.lastname: Parkes
authors.forename: H
authors.initials: H
authors.lastname: Adams
authors.forename: S
authors.initials: S
authors.lastname: Othman
authors.forename: R
authors.initials: R
authors.lastname: Hall
authors.forename: R
authors.initials: R
authors.lastname: John
authors.forename: J H
authors.initials: JH
authors.lastname: Lazarus
mesh_terms: D001323:Autoantibodies / Q000097:blood; D003165:Complement System Proteins; D005260:Female; D006801:Humans; D007453:Iodide Peroxidase / Q000276:immunology; D011644:Puerperal Disorders; D013961:Thyroid Gland / Q000000981:diagnostic imaging / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000000981:diagnostic imaging* / Q000276:immunology*; D014463:Ultrasonography
chemical_list: D001323:Autoantibodies; D003165:Complement System Proteins; D007453:Iodide Peroxidase