Therapeutic controversy: Screening for postpartum thyroiditis.

Abstract

Postpartum autoimmune thyroid dysfunction is briefly characterized as a postpartum exacerbation of subclinical autoimmune thyroid disease, wherein some immunological abnormalities are observed before the onset of thyroid dysfunction. Therefore, we can detect the high-risk group for postpartum thyroid dysfunction by screening, in early pregnancy, those with subclinical autoimmune thyroiditis. Among several methods for detecting thyroid autoimmunities, the measurement of anti-thyroid microsomal antibody (MCAb) or thyroid peroxidase (TPO) antibody is the most useful marker for detecting subclinical autoimmune thyroiditis and, therefore, for predicting the occurrence of postpartum thyroid dysfunction. When MCAb is positive, there is always lymphocytic infiltration into the thyroid, indicating subclinical autoimmune thyroiditis (15) that may be exacerbated after delivery. Sixty to seventy percent of women with positive MCAb in early pregnancy develop postpartum thyroid dysfunction (1). Other investigators have also reported that MCAb-positive subjects had approximately 20 –23 times the relative risk (over normal subjects) for developing postpartum thyroid dysfunction (16, 17). On the other hand, the prevalence of postpartum thyroid dysfunction in the MCAb-negative subjects in early pregnancy is estimated as 1/100 of that in MCAb-positive subjects (Fig. 1). So, when we screen 1000 early pregnant women in the general population, we can expect to find about 50 patients with postpartum thyroid dysfunction. Although MCAb is a good marker for the occurrence of postpartum thyroid dysfunction, it gives no information about the type of dysfunction that will occur. Among the various types of dysfunctions, postpartum Graves’ disease is clinically the most important and is predicted by the measurement of thyroid-stimulating antibodies (TSAb) with a sensitive bioassay (18). Our subsequent study (19) revealed that pregnant women with positive TSAb in early pregnancy had a much higher risk of developing postpartum Graves’ disease. We observed 71 pregnant women with positive MCAb from early pregnancy through the postpartum period. Among them, 7 showed positive TSAb, and 5 of those 7 (71%) developed postpartum Graves’ disease. Thyrotoxicosis in 3 of those 5 was transient and spontaneously improved within a year. Graves’ disease did not occur in the TSAb-negative subjects. AntiTSH receptor (TSHR) antibodies (TRAb) with conventional radio-receptor assay (thyrotropin binding inhibitory immunoglobulin; TBII) were not useful in predicting postpartum Graves’ disease. Figure 2 shows a protocol that we have tentatively employed to screen for postpartum thyroid dysfunction at the outpatient maternity clinic of the Osaka University Hospital for several years. In the protocol, MCAb-positive mothers are examined for thyroid status, measuring serum free thyroxine (FT4), serum free triiodothyronine (FT3), serum thyrotropin (TSH), anti-TSHR antibody (TRAb), and antithyroglobulin (TgAb), and are observed every Accepted March 8, 1999. Address correspondence and requests for reprints to: Alex StagnaroGreen, MD, Dean for Student Affairs and Medical Education, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1255, New York, New York 10029-6574. E-mail: stagnaro@smtplink.mssm.edu. Reprints of the Therapeutic Controversies will include all authors and all pages, as shown in the journal. 0021-972X/99/$03.00/0 Vol. 84, No. 6 The Journal of Clinical Endocrinology & Metabolism Printed in U.S.A. Copyright © 1999 by The Endocrine Society