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Thyroid and Endocrine Divisions, Department of Medicine (E.M., S.J.M.); and Reproductive Medicine Division, Department of Obstetrics, Gynecology, and Reproductive Biology (J.A.H.), Brigham and Women’s Hospital, Boston, Massachusetts 02115
Address all correspondence and requests for reprints to: Susan J. Mandel, Thyroid Division, Department of Medicine, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.
Abstract
We present a case series evaluating the development and characteristics
of thyroiditis following pregnancy loss. Five women were followed
prospectively with measurement of thyroid function and antithyroid
antibodies after pregnancy loss. Serum TSH concentrations were measured
by immunoradiometric assay and antithyroid antibodies by RIA and
hemagglutination techniques. All women had normal serum TSH
concentrations before conception or at the time of pregnancy loss, and
all but one had positive antithyroid antibodies. Pregnancy loss
occurred between 5–20 weeks gestation because of ectopic pregnancy or
either spontaneous or elective abortion. Two women had subclinical
hypothyroidism with peak serum TSH values of 8.7 mU/L and 5.4 mU/L at 2
and 7 months after pregnancy loss, respectively. Three women had
clinical hyperthyroidism with serum TSH values 
0.2 mU/L diagnosed
between 3–11 months after pregnancy loss followed subsequently by a
hypothyroid phase. Painless thyroiditis within 1 yr of pregnancy loss
in these women suggests that the immunological changes of a short-term
gestation may be sufficient to lead to thyroiditis.
ALTHOUGH POSTPARTUM autoimmune thyroiditis is well described after a full-term pregnancy, occurring in 3–16% of women (1), it has not been clearly associated with early termination of pregnancy by either spontaneous or elective abortion. Previously, there have only been two reports of thyroiditis occurring after pregnancy loss without prospective clinical evaluation (2, 3). In this article we report on five women with normal thyroid function before conception or at the time of pregnancy loss who developed thyroiditis within 1 yr of their loss.
Subjects and Methods
Patients
Peripheral blood was obtained for thyroid function studies during an evaluation for recurrent miscarriage or symptoms of hyperthyroidism at the Brigham and Women’s Hospital (Boston, MA) from five women with a history of recent pregnancy loss. When thyroid function test abnormalities were identified, any history of thyroid disease and prior thyroid function tests were obtained. The women were then followed prospectively for at least 20 months with measurement of thyroid function and antithyroid antibodies. The case series was approved by the Human Research Committee at the Brigham and Women’s Hospital, and informed consent was obtained from all women.
Assays
Serum TSH concentrations were measured using an immunoradiometric assay (Nichols Institute, San Juan Capistrano, CA) with normal ranges of 0.5–5.0 mU/L. (Some samples were analyzed with different assays with similar normal ranges). The T4 levels of patient 4 was measured using a flourescein polarization immunoassay (Abbott Laboratories, Chicago, IL) with normal range of 60–150 nmol/L. The free T4 assay was done by RIA (normal range 10–20 pmol/L). Serum thyroid peroxidase (TPO) antibodies were measured by either RIA kits (patients 1, 2, 3, and 5) or by the hemagglutination technique (patient 4).
Results
Patients
The characteristics of the patients are shown in Table 1
. The mean age of the five women at pregnancy loss was
32 yr (range 31–35 yr). All had normal serum TSH concentrations before
conception or at the time of pregnancy loss, and none had taken or were
currently taking thyroid hormone. There was no history of neck
tenderness or preceding upper respiratory tract illness before the
abnormal thyroid function tests were obtained, and none had palpable
thyroid nodules. All women, except patient 4, had positive tests for
TPO antibodies. At the time of pregnancy loss, the women were between
5–20 weeks of gestation (mean 10 weeks). Gestational age was
calculated from the start of each patient’s last menstrual period.
Pregnancy resulted in a spontaneous abortion in patients 1, 3, and 5,
and an ectopic pregnancy in patient 2. Patient 4 had an elective
abortion. Thyroiditis, defined as transient biochemical hypothyroidism
and/or hyperthyroidism within 1 yr of pregnancy loss, was diagnosed
between 2–11 months (mean 7 months) later in these five women.
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Two profiles of thyroiditis were seen.
Profile 1 (Fig. 1).
Two patients (patients 1
and 2) had subclinical hypothyroidism alone, with peak serum TSH values
of 8.7 mU/L and 5.4 mU/L at 2 and 7 months after a miscarriage and an
ectopic pregnancy, respectively. The hypothyroidism resolved within 1
month in both women. Patient 1 subsequently became pregnant 4 months
after her spontaneous abortion, and her thyroid function remained
normal throughout that pregnancy, which ended in a full-term
delivery. She remained euthyroid postpartum (TSH 2.4 mU/L and 3.2
mU/L at 1 and 9 months postpartum, respectively).
|
).
Hyperthyroidism was
diagnosed between 3–11 months after pregnancy loss (serum TSH
0.2 mU/L) in patients 3, 4, and 5 when they presented with palpitations
and tremulousness. Because of the proximity of the hyperthyroidism to
the pregnancy loss and thus the possibility of thyroiditis, they did
not receive antithyroid medication, and thyroid hormone levels were
followed. Within 8 weeks of the diagnosis of hyperthyroidism, all had
become hypothyroid, and all conceived again during their hypothyroid
phase. Patients 3 and 4 were treated with T4 (0.1 mg and
0.075 mg daily, respectively), and their dose requirement did not
change during their pregnancies. Both patients discontinued
T4 after delivery and remained euthyroid (patient 3, TSH
4.0 mU/L at 10 months postpartum; patient 4, TSH 1.3 at 5 months
postpartum). Patient 5 had a spontaneous abortion 1 week after
hypothyroidism was diagnosed. She was not treated, and her serum TSH
returned to normal during the next 2 months. She subsequently became
pregnant again and thyroid function remained normal throughout a
full-term gestation. Postpartum, she developed thyroiditis with both
hyper- and hypothyroid phases, with eventual return of normal thyroid
function.
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The occurrence of thyroiditis in these five women illustrates that the immunological changes of a short-term pregnancy may be sufficient to lead to painless thyroiditis after pregnancy loss. Only three patients with thyroid dysfunction after abortion have been previously reported. In an early report of postpartum thyroiditis, Amino and colleagues (2) described two cases of transient hypothyroidism occurring at 2 weeks and 2 months after elective abortions, but no clinical follow-up was provided. A recent retrospective case report described transient hypothyroidism 8 months after a 47-day gestation spontaneous abortion (3). A recent prospective study reported no episodes of thyroiditis in 24 women followed 9 months after elective and spontaneous abortions (4). However, only four of these women were antithyroid antibody positive. Women who are antithyroid antibody positive have a greater risk of developing postpartum thyroiditis. Therefore, the incidence of thyroiditis after pregnancy loss in antibody-positive women would be higher than this study would suggest; our experience supports this.
Because the incidence of miscarriage in thyroid antibody-positive women is twice that of antibody negative women (5, 6), painless thyroiditis may not be uncommon in patients with spontaneous abortions. Because many of these women may be attempting to conceive again, evaluation of thyroid function is warranted to optimize maternal thyroid status in early pregnancy before the development of fetal thyroid function (7).
Footnotes
1 This study was supported in part by NIH Grants DK02221, HL07609,
HD23547, HD00815, and GCRC M01 RR02635. 
Received March 5, 1997.
Accepted May 6, 1997.
References
This article has been cited by other articles:
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M. Abalovich, N. Amino, L. A. Barbour, R. H. Cobin, L. J. De Groot, D. Glinoer, S. J. Mandel, and A. Stagnaro-Green Management of Thyroid Dysfunction during Pregnancy and Postpartum: An Endocrine Society Clinical Practice Guideline J. Clin. Endocrinol. Metab., August 1, 2007; 92(8_suppl): s1 - s47. [Abstract] [Full Text] [PDF]
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A. Stagnaro-Green Postpartum Thyroiditis J. Clin. Endocrinol. Metab., September 1, 2002; 87(9): 4042 - 4047. [Full Text] [PDF]
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 A. F. Muller, H. A. Drexhage, and A. Berghout Postpartum Thyroiditis and Autoimmune Thyroiditis in Women of Childbearing Age: Recent Insights and Consequences for Antenatal and Postnatal Care Endocr. Rev., October 1, 2001; 22(5): 605 - 630. [Abstract] [Full Text] [PDF]
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