A. B. Parkes

A LONG‐TERM FOLLOW‐UP OF POSTPARTUM THYROIDITIS

To investigate the long‐term outcome of postpartum thyroiditis (PPT), 43 patients with PPT and 171 control women were evaluated 3.5 (range 2‐4) years postpartum. Ten (23%) PPT patients were hypothyroid compared to none of the controls (P<0.001). Factors associated with the development of hypothyroidism were high antimicrosomal antibody titre measured at 16 weeks gestation (P < 0.01), severity of hypothyroid phase of PPT, multiparity, and a previous history of spontaneous abortion. The presence of microsomal antibody but no PPT in one pregnancy did not prevent the occurrence of PPT in the next pregnancy in two patients and a further five patients had PPT in two successive pregnancies. There was no association between HLA haplotype, family history of thyroid disease, smoking or frequency of oral contraception, and the development of long‐term hypothyroidism after PPT. It is concluded that permanent hypothyroidism is an important sequel to PPT and patients with PPT should be followed up appropriately.

Effect of low dose iodide supplementation on thyroid function in potentially susceptible subjects: are dietary iodide levels in Britain acceptable?†

objective The aim of the study was to evaluate the risk of exposure to an Increase in dietary Iodide Intake amongst potentially susceptible population groups in Britain.

The Sonographic Appearances in Postpartum Thyroiditis

During the postpartum period about 50% of women with circulating thyroid autoantibodies develop a transient autoimmune thyroiditis. To determine the sonographic appearances in postpartum thyroiditis (PPT), serial ultrasound (US) scans of the thyroid were performed in 135 postpartum women who were divided into three clinical groups: Group 1, 37 antibody positive subjects who developed PPT; Group 2, 28 antibody positive subjects in whom thyroid function remained normal; Group 3, 70 antibody negative controls. Thyroid hypoechogenicity was observed in 14/31 patients (45%) who were scanned between 4 and 8 weeks postpartum and who subsequently developed PPT (Group 1) compared with 4/24 patients (17%) in Group 2 (P less than 0.05) and 1/65 patients (1.5%) in Group 3 (P less than 0.001). In antibody positive patients, the positive predictive value of an abnormal scan during this period was 78%. Between 15 and 25 weeks postpartum thyroid hypoechogenicity was present in 32/37 patients (86%) in Group 1 compared with 11/28 patients (39%) in Group 2 (P less than 0.001) and 2/70 patients (3%) in Group 3 (P less than 0.001). Sonographic abnormality persisted beyond 32 weeks postpartum in 36/41 antibody positive patients (87%) who had exhibited thyroid hypoechogenicity earlier during the study and who had late scans. The characteristic US appearance in PPT is thyroid hypoechogenicity. The role of sonography in the prediction, diagnosis and follow up of patients with PPT is discussed.

Serum thyreoglobulin: an early indicator of autoimmune post‐partum thyroiditis

OBJECTIVE The aim of this study was to assess whether autoimmune thyroid damage in post‐partum thyroiditis was accompanied by a significant rise in the concentration of thyroglobulin in the serum and whether its measurement could be useful In the prediction of the risk and severity of an episode of post‐partm thyroid dysfunction.

Is there an association between life events, postnatal depression and thyroid dysfunction in thyroid antibody positive women?

Background: Postnatal depression is more common in women positive for thyroid autoantibodies, independent of thyroid hormone dysfunction, but the basis of this association is unclear. Aims: The objective of the work reported here has been to investigate from data obtained from previously published research, a possible association between life events, postnatal depression and the development of thyroid dysfunction in women who are positive for thyroid autoantibodies. Method: A cohort of pregnant women whose thyroid antibody status was positive (N = 115), was identified at antenatal booking (approximately 16 weeks). These, and a group of women negative for thyroid antibodies (N = 123), were assessed for depression at six to eight weeks postpartum and then at 12, 20 and 28 weeks postpartum according to Research Diagnostic Criteria (RDC). The number and type of life events over the preceding year were also assessed at eight weeks postpartum using Paykels Life Event Schedule. At four weekly intervals postpartum until six months, thyroid antibody levels and thyroid function (plasma T3 T4 and TSH) were measured. Results: As anticipated, the thyroid antibody status remained the same throughout the study, and there was no difference in the number or type of life events reported in the preceding year, between antibody positive and antibody negative women. Postnatal depression was associated with an excess of both total and negative life events, independent of thyroid antibody status or actual thyroid hormonal status. Women who developed thyroid dysfunction did not report an excess of life events (total, negative or neutral) in the preceding year. Conclusion: There was an excess of reported total and negative life events in women with postnatal depression, but this was independent of thyroid antibody status or function.

High leptin levels in women developing postpartum thyroiditis

background  There is experimental evidence that leptin is required for the development of T helper 1 (Th1)‐mediated autoimmune diseases. However, to our knowledge, there are no studies demonstrating such a role in human autoimmune thyroid disease.

Thyroglobulin epitope recognition in a post iodine-supplemented Sri Lankan population.

objective We previously reported a high prevalence of raised thyroglobulin autoantibodies (TgAb) in apparently healthy Sri Lankan schoolgirls following salt iodination. To characterize these antibodies further we determined the epitopes on thyroglobulin (Tg) with which they react and compared these with serum obtained from both healthy subjects and established autoimmune thyroid disease (AITD) patients from the UK. To extend our study to a wider population within Sri Lanka, we in addition determined the epitopes recognized by a group of AITD patients selected from a thyroid clinic in Sri Lanka, as well as apparently healthy female Sri Lankan tea workers of distinct ethnicity from the schoolgirls and AITD patients.

Post-Partum Thyroid Dysfunction

Normal pregnancy is associated with two major series of alterations in the endocrine system. On the one hand hormonal changes necessary for the maintenance of pregnancy must occur and on the other pregnancy itself may influence the function of endocrine glands, such as the thyroid, which are not themselves directly involved in the maintenance of the pregnancy. In pregnancy therefore, and as a result of these normal physiological regulatory mechanisms, thyroid function must be interpreted with caution (Table 1). The situation is further complicated in those women with known (or previously unrecognised) thyroid disease, particularly if the aetiological basis of their disease is autoimmune (Table 1). In these women pregnancy may have a profound impact on their disease with amelioration during the pregnancy itself but with exacerbation in the post-partum period. In addition and as a result of their thyroid disease, alterations in the function of the foetal and neonatal thyroid may occur. Considerable interest has been focussed recently on alterations in thyroid function in pregnancy and the post-partum period in both normal women and women with known autoimmune thyroid disease and has been extensively reviewed (1-3). In the present study we have sought to examine prospectively the thyroid function of a group of normal women with no known history of thyroid disease, through pregnancy and the post-partum period. Our aim was to define the true prevalence of post-partum thyroid dysfunction (PPTD) in such women, to characterise the syndromes of PPTD developing and to determine the factors associated with their development.

Thyroid stimulation by (FAB)2 and FAB fragments of TSH receptor antibody

The TSH receptor binding and thyroid stimulating properties of (Fab)2 and Fab fragments of Graves’ IgG have been investigated. (Fab)2 fragments were prepared by pepsin digestion of IgG and Fab fragments by reduction of (Fab)2 or papain digestion of IgG. (Fab)2 and Fab were effective in inhibiting TSH binding to its receptor with all five patients’ sera studied and both preparations stimulated cyclic AMP release from isolated thyroid cells. However Fab fragments were less active thyroid stimulators than their parent (Fab)2 in all five cases. These studies indicate that antibody divalency is not essential for thyroid stimulation by TSH receptor antibodies.

Antenatal depression and thyroid antibodies

Depressive illness has a high prevalence in the puerperium (Paykel et ai 1980). Antenatal psychiatric disorders have received less attention; however, there are now several studies that suggest that rates of antenatal depression are comparable to those of postnatal depression (see review: Green and Murray 1994). Little is known about the etiology of antenatal depression. Studies have shown that women positive for thyroid antibodies, independent of thyroid hormone status, are prone to episodes of postnatal depression (Hams et al 1989, 1992; Pop et al 1991). No study to date has investigated whether the presence of gestational thyroid antibodies are associated with antenatal mood disturbance. The aim of this study was to assess prevalence of antenatal depressive symptoms and the relationship, if any, to thyroid antibody status.