C. J. Richards

Association between postpartum thyroid dysfunction and thyroid antibodies and depression.

OBJECTIVE--To define the relation between mood and autoimmune thyroid dysfunction during the eight months after delivery. DESIGN--Double blind comparison of the psychiatric status of women positive and negative for thyroid antibodies. Clinical examination and blood sampling for free triiodothyronine and thyroxine, thyroid stimulating hormone, and thyroid antibody concentrations at four weekly intervals. Psychiatric assessment at six, eight, 12, 20, and 28 weeks post partum. SETTING--Outpatient department of district hospital. PATIENTS--145 antibody positive women and 229 antibody negative women delivering between August 1987 and December 1989. MAIN OUTCOME MEASURES--Thyroid status. Number of cases of mental ill health by the general health questionnaire, research diagnostic criteria, Hamilton 17 item depression scale, hospital anxiety and depression scale, and Edinburgh postnatal depression scale. RESULTS--Six weeks after delivery the general health questionnaire showed 62 (43%) antibody positive women and 65 (28%) antibody negative women had mental ill health (chi 2 = 8.18, p less than 0.005). Follow up of 110 antibody positive and 132 antibody negative women showed significantly greater depression by research diagnostic criteria in antibody positive women (47%) than antibody negative women (32%) regardless of thyroid dysfunction. Antibody positive women showed higher mean scores for depression on the Hamilton (6.01 v 3.89, p = 0.0002), Edinburgh (7.45 v 5.92, p = 0.031), and hospital depression scales (4.95 v 3.79, p = 0.003). CONCLUSION--Depressive symptoms are associated with positive thyroid antibody status in the postpartum period.

Postpartum thyroid dysfunction in Mid Glamorgan

A high prevalence of postpartum thyroid dysfunction has been reported in several countries, but there have been no systematic studies of its prevalence in Britain. Among a group of 901 consecutive, unselected pregnant women thyroid autoantibodies were detected in 117 (13%) at booking. The clinical course of postpartum thyroid dysfunction, factors associated with its development, and its likely prevalence were defined in 100 of these women with thyroid antibodies and 120 women with no such antibodies who were matched for age. None of the women had a history of autoimmune thyroid disease. Normal reference ranges for thyroid function during pregnancy and post partum were established in the 120 women negative for thyroid antibodies. On the basis of these observations postpartum thyroid dysfunction was observed in 49 (22%) of the 220 women studied, and the prevalence in the total group of 901 women was estimated to be 16·7%. Thyroid dysfunction, mainly occurring in the first six months post partum, was usually transient and included both destruction induced hyperthyroidism and hypothyroidism. The development of the syndrome was significantly related to smoking more than 20 cigarettes a day and the presence of thyroid microsomal autoantibodies at booking. Of the 16 women with a family history of thyroid disease in whom thyroid microsomal autoantibody activity was detectable at booking, 11 developed thyroid dysfunction. Age, parity, presence of goitre at presentation, duration of breast feeding, and the sex and birth weight of the infant were not associated with the development of postpartum thyroid dysfunction. The mood changes experienced by women post partum may in part be associated with altered thyroid function during this time.

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.

Transient post-partum thyroid dysfunction and postnatal depression

In the course of a population study of thyroid dysfunction in pregnancy and the post-partum period, 65 women, considered to be antibody-positive (microsomal and thyroglobulin), and 82 antibody-negative women were assessed for postnatal depression at 6-8 weeks post partum. The women were also assessed for the development of post-partum thyroid dysfunction. Of the 147 women, 22 met DSM-III criteria for major depression. The presence of autoantibodies showed little association with depressed mood but there was a minor association of postnatal depression with actual thyroid dysfunction in that incidence of the latter condition was higher in depressed women (Raskin scale P less than 0.01; Edinburgh scale P less than 0.05; Montgomery-Asberg scale P less than 0.1). Three of eight mothers with thyroid dysfunction had major depression and were depressed on all three scales.

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.

Postpartum thyroid dysfunction and HLA status

Abstract. Nine‐hundred‐and‐one women presenting in an antenatal clinic at the 60th week of pregnancy were tested for antithyroid antibodies. A group of 113 antibody‐positive women and 108 antibody‐negative age‐matched controls were HLA typed and followed prospectively at 6‐weekly intervals through pregnancy and for 12 months postpartum. Forty‐five of the women developed biochemical evidence of postpartum thyroid dysfunction (PPTD) of whom 36 were antibody positive. Compared with a local control population (n = 600), and using multiplex analysis, there was a significant increase in the combinations HLA B8, DR3 and HLA Al, B8, DR3 from 22.5% to 40.0% (P<0.02) and from 18.6% to 35.6% (P<0.01) respectively in the women who developed PPTD. The well‐recognized association of these haplotypes with other organ‐specific autoimmune diseases provides further support for autoimmune events being implicated in the development of PPTD.

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.

Autoimmune thyroid disease and pregnancy.

The cholinergic drug pilocarpine may cause sweating and salivation, nausea, vomiting and diarrhoea, and bronchospasm. Finally, any mydriatic at all used by a casualty officer in an unconscious patient will produce a severe systemic adrenergic reaction-in the neurologist or neurosurgeon who receives the patient. The casualty officer should never forget that the size and reactions of the pupils are important in the management of patients in coma, with head injuries, or with many other neurological diseases.