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Andreas Vesalius described the human thyroid lobes very distinctly in his De humani corporis fabrica in 1543 calling them glandulae laryngis. Before him Leonardo da Vinci had depicted the human thyroid gland in his anatomical drawings. The first publication which could be called a textbook of human anatomy, because it was used as the basis for cathedral teaching in human anatomy for about two centuries, was the Anothomia of Mundinus Liucius, Mondino de'Liuzzi, published in 1316. In the chapter on the blood vessels of the neck he describes two glands, which he calls amigdalae, situated under the longitudinal muscles and below the larynx. Their function should be 1) to wet the trachea; 2) to fill the grove below the larynx because the neck was broader above due to the large larynx but much slender below because of the narrower trachea. And 3): they should function as a shield for the deep arteries and veins. Later anatomists at the beginning of the 15th and the 16th century, like Achillini, Massa and Zerbus, all used the text of Mundinus but obviously they tried to locate the glands of Mundinus to the tonsils apparently only because he used the denomination amigdalae. Berengario da Carpi, however, who was a much experienced anatomist, published a large treatise Commentaria super Anothomia Mundini in which he confirms the location of the glands of Mundini below the larynx. Obviously the two glands in the neck Mundinus mentions are the two thyroid lobes. According to his description they cannot be the tonsils because 1) of their location below the larynx, and 2) their function of adequating the appearance of the neck and 3) shielding, at least to some extent, the deep vessels in the neck. Before Mundini there is no similar description of the anatomy of the human neck in the literature, so what he describes must he based upon his own experience. Furthermore, he did the autopsies himself and did not use the assistance of a prosector as the professors after him used to do.

Visual evoked potentials (VEP) were tested in patients with ophthalmopathy (OP) of Graves' disease (GD) before treatment and half-a-year and 5-7 yr after orbital decompression (7 patients) or retrobulbar irradiation (3 patients). Five patients not requiring treatment for OP and 16 healthy subjects served as controls. Treatment of OP was given on clinical grounds including decreased visual acuity (VA) indicating optic neuropathy. Before treatment VA was decreased in 5 out of 19 eyes whereas VEP were abnormal in all. The mean latency at N60 both in the operated (83.1 +/- 21.6 ms) and in the irradiated groups (80.9 +/- 7.0 ms) was significantly different from that in the untreated group (62.6 +/- 8.2 ms; p < 0.001) and the healthy subjects (58.9 +/- 6.3; p < 0.001). At P120 only the latency of the operated group differed significantly from that of the other groups (p < 0.001). There was a relationship between the eye muscle changes seen on CT scans and the ophthalmopathy score (according to the classification of the American Thyroid Association) and the latency both at N60 and P120. A change from a V-shape to a W-shape of the waves occurred more often in the treated patients before therapy than in the other groups. Two patients had multiphase VEP in both eyes which improved after treatment. After adequate clinical response the visual acuity improved in one of the 5 patients with initially depressed VA. VEP, initially abnormal in all, improved in 7 of the 19 eyes (37%) but further deterioration was observed in 8 (42%).(ABSTRACT TRUNCATED AT 250 WORDS)

Endemic goitre occurs when the prevalence of thyroid enlargement in the population of an area exceeds 10%. With few exceptions its cause is iodine deficiency superimposed on other goitrogenic factors normally present and responsible for sporadic goitre. Iodine deficiency causes significant health problems and so, the term iodine deficiency disorders (IDD) has been introduced. The earliest sign of IDD is goitre, but these disorders also include cretinism, neonatal hypothyroidism and congenital defects, as well as retardation of mental and physical development etc. IDD are a worldwide problem: WHO estimates that substantially more than 800 million people are at risk and more than 190 millions suffer from IDD; over 3 million people have cretinism and in the largest and worst affected areas many millions suffer from mental and physical developmental defects. IDD can be totally eliminated by prophylaxis using iodine administered in salt, oil or some other vehicle. Problems over preventing iodine deficiency relate to difficulties in the handling and distribution of the iodized vehicle in some parts of the world and on the political will to introduce preventive schemes. In only a very few areas does the presence of goitrogenic agents in the environment cause endemic goitre despite adequate iodine supply. In a limited number of places excessive iodine from seaweed used as staple food results in endemic goitre.

VEP are an objective and a more sensitive sign of optical neuropathy in Graves' ophthalmopathy than is visual acuity. A correlation exists between VEP and the changes in the external eye muscles as visualized on CT scans. VEP should always be registered if CT changes are present. Improvement of optic neuropathy as evaluated from VEP seems to be remarkably infrequent.

The common occurrence of increased serum PBI concentration in patients with lysinuric protein intolerance (LPI) was elucidated by further studies. The reason was found to be an increase in the concentration of thyroid binding globulin (TBG), concomitantly with an increase in the binding capacity of TBG. The concentrations of serum thyroxine and triiodothyronine were elevated, whereas the free thyroxine index remained normal. The free triiodothyronine index was slightly increased. The binding capacity of thyroid hormone binding pre-albumin (TBPA) was significantly decreased. The concentrations of reverse triiodothyronine (3,3',5'-T3) and of 3,3'-diiodothyronine were normal. In all patients serum lactic acid dehydrogenase activities and ferritin concentrations were elevated. The reason for the almost constant increase in TBG remains obscure. It may be related to the primary disorder of LPI, a defect in diaminoacid transport.

Computed tomography of the pituitary fossa was performed in 12 patients with primary hypothyroidism before and after thyroxine treatment. In three, herniation of the diaphragma sellae precluded accurate measurement of the density of the hypophysis. Eight of the remaining patients showed abnormally increased density of the pituitary gland after intravenous injection of contrast substance which was significantly correlated with the serum TSH-level (r = 0.913, P less than 0.001). After thyroxine treatment the intrasellar density decreased substantially in all but one. We suggest that the observed contrast enhancement reflects increased pituitary circulation associated with the augmented function of TSH-producing cells in response to thyroid hormone deficiency.

Blood cortisol, ACTH, thyroxine, triiodothyronine, reverse triiodothyronine, thyroid stimulating hormone (TSH) and vasopressin concentrations were determined in 9 runners (29-56 years old) and one 80 year old man taking part in a non-competitive Marathon in Athens, Greece on October 1976. After the run the mean concentrations of cortisol, ACTH and vasopressin showed a significant rise. The thyroid function variables and TSH did not differ from the control values. There was a significant correlation between the cortisol and ACTH levels after the race and also between their increments from the corresponding base values. A significant correlation was found between the physical fitness (as measured by indirect determination of VO2max) and the post-race cortisol levels. One of the well trained runners with a fairly good running time had the highest post-race values for 6 of 7 hormones studied.

The occurrence of thyrotropin binding inhibiting immunoglobulins (TBII) was studied in 144 patients with different types and stages of Graves' disease (GD) including 2 patients with primary hypothyroidism which changed into hyperthyroid GD. TBII were also studied in 17 patients with toxic nodular goitre (TNG) and 29 patients with autoimmune thyroiditis. TBII was determined with a radioligand receptor assay and expressed as a TBII index which was defined as percentage binding of 125-I-labelled bovine TSH to a thyroid membrane fraction in the presence of test immunoglobulins in comparison with the maximal binding. TBII were positive in 69% of patients with untreated hyperthyroid GD, in 65% after 3-6 months of antithyroid treatment, and in 30-40% 3-114 months after discontinuation of therapy. During treatment the TBII index increased slowly towards normal levels differing significantly from the value before therapy not earlier than after at least 12 months' treatment. Both patients with primary hypothyroidism who developed hyperthyroid GD were strongly TBII positive. In patients with TNG TBII were positive in 24%. In about 30% of the patients with Hashimoto's thyroiditis and with spontaneous hypothyroidism positive TBII were registered. Also in 2 out of 9 patients (22%) with symptomless autoimmune thyroiditis TBII were positive. TBII are not specific for hyperthyroid GD but nevertheless useful humoral markers in several types of thyroid disorder.

The EGF and TSH receptor properties in malignant thyroid tumours and adjacent normal thyroid tissues were characterized using radioreceptor assays. Ten patients with papillary, 4 with medullary, 1 with Hürthle cell type follicular carcinoma, and 2 with anaplastic thyroid carcinoma were studied. In 10 out of 12 patients with papillary and anaplastic thyroid carcinomas, more EGF receptors were found in the neoplastic tissue than in the adjacent normal tissue (P less than 0.01). The affinity of the EGF receptors varied between patients (from 0.5 X 10(9) l/mol to 1.9 X 10(9) l/mol), but was in each patient the same in the neoplastic and in the normal tissue. In medullary carcinomas and a follicular Hürthle thyroid carcinoma, the EGF receptor content was very low. The receptor number was unaltered or decreased in papillary carcinomas when compared with adjacent normal tissue. In anaplastic medullary and follicular (Hürthle cell) carcinomas, the neoplastic tissue had very few high affinity TSH receptor sites. The alterations in TSH receptor characteristics when thyroid neoplastic tissue was compared with adjacent normal tissue did not correlate to changes in EGF receptor characteristics. Our results demonstrate that the amount of EGF receptors in papillary and anaplastic thyroid carcinomas differ significantly from that in follicular and medullary carcinomas and that alterations in EGF receptor content in malignant thyroid tissues are independent of TSH receptor content.

Out of 54 patients with hyperthyroid Graves' disease 35 remained euthyroid after treatment with antithyroid agents and have been continuously followed from 1 to 9 yr (4.85 +/- 2.55 yr, mean +/- SD). In 4 patients an exaggerated TSH response to TRH developed from 30 to 111 months after interrupting the treatment and one of them became hypothyroid 50 months (5.0 yr) thereafter. The annual incidence of subclinical hypothyroidism (exaggerated response to TRH) as calculated from the total number of observation yr was 2.5% and that of overt hypothyroidism was 0.6%. These figures are similar to those reported recently in 2 retrospective studies.

Endemic goitre of moderate severity was mainly found in the east of Finland in the 1930's. Studies in the 1950's showed an average daily iodine intake of 65-70 micrograms in the west and 50-65 micrograms in the east of the country. The use of iodized salt was introduced in the late 1940's but added only 15 micrograms of iodine to the daily intake. In the late 1950's iodine prophylaxis was intensified and the use of salt containing 25 mg KI/kg was recommended. In 1978 about 95% of all household salt used in the Savonlinna area was iodized. This region in the east of Finland has been used as an area of surveillance and studies have been carried out there in 1959, 1969 and 1979. During this period the thyroidal uptake decreased from 67 to 23% in non-goitrous subjects and from 62 to 28% in goitre patients the difference between the two last figures being statistically significant. The goitre patients also had significantly higher serum thyroxine and triiodothyronine levels. During the same period the urinary excretion of stable 127I increased from 45 micrograms to about 250 micrograms a day. Concomitantly the goitre prevalence among school children has decreased. Having been in the early 1950's in most parts 15-30% it is generally now 1-4%. It seems that the iodine intake is now adequate and that the endemia is gradually subsiding.

A follow-up study was performed on subjects with symptomless autoimmune thyroiditis in order to obtain information on the natural course of the disease. Seven out of the twenty-two subjects with symptomless autoimmune thyroiditis became hypothyroid within 4-48 months of observation, whereas fifteen subjects were still euthyroid after an observation period of 26-102 months. The yearly incidence of hypothyroidism in symptomless autoimmune thyroiditis was 7.3%. The basal serum thyrotrophin (TSH) level as well as the response in serum TSH to thyrotropin releasing hormone (TRH) was initially elevated in all subjects who developed hypothyroidism. The annual incidence of hypothyroidism was 26% in the subjects with an initially elevated TSH level. Serum TSH was initially normal in all but one of the eleven subjects with symptomless autoimmune thyroiditis in whom it was measured, and who remained euthyroid. In this group the TRH response was initially slightly exaggerated in three out of ten subjects. It was not performed in five subjects. During the follow-up, serum TSH and its response to TRH also became normal in these cases. An elevated basal serum TSH value is thus highly indicative of subsequent hypothyroidism, and these subjects with symptomless autoimmune thyroiditis should be carefully followed-up.

Serum thyroglobulin (Tg) was measured in 52 patients 3 months to 15 years (mean 5.3 years) after thyroidectomy with or without subsequent radioablation for differentiated thyroid carcinoma, before and after the interruption of suppressive thyroxine (T4) replacement therapy for 5 weeks. Whole body scintigraphy was carried out at the end of the T4 withdrawal period. Serum Tg was undetectable (less than 3 micrograms/l) in 38 patients on T4 therapy, in 18 the scintigraphy showed a minimal accumulation in the neck region and in 20 no uptake anywhere after withdrawal of T4. In the former group Tg rose in 10 patients to 4-21 micrograms/l when off T4 which seemed to correspond to the normal tissue left in situ, in the latter group Tg rose only in 2 patients to 5 and 21 micrograms/l, respectively. Two patients out of 14 with detectable Tg on T4 had pulmonary metastases as uncovered by whole body scintigraphy (in one of them Tg rose from 12 micrograms/l on T4 to 1200 micrograms/l off T4) and 6 patients were suspected for having recidual cancer tissue (2 patients had a negative scintigraphy) because the Tg rose (66-215 micrograms/l) over the upper limit of the reference range (less than 50 micrograms/l) after T4 withdrawal. In conclusion, in the follow-up of patients with differentiated thyroid carcinoma no routine scans are needed as long as serum Tg remains undetectable but further examinations are shortly warranted when detectable Tg is obtained during T4 suppression.

The effect of chlorpromazine (CPZ), thioridazine (TR), L-dopa, fusaric acid (FA), pimozide (PZ) and propranolol (P) in the i.v. thyrotropin-releasing hormone (TRH) stimulation test was studied in 75 subjects. It was found that chronic treatment with CPZ, TR and L-dopa inhibits the response to TRH. FA may to some extent counteract the effect of L-dopa. The results indicate that the response of the pituitary to TRH as regards the secretion of TSH is mainly regulated by norepinephrinergic alpha-receptors.

During 30 yr of iodine prophylaxis endemic goiter in school children had disappeared in the Savonlinna area which has been the location of continuous surveillance in the East of Finland. In adults goiter is still found to some extent especially in older people. The iodine intake has increased from about 50 to 300 micrograms per day during these yr and the thyroidal uptake of radioactive iodine has decreased from over 60% to between 20 and 30%. However, there is a significant difference in this regard between nongoitrous individuals and goiter patients. In the present study comprising only goiter patients it was found that the thyroidal uptake was significantly higher in the group of patients with a subnormal response to TRH. These patients also had larger goiters and more palpable thyroid nodules than those with a normal response to TRH. The mean age was significantly higher (60.3 yr) as compared to that in the group which had a TSH-response to TRH of greater than 20 mU/l, smaller glands and less thyroid nodules (45.1 yr). The data fit well with the reports on increasing autonomy with increasing age in nontoxic goiter.

Eleven pregnant women were treated for hyperthyroidism with carbimazole (CZ) and one with propylthiouracil (PTU). Based upon a previous study it was decided that lactation should be permitted if the dose required after delivery did not exceed 15 mg of CZ or 150 mg of PTU. In the patients studied here the daily dose of CZ varied from 5 to 15 mg and that of PTU was 125 mg. TSH was measured in cord blood and in the blood of the newborn infants usually after 2 and 3 weeks of lactation. Serum T4 was measured serially in the infants' blood from day 4 up to 21 day of age, at least. In all instances the TSH concentration in cord blood remained below 45 mU/l the level used in screening for neonatal hypothyroidism. Serum TSH and T4 were all within the appropriate reference limits during the 3 weeks of study with only one exception. In the infant whose mother was treated with PTU the serum T4 measured 5 d after birth was slightly below the lower limit but later returned to normal. Since serum TSH and T4 did not deviate from the reference range in newborn infants during lactation, we conclude that breast-feeding can be permitted if the daily dose of CZ does not exceed 15 mg (or 150 mg of PTU) and if facilities are available for measuring neonatal serum TSH and T4.

A female patient with acromegaly, TSH-induced hyperthyroidism and a large eosinophilic pituitary adenoma is reported. Granules in the adenoma cells were by immunohistochemical methods shown to contain GH and with monoclonal TSH-antibodies it was shown that 5-10 per cent of the cells secreted TSH. The basal serum TSH was elevated in the hyperthyroid phases and was not suppressible by exogenous T3 but decreased markedly with dexamethasone. There was a small subnormal rise in serum TSH after TRH injection which was totally suppressed by T3 (but not dexamethasone). L-dopa, bromocriptine and somatostatin caused a 20-30 per cent decrease in serum TSH. The alpha-subunit concentration was also elevated and was equally depressed by bromocriptine and somatostatin. The urinary excretion of TRH was within reference limits. This mixed tumour obviously secreted an excess of both GH and TSH causing acromegaly and hyperthyroidism.

During the period 1965-1976, 43 pregnancies in 42 thyrotoxic mothers were seen. Thirty-nine pregnancies in 38 patients were analyzed further. Twenty-six patients (27 pregnancies) were treated with antithyroid agents with (9) or without (17) supplemental thyroid hormone therapy and 5 were subjected to subtotal thyroidectomy. In these groups spontaneous abortion occurred in 4 patients (12.5%), prematurity in 3 (9.4%) and perinatal death in one whereas 25 pregnancies ended at term (78%). Two pairs of twins were born and the number of live children in these 32 pregnancies was 29. Hypothyroidism developed in one patient after operation. Thyroid crisis occurred at delivery in one patient in whom the antithyroid therapy was interrupted before labour. Seven patients were not treated with specific antithyroid therapy. In this group there was one twinbirth, one premature birth, one stillbirth and one child died shortly after birth. Thyroid crises developed at delivery in two mothers. The authors use subtotal thyroidectomy if usual indications for operation are present and antithyroid therapy when the thyroid gland is small and diffuse. Beta-receptor blocking agents are recommended only as adjuncts to the antithyroid therapy. A close surveillance of the patients and the free thyroid hormone level during therapy is important and after thyroidectomy treatment with thyroid hormone is recommended until after delivery.

Fifteen patients, 11 females and 4 males, aged 4-16 years with follicle-derived differentiated thyroid carcinoma treated at the Helsinki University Central Hospital during 1953 through 1984 are reported. Histologically 13 carcinomata were papillary, 1 follicular and 1 was suspected to be follicular carcinoma (atypic adenoma). Eleven (73%) had cervical lymphnode metastases and 4 (25%) pulmonary metastases as well. All patients were initially operated on; total thyroidectomy was performed in 11 and subtotal in 4 patients. In 5 patients there was invasion into the thyroid capsule, perithyroid tissues and blood vessels; 4 patients with pulmonary metastases belonged to this group. Postoperatively 5 patients received radioactive iodine, 4 patients external irradiation to the neck and 6 were given both types of radiation. Pulmonary metastases were treated with radioactive iodine. The patients have been given suppressive doses of thyroxine. The follow-up ranged from 3.5 to 33 years. One patient with extensive pulmonary metastases died 6 years after the initial treatment, all others are still alive. Twelve patients have been followed for 9 to 33 years, in 10 serum thyroglobulin was determined. Tg was undetectable in 9 patients when measured during thyroxin therapy; in 1 patient followed for 33 years, the dose was not suppressive, and there were no signs of disease and Tg in the normal range. In 2 patients Tg could not be determined but they had no signs of disease 18 and 22 years after initial treatment. It is, therefore, presumed that these patients, forming 80% of the material, are cured. Two patients followed for 3.5 years are still under treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Endemic goitre of moderate severity was mainly found in the East of Finland still in the 1950s but the whole country was moderately iodine deficient. The daily iodine intake determined both from food consumption and from the urinary excretion in population samples was 50-70 micrograms being lower in the East. The main iodine sources were milk products, about 50% of the daily intake being derived from these. Iodized salt was available but its use was very low and the iodine content insufficient so that only about 20% came from this source. In the late 1950s iodine prophylaxis was activated and since then only salt containing 25 mg KI/kg has been imported. However, during the last decades the consumption of salt has declined from 7-8 g to less than 4 g per day. Today the iodine intake in Finland is about 300 micrograms per day, the highest in Europe. The main sources are milk products and eggs which provide about 2/3 of the daily iodine intake due to an active iodine prophylaxis of house animals and only 20% comes from iodized salt. The origin of endemic goitre in Finland has obviously been multifactorial autoimmunity, natural goitrogens and possibly genetic factors being superimposed upon the basic iodine deficiency. The iodine supply is now adequate and there is no more goitre in neonates and no endemic goitre in school children in whom the prevalence is usually below 1%. Concomitantly, the nosology of hyperthyroidism has changed. Whereas more than 80% of hyperthyroid patients in the 1950s had nodular goitre the main type of hyperthyroidism today is Graves' disease proper with a small or normal-sized thyroid gland without nodules obviously due to disappearance of the endemic nodular goitre.

A relatively high percentage of patients with affective disorders have abnormalities of thyroid function, and over 60% of endogenously depressed and most manic patients show a blunted thyroid-stimulating hormone (TSH) response to thyroid-releasing hormone (TRH) injections. We now replicate earlier findings concerning relatively high 3,3',5'-triiodothyronine (reverse T3) levels in unipolar depressives and find similarly high levels in manic women. The significance of the present finding is unknown, but measurement of reverse T3 levels as a potential tool in differential diagnosis of affective disorders and in psychobiological research should be explored further.

Thirty-one patients who had been treated for acromegaly for 1-21 years with conventional pituitary irradiation were re-examined. Immunoreactive growth hormone (GH) was measured in connection with an oral glucose load. Adrenal and gonadal functions were assessed on the basis of plasma cortisol and the urinary excretion of 17-ketogenic steroids, 17-ketosteroids and gonadotrophins. In evaluating the thyroid-pituitary axis the thyrotrophin-releasing hormone stimulation test (TRH) was used. Initially 30 patients had experienced definite benefit from the treatment but at the time of re-examination 10 still had clinically active disease and required another type of treatment. Normal GH levels (less than 5 ng/ml/1) were seen in only 12 patients. Skin thickness was normal in 15 out of 30. Thus the remission rate can be evaluated as being 67% as regards clinical activity, 50% with regard to skin thickness and 39% in terms of GH levels. Hypogonadism occurred in 12 patients (39%) and adrenal and thyroid failure in 5 patients each (16%). The response to TRH was within the normal range in 2 of the hypothyroid patients. In 22 euthyroid patients the mean increment in serum TSH in response to 200 mug of synthetic TRH was only 5.8 mU/1 which was significantly below the normal mean 12.5 mU/1. Furthermore, in 7 of these patients (32%) the response was absent or subnormal (less than 3.0 mU/1). This indicated that the pituitary is capable of secreting enough TSH for maintenance of an euthyroid state but that its capacity is limited. Conventional pituitary irradiation is not a very effective treatment in acromegaly but may still be recommended in selected cases.

Thirty-four hypothyroid women on thyroid hormone substitution were followed through 37 pregnancies, and 16 women having previous surgery for thyroid carcinoma and thereafter placed on suppressive thyroxine treatment were followed through 19 pregnancies. The thyroxine treatment needed readjustment in 13 pregnancies (23%) to maintain euthyroidism. At delivery, the maternal free thyroxine index was 126 nmol/L in the group of patients treated for hypothyroidism and 146 nmol/L in the patients with treated thyroid carcinoma. The amniotic fluid thyroxine level in normal pregnancies was 6.7 nmol/L, in hypothyroid patients 6.7 nmol/L, and in patients with thyroid carcinoma 5.6 nmol/L. The amniotic fluid reverse triiodothyronine level in normal pregnancies was 0.51 nmol/L, in hypothyroid patients 0.66 nmol/L, and in patients with thyroid carcinoma 0.70 nmol/L. All infants were euthyroid.

The occurrence of permanent overt or subclinical hypothyroidism following subacute thyroiditis (SAT) was studied in 32 patients during 0.75-13 years (mean 4.2 years) of follow-up. Permanent hypothyroidism developed in 2 patients in whom a characteristic feature was persistent of circulating thyroid antibodies in high titres from the onset of SAT indicating the presence of autoimmune thyroiditis. One also showed cytological evidence of autoimmune thyroiditis. In another patient subclinical hypothyroidism demonstrated by an exaggerated TSH-response to TRH, persisted after hemithyroidectomy during the acute phase. In addition, transient overt hyperthyroidism developed immediately after the acute phase in 3, and subclinical hypothyroidism in 2 patients. Apart from the 2 patients with evidence of autoimmune thyroiditis, circulating thyroid antibodies were found in 15 others. The titres were usually low and disappeared in most cases after a transient rise. It is concluded that permanent hypothyroidism is likely to develop after SAT only in the presence of autoimmune thyroiditis or after thyroid surgery.

Eleven pregnant women with concomitant hyperthyroidism were treated with antithyroid drugs. At monthly intervals serum thyroxine (T4) and triiodothyronine (T3) were measured with radioimmunoassay, the Sephadex uptake of radioactive triiodothyronine (T3U) determined the free T4 and T3 indices calculated (FT4I, FT3I). TSH-binding inhibiting immunoglobulins (TBII) were determined by the radiomembrane assay. Serum TSH and T4 were measured at delivery from cord blood and/or from the newborn infants some days after birth. Serum TSH was significantly elevated in one infant. There was an inadequate post-partal rise in serum T4 concentration in this child and in another who showed only a marginal elevation of TSH. The mothers of these infants were given carbimazole in doses of 30 and 25 mg/day, respectively, at the time of delivery. No significant changes were seen in other infants, the daily doses being 20 mg of carbimazole or less. There was no clinical indication of hypo- or hyperthyroidism in any of the newborn. The TBII were positive in most patients and there was a trend of normalization during treatment. No relationship between the dose of antithyroid drug and the level of TBII could be seen. During treatment the dose was adjusted according to the FT3I values. This seems to be an adequate laboratory test for this purpose.