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Bengt Skanse and G. Eberhard Nyman

It is known that the increased impact of thyroid hormone in thyrotoxicosis produces a number of symptoms involving the central nervous system. Thyrotoxicosis can even produce such gross neurological phenomena as coma, bulbar palsies, athetotic and choreiform movements, as has been well demonstrated by Waldenstrom (1945).

It is thus not surprising that electroencephalographic (EEG) abnormalities occur in the presence of thyrotoxicosis. In normal subjects Lindsley & Rubinstein (1937) found a correlation between the alpha frequency and the basal metabolic rate. This correlation was also demonstrated in a subject whose metabolic rate was increased by the administration of thyroxine. Ross & Schwab (1939) observed a similar correlation between the alpha frequency and the basal metabolic rate in a group of 12 patients with myxedema and 22 patients with thyrotoxicosis. They pointed out, however, that this correlation was not so close during the basal state (patient fasting and resting one half hour

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W. A. Scherbaum

Abstract. Among the various autoantibody tests applied in research and clinical practice, the determination of thyroid microsomal (TMAb) and thyroglobulin antibodies (TgAb) still retains its strong value in the screening for thyroid autoimmunity. The presence in the serum of TMAb is almost invariably associated with thyroid autoimmune disease or focal thyroiditis. The appearance of TMAb together with elevated serum-TSH in subclinical autoimmune thyroiditis strongly suggests progression to overt hypothyroidism. Pregnant women with positive TMAb and/or TgAb run an increased risk for post-partum painless thyroiditis with transient thyrotoxicosis and subsequent hypothyroidism. After delivery also a relapse of previously unrecognized Graves' thyrotoxicosis may occur. Thyroid antibody determination is not a valuable tool to discriminate autoimmune thyroiditis from thyroid malignancies. TMAb and TgAb determination helps to recognize individuals with thyroid autoimmunity among patients with non-thyroid autoimmune diseases such as Addison's disease and Type I diabetes mellitus.

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Enio Martino, Alessandro Pacchiarotti, Fabrizio Aghini-Lombardi, Lucia Grasso, Giovanni Bambini, Lidio Baschieri, and Aldo Pinchera

Abstract. The serum free thyroxine concentration was measured by direct radioimmunoassay in 38 untreated T3-thyrotoxic patients with elevated serum total and free triiodothyronine, normal serum thyroxine and free thyroxine index, no TSH response to TRH, and with clinical evidence of hyperthyroidism. An elevation of circulating free thyroxine values was observed in 58% of the patients, whereas total serum thyroxine concentration was within the normal range. It is suggested, therefore, that T3-thyrotoxicosis should be reserved for patients with elevated serum total T3 and free T3 concentrations and normal serum total T4 and free T4 concentrations. Serum thyroxine-binding globulin concentrations were significantly lower (P < 0.025) in patients with an elevated serum free thyroxine (18.7 ± 3.6 μg/ml: mean ± sd) as compared with those in patients with a normal free thyroxine concentration (23.4 ± 2.6 μg/ml). In addition, no daily fluctuations in total and free thyroxine concentration were observed in 6 patients over a 4–8 day period.

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J. Penhaligon and M. L. Wellby


A kindred with a high prevalence of hereditary serum thyroxine-binding globulin (TBG) is described. Seventeen of the 29 members of the kindred have the increased TBG trait as demonstrated by a combination of increased serum total thyroxine (T4) and total triiodothyronine (T3) and decreased T3 resin uptake. In 12 of the 17, the anomaly was confirmed by measuring serum TBG activity as maximum binding capacity of T4. The pattern of increased TBG is consistent with X-linked inheritance. One of the affected members had proven thyrotoxicosis and two others were subjected to sub-total thyroidectomy.

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Kyuzi Kamoi, Terunori Mitsuma, Hiroshi Sato, Motoharu Yokoyama, Kazuo Washiyama, Rhuichi Tanaka, Okuhiro Arai, Nobuyuki Takasu, and Takashi Yamada

Abstract. A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its α-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas β-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. l-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH.

Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, α-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its α-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour.

It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.

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Angel A. Zaninovich


The peripheral metabolism of thyroxine (T4) was studied before and after the administration of oestrogens in 21 patients with Graves' disease and in 5 subjects with thyrotoxicosis factitia. In addition, 6 patients with Graves' disease while receiving oestrogen treatment were given 600 mg of diphenylhydantoin (DPH) orally daily; the study on the peripheral metabolism of T4 was similarly performed. Oestrogens induced the following changes in T4 metabolism: a decrease in the concentration of free T4 in the serum, an increase in serum total T4, slowing of the fractional turnover, and contraction of the distribution space. The extrathyroidal T4 pool remained unchanged. These changes led to a decrease in daily T4 degradation rate from 469 μg in the control period to 348 μg during oestrogen therapy (P < 0.001). Fifteen of these patients showed apparent clinical improvement. The 2 subjects with T4-thyrotoxicosis factitia had decreased T4 degradation and remission of symptomatology following oestrogen administration; on the other hand, 3 subjects with T3-thyrotoxicosis factitia had no appreciable amelioration of their symptoms. The administration of DPH to oestrogen-treated patients with Graves' disease induced a slight acceleration of the absolute T4 turnover. It is concluded that the decreased T4 degradation induced by oestrogens in spontaneous and iatrogenic hyperthyroidism was mediated by an increase in T4-binding globulin capacity in the serum.

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Csaba Bános and József Takó


Agar gel electrophoretic studies were performed on 11 patients suffering from auto-immune thyroiditis in order to evaluate the distribution of tracer 125I-thyroxine in plasma proteins as well as their maximal thyroxine binding capacity. The thyroxine binding of the plasma proteins did not show any appreciable difference from that of the control group. Following treatment with 3 × 10 IU thyrotrophin (Ambinon®) the thyroxine binding capacity of prealbumin remained unchanged while that of thyroxine binding globulin increased in 5 of the 6 cases, the thyroid hormone secretion was normally enhanced and the serological reactions to thyroid auto-antibody formation showed no appreciable alterations. It seems unlikely that proteins other than the usual thyroxine binding plasma proteins are substantially involved in the transport of thyroid hormones in auto-immune thyroiditis.

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Bernhard E. Schreiber, Hugo M. Ortner, Georg Leb, and Otto Eber


An assay of stable 3,5,3′-triiodo-L-thyronine (T3) in serum of 54 patients was performed, using a new simple chromatographic procedure. With samples of 5 ml serum, the lower detection limit was 0.04 μg/100 ml. The total time required for a complete analysis was less than 3 hours, which was accomplished by partial automatization of the procedure. The range of the T3-concentration was 0.22 ± 0.05 (sd) μg/100 ml in 18 normal subjects, 0.67 ± 0.3 in 15 thyrotoxic patients and 0.08 ± 0.04 in 8 patients with hypothyroidism. Among 13 patients with normal serum thyroxine (T4) levels after thyroid surgery owing to thyrotoxicosis, there were 3 with marked increases in serum T3. In spite of normal T4-levels, symptoms of hyperthyroidism were still present in these patients. It is concluded, that serum T3-determinations may be useful for diagnosing cases of hyperthyroidism where clinical findings do not correspond with serum T4 or PBI-findings.

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J Tani, K Mori, S Hoshikawa, T Nakazawa, J Satoh, Y Nakagawa, S Ito, and K Yoshida

OBJECTIVE: Interferon regulatory factor-1 (IRF-1) is a critical regulator of interferon-gamma(IFNgamma)-mediated immune responses. To determine whether IRF-1 is involved in the pathogenesis of thyroiditis in animal models, we evaluated the incidence of iodide-induced lymphocytic thyroiditis (LT) in non-obese diabetic (NOD) mice lacking IRF-1 as well as IRF-1 +/+ and +/- mice. DESIGN: IRF-1 +/+, +/- and -/- NOD mice at 6 weeks of age were fed water (group 1) or iodide water (group 2) for 8 weeks. METHODS: Thyroids were examined histopathologically and intrathyroidal lymphocytic infiltration was arbitrarily graded. Serum thyroxine (T(4)) and anti-mouse thyroglobulin antibody (anti-mTgAb) levels were measured. Spleen cell population was analyzed by flow cytometry, and IFNgamma and interleukin-10 produced by splenocytes were measured by enzyme-linked immunosorbent assay. RESULTS: In group 1, only 4.3% of NOD mice developed LT. In contrast, 67.6% of mice in group 2 developed the disease. Iodide treatment induced LT in more than 80% of IRF-1 +/+ and +/- mice. However, no IRF-1 -/- mice in group 2 developed LT. There was no difference in both serum anti-mTgAb and T(4) levels among the three IRF-1 genotypes of NOD mice. Numbers of splenic CD8(+) T cells and IFNgamma production by Concanavalin A-stimulated splenocytes were markedly decreased in IRF-1-deficient NOD mice. CONCLUSIONS: IRF-1 is involved in the development of iodide-induced LT in NOD mice.

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C. Ferrari, M. Boghen, A. Paracchi, P. Rampini, F. Raiteri, R. Benco, M. Romussi, F. Codecasa, M. Mucci, and M. Bianco

Abstract. Circulating thyroglobulin antibodies (TgAb) and microsomal antibodies (MsAb) and thyroid function (total and free T4 and T3, TSH basal and after TRH) have been evaluated in 92 hyperprolactinaemic patients (82 females and 10 males; 9 with macroprolactinoma, 22 with microprolactinoma, 4 with acromegaly, 5 with organic lesions of the hypothalamus, 2 with empty sella, 2 with idiopathic hypopituitarism, 2 with primary hypothyroidism, and 46 with idiopathic hyperprolactinaemia). Thyroid function was normal in all cases except 3 with hypothalamic disease and central hypothyroidism, the 2 patients with primary hypothyroidism and 2 with thyrotoxicosis (one due to Graves' disease and one to autonomous thyroid adenoma). High titres of TgAb (≥1/1250) and/or MsAb (≥ 1/1600) were found in the subject with Graves' disease, in one acromegalic, in the 2 primary hypothyroids, and in 12 women with either adenomatous or idiopathic hyperprolactinaemia; low titres of one or both antibodies were found in 9 other euthyroid women and in the one with toxic adenoma. In a control population of 185 subjects studied with the same methods, the prevalence of TgAb and/or MsAb positive (low titres) was 3.3% in females and 2.5% in males. Diffuse thyroid hyperplasia was clinically detectable in 12 euthyroid women and in the one with Graves' disease; 3 others had been previously operated for nodular goitre with histological evidence of Hashimoto's thyroiditis (2 cases) or for a cold nodule; a single thyroid nodule was present in the woman with toxic adenoma and in one euthyroid woman. Most of these subjects also had circulating TgAb and/or MsAb, and a few had increased TSH secretion. No significant differences were found in mean thyroid hormone and TSH levels between euthyroid hyperprolactinaemic subjects and healthy controls, but TRH-stimulated TSH levels were significantly higher in thyroid antibodies positive than negative subjects. These data, in agreement with a few previous reports, suggest that autoimmune thyroid disorders (especially asymptomatic autoimmune thyroiditis) occur in hyperprolactinaemic women with a prevalence far exceeding that observed in many surveys in the general population.