For the past 3 years, 1649 patients with thyroid diseases have been examined in our thyroid clinic. Among them, 685 patients have hyperthyroidism, and 315 patients have chronic thyroiditis. Since a number of laboratory tests are available at present, diagnosis of hyperthyroidism is not difficult. However, hyperthyroid patients without goiter are sometimes misdiagnosed as having heart disease. Four hundred seventy one hyperthyroid patients were treated with propylthiouracil or methimazole for at least 12 months. About 60% of hyperthyroid patients showed a decrease of thyroid size after propylthiouracil treatment, whereas only 30% of hyperthyroid patients showed a decrease of thyroid size after methimazole therapy. In contrast, re-enlargement of the thyroid has often been found after methimazole therapy. This enlarged thyroid can be reduced by the administration of desiccated thyroid or triiodothyronine without affecting thyroidal radioiodine uptake, suggesting that partial re-establishment of pituitary-thyroid feedback mechanism is achieved shortly after starting goitrogen. A combined use of thiocyanate and propylthiouracil is advisable for an acute control of hyperthyroidism, since such therapy produced a rapid fall of PBI, BMR, thyroidal radioiodine uptake and resin sponge T₃ test (RSU), without producing any side effects. Two hundred twelve patients were treated with radioiodine. Eleven patients were actually hypothyroid states as evidenced by laboratory tests. Fourteen patients have suggestive signs of hypothyroidism but the data of laboratory tests were all within normal range. If overt and such subclinical cases were combined, incidence of hypothyroidism 10 years after radioiodine was about 12%, making a sharp contrast with the data of foreign country in which 30 to 75% of the treated patients were hypothyroid.
Among 315 patients with chronic thyroiditis, 117 patients received needle biopsy for histological examination. Analysis of the data obtained in those patients indicated that a) incidence is high at older age, b) size of the goiter is more in chronic thyroiditis than in simple goiter, c) hardness of the thyroid is increased particularly at upper half of the thyroid, d) a decrease of thyroid size hardly occurs after thyroid hormone but occurs in most cases after steroid therapy, e) thyroid autoantibody was found in most patients. Analysis of these findings makes us possible to do diagnosis of chronic thyroiditis without doing further histological examination.
Since the terms myxedema and hypothyroidism were used in the same manner, an analysis of overt and subclinical hypothyroidism was performed using thiocyanate and iodide loading tests. Through these particular tests, 3 types (A, B, C) of subclinical hypothyroidism have been classified and were designed as masked hypothyroidism. Type A does not have goiter and showed discharge of thyroidal iodide before and/or after iodide loading. BMR, thyroidal radioiodine uptake and RSU also decreased after iodide loading. Type B has goiter and does not show iodide discharge before iodide loading, but otherwise similar to Type A. Type C has goiter and does not show any abnormality before and after iodide loading except that thyroidal radioiodine uptake decreased markedly after iodide administration. Myxedematous patients without any detectable abnormality either in laboratory tests or in special tests should not be regarded as subclinical hypothyroidism, although the patients responded well to thyroid therapy.

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Mechanism through which homeostatic adaptation to severe iodine deficiency is produced have been studied in the rat. Within 24 hours after institution of a Remington low-iodine diet (LID) containing 30 μg I/kg there is a 50% increase in the 131-I uptake by the thyroid. The 4-hr uptake increases linearly from approximately 5% in Purinafed rats to 70% after 30 days LID. Thereafter the increase is very gradual, the 4-hr uptake averaging 80-90% between 4 and 15 months. Within one week of starting LID there is a statistically significant increase in thyroid size. The increase in relative thyroid weight is linear up to 5 months, going from 6.5 mg/100 g B.W. to approximately 60; there is a slow further increase up to at least 15 months. Total iodine content of the thyroid remains relatively constant for the first 1-2 weeks, then rapidly falls to 5% of the initial value by one month. This is associated with a rapid fall in serum PBI from 4 to 0.5 ug/100 ml between 2 and 4 weeks. In spite of maintenance of this extremely low PBI for more than one year on LID, the rats continue to grow, remain healthy, and are not “clinically” hypothyroid, as occurs after thyroidectomy or propylthiouracil administration. The thyroid MIT/DIT ratio begins to rise as soon as the rats are given LID, but the T3/T4 ratio does not begin to rise until about 2 weeks after institution of LID, coincident with fall in serum PBI and depletion of thyroid iodine stores. The T3/T4 ratio of iodothyronines secreted by the thyroid rises even faster in the gland, going from 0.2 in rats fed a high iodine diet to 3 after several month of LID. The preferential secretion of T₃ in iodine deficiency accounts for the maintenance of a relatively euthyroid state in spite of a very low PBI. T₃ is four times as potent as T₄ but contains only 75% as much iodine per mol molecule. It is thus teleologically sound for this qualitative adaptation of thyroid secretion to occur during periods of grossly inadequate availability of dietary iodine. All adaptive changes are dependent on increased TSH secretion and are abolished by hypophysectomy. However, they are not reproduced by administration of TSH unless the thyroid is simultaneously depleted of iodine. Thus the adaptation is synergically produced by autonomous and TSH-induced intrathyroidal mechanisms. The changes in thyroid iodine metabolism produced by iodine deficiency in the rat are consistent with observations in humans with endemic, iodine-deficiency goiter and provide a valuable experimental model.

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従来用いられて来た gonadotropinのrodioimmunoassayは結果が判明する迄長時間を要する欠点があつた.この点を解決する為にanti-HCGそのものをethyl chloroformateにてpolymerizeし, これをimmunoadsorbentとして¹²⁵I-HCGと直接結合させる反応系を用いてone step radioimmunoassayを考案した.その結果HCGを含む検体と本反応系を混合して, 37℃, 60分 incubateするのみで従来のradioimmunoassayに劣らぬ感度で測定が可能になり, LH定量にも応用しうることが判明した.

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ラットを用い心筋ホスホリラーゼ活性, 心搏数を指標として甲状腺ホルモンとカテコールアミンの関係を知ろうとした.サイロキシンおよびアドレナリンの単独投与では心筋ホスホリラーゼ活性の上昇, 心搏数の増加が観察されたが, 両ホルモンの投与ではこの効果が認められなかつた.また内因性カテコールアミンの態度とサイロキシンの作用との間にも関係が認められず, 甲状腺機能充進状態ラットにおいてrcceptorの機能が充進しているという証拠もえられなかつた.

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血中cortiso1の日内変動は睡眠・覚醒周期により確立されるとされているが諸疾患時における日内変動を検討した.また日内変動とnegative feedback機構の関係を検討するため中枢神経障害患者にMetopironeテストを行なつた.高血圧症, 脳腫瘍, 甲状腺機能f進症, Cushing症候群, 髄膜炎などに特有の日内変動の異常がみられた.またnegative feedback機構に側頭葉領域が何らかの関係をもつことが示された.

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人成長ホルモン (HGH) のchromatoelectrophoretic radioimmunoassayについて基礎的に検討し, 健常人における血中HGH値を測定した.測定法は感度0.5mμ9/m1, 測定範囲0.5から16.0mμg/m1, 再現性100±14.7%, 回収率84.8～124%で.TSH, 合成FSHおよびACTHに影響をうけず, 未端肥大症患者血清の希釈曲線は標準曲線とよく平行した.健常人の空腹安静時における血中HGH値は殆んど5mμ9/m1以下で, insulin, arginineおよび運動負荷により血中HGHは著明な上昇反応を示した.

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間脳・下垂体および甲状腺疾患時の血中HGH値をradioimmunoassayにより測定した.末端肥大症および神経性食思不振症では空腹安静時の血中HGHは高値で, 下垂体機能低下症および下垂体性徐儒性ではinsulin負荷によるHGH上昇反応が欠除し, 前葉ホルモンはHGHとgomadotropinの分泌障害を示す症例が多かった.HGH単独欠損症, 反応解離型のHGH分泌障害による條儒症の存在を認めた.末治療の甲状腺機能低下症では, insulin負荷によるHGH分泌は低下していた.

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イヌ睾丸静脈血中のC₁₉ステロイドを分析し, testosterone, androstcnedione, dchydroepiandrosterone, androstenediolを単離, 同定した.これらは何れもLH投与後明らかな増量を示した.androstenediolのtestosterone生合成に於ける意義を知る目的で放射性同位元素標識ステロイドのイヌ睾丸灌流実験を行なつた.その結果, androstenediolがイヌ睾丸に於けるtestosteronc生合成に重要な位置を占めることを確認した.

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カイウサギに大量のカルシウムおよびビタミンD₂を長期間投与して, 上皮小体実質細胞の機能を著明に低下せしめ, その後の実質細胞の再生あるいは機能の回復過程を電子顕微鏡的に観察した.その結果, カルシウムおよびビタミンD₂最終投与4日後の上皮小体では, すでに機能の低下した実質細胞は著明に減少し, 14日後では, 形態学的にみて, 全く正常の実質細胞のみ認められた.

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