Katsumi Iwase

Asahi Kasei (Germany)

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Congenital Goiter Sustaining Normal Level of Serum Triiodothyronine

Hormone and Metabolic Research (1986)

Akio Nagasaka N Nihei Y Hirooka Terunori Mitsuma Kunio Kataoka

We attempted to elucidate the deficient site of thyroid hormone biosynthesis in the thyroid gland and the mechanism of sustaining normal T3 level in sera of a patient with congenital goiter. TY, a 8-yr-old boy, first noted the onset of a diffuse goiter at the age of 2. There was no clinical evidence of hypothyroidism except for the slight impairment of intellectual development and the awkward physical activity. BMR, T3-RSU and T4 showed low values (-13%, 20.8% and 2.2 micrograms/dl), but serum T3 was normal (180 ng/dl). Serum TSH was 18 microU/ml. The intrathyroidal T3 and T4 were slightly low. Thyroidal 131I uptake was high, but KSCN discharge test was negative. Percent distribution of 131I labelled amino acids in the pancreatin digested thyroid homogenate was 17.4% in MIT, 33.4% in DIT and 11.3% in T3 and T4. Thyroid iodide peroxidase activities in mitochondrial and microsomal fractions were slightly low (19.6 and 26.8 (normal: 32 +/- 3.0 and 37.4 +/- 9.5) mumoles/mg protein). The activity was not increased by the addition of hematin. Thyroglobulin was found to be normal. A biological half life of 131I labelled T4 was shorter (3.5 days) than that of the normal. Electron microscopic examination exhibited the increment and expansion of endoplasmic reticulum in the follicular cell. Low iodide peroxidase activity of this patient may correlate to low T3 and T4 level in the thyroid cell. Moreover, shortened biological half life of T4 implies that normal T3 level in serum is sustained by the accelerated conversion of T4 to T3 in peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Thyroglobulin

Thyroid peroxidase

10.1055/s-2007-1012457

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Citations (4)

Cytosol components from human placenta and rat liver in iodothyronine 5- and 5′-deiodination

Biochemistry and Cell Biology (1989)

Katsumi Iwase Brian C. W. Hummel Paul G. Walfish

Using either human placental microsomal 5-deiodinase as enzyme (5-DI) and thyroxine as substrate or rat liver (RL) microsomal 5′-deiodinase (5′ DI) as enzyme and reverse [(3′- or 5′-)- 125 I]triiodo-L-thyronine ([ 125 I]rT3) as substrate, activation of 5′-DI in the presence of NADPH was observed using either human placental or rat liver cytosolic components, but there was no activation of 5-DI. Both could be activated by DTT, with higher concentrations being required for 5-DI than for 5′-DI. Iopanoic acid, dicumarol, and sodium arsenite inhibited 5′-DI and 5-DI activated by DTT. In the presence of DTT, 1 mM 6-propyl-2-thiouracil had no effect on 5-DI but inhibited 5′ DI. Thus, human placental and rat liver cytosolic components are interchangeable in activating hepatic 5′-DI in the presence of NADPH. However, if an endogenous cofactor system involved in the activation of human placental 5-DI exists, it probably differs from the activator of liver 5′-DI.Key words: iodothyronines, deiodination cofactors, placenta, liver, cytosol.

Dithiothreitol

10.1139/o89-009

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A CASE OF RADIATION INDUCED CARCINOMA OF THE CERVICAL ESOPHAGUS

The journal of the Japanese Practical Surgeon Society (1980)

Katsumi Iwase Kaoru Miura Kyohei KAWASE Akihiro Yamaguchi Shigehiko Kondo

[in Japanese]

10.3919/ringe1963.41.622

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The influence of hyper- and hypothyroid states on the incidence of 3-methylcholanthrene-induced tumor in DDY mice.

PubMed (1981)

M Ohkoshi Akihiro Yamaguchi Akio Nagasaka Katsumi Iwase N Nihei

In female DDY mice. the incidence of 3-methylcholanthreneinduced skin tumors was increased in the hypothyroid state produced by the administration of Endojodin or l-methyl-2-mercaptoimidazole (p < 0.0 I) and decreased in the hyperthyroid state produced by L-thyroxine administration (p < 0.05) compared with controls. The calorigenic effect or the direct action of thyroid hormones may correlate with tumor induction in mice.

Methylcholanthrene

Skin tumor

Source

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A CASE OF MALIGNANT LEFT ADRENAL PHEOCHROMOCYTOMA WITH METASTASIS TO THE SACRUM WHICH WAS SURGICALLY RESECTED

Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) (2003)

Shin Jimbo A. Inagaki Naomi Kobayashi HARUO YAMAMOTO Katsumi Iwase

症例は54歳,男性. 1994年6月,腹痛を主訴にCT検査を受け,左副腎腫瘤を指摘された.高血圧症は認めないが,尿中カテコラミン(CA)は高値を示した. CT, MRIでは,左腎門部と大動脈に接し,腎動静脈の間に発育する境界明瞭で嚢胞性変化を伴う最大径約10cmの腫瘤を認めた. 131I-MIBGシンチで腫瘤部と骨盤部に集積を認め, CTで仙骨部に腫瘤を確認し,仙骨転移を伴う左副腎悪性褐色細胞腫(無症候性)と診断した. 10月,左腎合併左副腎摘出術を施行.腫瘍は径10×6×4.5cm,重量145gで腎実質への浸潤はなかった.組織学的には,分泌顆粒を持つ大小不同の好塩基性細胞の充実性増殖を認め,褐色細胞腫と診断された,術後,尿中CAおよび代謝物は高値を持続し, 4カ月後に仙骨部分切除術施行後には,全ての尿中CAは正常化した. 4カ月後歩行可能となり退院.術後8年経過した現在,再発を認めない.悪性褐色細胞腫の治療には手術,化学療法,動脈塞栓, 131I-MIBG内照射などが挙げられるが,いまだ確立されてはいない.われわれは仙骨部に単発性転移を伴った悪性副腎褐色細胞腫に対して,原発および転移病変の二期的切除を施行し良好な結果を得た.

10.3919/jjsa.64.3173

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High levels of DNA polymerase β mRNA corresponding with the high activity in Graves’ thyroid tissue

Journal of Endocrinological Investigation (2016)

Naohiro Hayakawa Yukihiro Sato Akiomi Nagasaka Y. Mano T. Nagasaka

Trab

Thyroid peroxidase

Thyroid hormone receptor

10.1007/s40618-016-0571-0

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High-dose chemotherapy with peripheral blood stem cell transplantation as adjuvant therapy for primary breast cancer

European Journal of Cancer (1998)

Katsumi Iwase Fumio Maruyama Satoshi Ohtani Tohru Tsujimura A. Inagaki

Adjuvant Chemotherapy

Adjuvant Therapy

10.1016/s0959-8049(98)80048-8

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Effect of Calmodulin Inhibitors on Thyroid Hormone Secretion

Springer eBooks (1986)

Akira Nakai Akio Nagasaka Takako Ohyama Toshihiro Aono Rumi Masunaga

10.1007/978-1-4684-5260-0_55

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Cu/Zn- and Mn-Superoxide Dismutase Distribution and Concentration in Adrenal Tumors

Journal of Surgical Research (2006)

Katsumi Iwase Akio Nagasaka Kanefusa Kato Asako Itoh Shin Jimbo

Dismutase

10.1016/j.jss.2006.03.027

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Citations (6)

A CASE OF METASTATIC FOLLICULAR CARCINOMA OF THE THYROID. CAUSING HYPERTHYROIDISM (T3 TOXICOSIS)

The journal of the Japanese Practical Surgeon Society (1991)

Katsumi Iwase Susumu Ohtani Toru Tsujimura A. Inagaki Shuichi Miyakawa

We experienced a rare case of lung, and bone metastases from follicular carcinoma of the thyroid, presenting with hyperthyroidism induced by triiodothyronine (T3), which was secreted from metastatic lesions after surgery for primary lesion.A 42-year-old female suffering from a tumor of the neck for past 3 years consulted us in Mar. 1977. It was a thyroid tumor of 7 by 5 cm in size, elastic hard and smooth surface in palpation. She didn't have thyroid dysfunction. Under a clinical diagnosis of thyroid adenoma, left hemithyroidectomy was performed. Although the tumor was histologically diagnosed being follicular carcinoma, she was followed without any other treatments. Three years after surgery, modified neck dissection was done for regional lymph nodes metastases, and TSH suppression therapy was added. Seven years after the first surgery, lung and liver metastases were found and remained thyroid was removed for the 131I irradiation. Following 3 years, twice 131I and external irradition for pain control of sacral metastasis were performed. TSH suppression therapy by T3 (25 μg/day) and T4 (100 to 200 μg/day)administration was also continued, but the metastatic lesions gradually enlarged. Eleven years after the first surgery, the elevation of serum T3 and TSH receptor antibody were found, and one year after that she manifestated palpitation as a symptom of hyperthyroidism. The stop of T3 and T4 administration failed to control the thyrotoxicosis, and methylmercaptoimidazol (30 μg/day) was needed. The patient died of respiratory insufficiency caused by the enlarged pulmonary metastasis.T3 production in the metastatic lesions and the increase of its release to blood according to tumor growth were thought to be main factors for hyperthyroidism in this patient. Autoimmune disorder also may participate in the occurrence of hyperthyroidism.

10.3919/ringe1963.52.1024

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