Folia Endocrinologica Japonica
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
Volume 67, Issue 2
Displaying 1-5 of 5 articles from this issue
  • Toshiki MANO, Masahiro YAMAMOTO, Kozo SUZUKI
    1991 Volume 67 Issue 2 Pages 57-64
    Published: February 20, 1991
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    A 37 year-old female with Kallmann syndrome and NIDDM who had two successful deliveries is reported.
    She had experienced no menstruation until she had treatment with gestagen in her early twenties. She had withdrawal bleeding only once. At the age of 25, she consulted her family doctor, complaining of amenorrhea. Estrogen progesterone cyclic therapy caused withdrawal bleeding, and clomiphene citrate failed to induce apparent ovulation. In January 1978, 150IU of hMG was administered daily for 9 days, and then 3000IU of hCG daily for the following 2 days. This therapy induced pregnancy, which failed spontaneously on June 4th. A year later, in January 1979, 150IU of hMG was again administered daily for 7 days followed by 6000IU of hCG for 3 days. This therapy again induced pregnancy. On September 27th, 1979, she delivered a girl vaginally, weighing 3830g.
    After this delivery, she experienced no menstruation. In June 1985, she consulted her family doctor again, and she was diagnosed as being pregnant. Since her fasting blood glucose was 145mg/dl, she was admitted to Kosei Hospital to control her blood glucose. On October 15th, she delivered a girl weighing 2600g.
    On June 13th, 1989, she was referred to Kosei Hospital by her family doctor to achieve an accurate control of her blood glucose. During this admission, she was diagnosed as having Kallmann syndrome because of congenital anosmia and hypogonadotropic hypogonadism without any abnormal morphological changes. Vitamin Bi infusion test was negative. Intravenous infusion of LH-RH resulted in a delayed response in serum LH with a peak 60 minutes after administration, and a delayed and small increase in serum FSH with a plateau after 60 minutes. TRH induced a small increase in serum TSH. No abnormal finding was detected with CT and MRI imagings in the hypothalamus and the pituitary.
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  • Takashi TOKUYAMA, Mototaka YOSHINARI, Ken OKAMURA, Hiroshi IKENOUE, Ka ...
    1991 Volume 67 Issue 2 Pages 65-74
    Published: February 20, 1991
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    The role of dopaminergic agents (DA) in the regulation of growth hormone (GH) secretion was investigated in patients with untreated acromegaly. TRH (0.5mg iv), bromocriptine (Br) (2.5mg orally) or L-Dopa (500mg orally) loading tests were performed, and serum levels of TSH, GH and prolactin (PRL) were measured. Patients were defined as responders to TRH when peak TSH level after TRH test was higher than 5 μU/ml. Br or L-Dopa was considered to be effective when serum GH or PRL levels were suppressed more than 50% of the basal value. The patients were classified into large adenoma group with suprasellar extension or cisternal herniation (L group, n=7) and intrasellar small adenoma group (S group, n=11) which was further divided into TRH responder (Sr group, n=4) and TRH non-responder with suppressed TSH (Ss group, n=7).
    Br was effective in 7 or 100% of 7 patients in the Ss group but only in one or 25% of 4 patients in the Sr group. Br was also effective in 5 or 71% of 7 patients in the L group, although most of them were responders to TRH. Percent inhibition of serum GH levels by Br was significantly higher in the Ss group (82.3-1712.3%, p<0.001) and in the L group (64.7±20.5%, p<0.05) compared with that in the Sr group (29.3±21.6%). Suppression of serum GH level by L-Dopa was also observed in the Ss group. In contrast to the difference in the response of GH, serum PRL level was equally suppressed by Br or L-Dopa in each group. Suppression of TSH by administration of exogenous T4 had no effect on the GH suppression effect of Br in the Sr group.
    Considering the dual effects of DA to enhance growth hormone-releasing hormone (GHRH) secretion in the hypothalamus and to suppress GH secretion in the pituitary gland, these findings suggest that the paradoxical effect of DA to suppress serum GH level is observed when the hypothalamo-pituitary axis is disturbed mechanically by large adenoma in the L group or functionally in the Ss group probably due to enhanced secretion of somatostatin which suppresses TSH secretion and impairs the effect of GHRH.
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  • Nobuhiko FUKASAWA, Makoto IITAKA, Yoshihito HARA, Morifumi YANAGISAWA, ...
    1991 Volume 67 Issue 2 Pages 75-83
    Published: February 20, 1991
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Two patients with Graves' disease treated with methimazole (MMI) showed a discrepancy between serum free T4 (FT4) values and other hormone values (especially total T4) which was due to the presence of potent binding activity to labelled T4 analogue (125I-aT4) in their serum. This activity was demonstrated to be in immunoglobulin G (IgG) with κ light chain isotype in both patients. The binding of 125I-aT4 to their serum was inhibited by unlabelled T4 in a dose-dependent manner. Autoantibodies had almost identical binding affinity to T4 and aT4, although they precipitated more radioactivity when 125I-aT4 was used. The binding of IgG purified from patients' sera to labelled T4 or aT4 was not greater than the corresponding sera, suggesting that the thyroxine binding proteins did not interfere with the assay. Since the specific radioactivity of 125I-aT4 is almost 10 times higher than that of 125I-T4, autoantibodies can precipitate almost 10 times more radioactivity in the FT4 assay than the total T4 assay, thus leading to the spuriously high FT4 values and large discrepancy between FT4 and TT4 values.
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  • A comparative study of the effect of 1 α-hydroxycholecalciferol (1 α-OHD3) on senile osteoporosis
    Masataka SHIRAKI, Hajime ORIMO
    1991 Volume 67 Issue 2 Pages 84-95
    Published: February 20, 1991
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    In order to assess the effect of sex steroids on bone mineral density in Japanese with senile osteoporosis, the bone mineral density in 1/3 distal site of radius was measured serially before and after treatment for 2 years using single photon absorptiometry.
    Sixty seven old females with senile osteoporosis were divided into 4 groups, Group 1 (n=28, mean age; 74.4±1.3y. o., mean±SEM) was the control group, Group 2 (n=14, mean age; 73.7±1.7y. o.) was treated with 0.5-1.0μg/day of 1 α-OHD3, Group 3 (n=12, mean age; 75.4±2.9y. o.) was treated with conjugated estrogen (Premarin ®) in a dose of 0.3125mg/day (3~4 weeks administration followed by 1 week rest) and Group 4 (n=13, mean age; 76.4±1.8y. o.) was treated with sex-steroids (pregnenolone: androstenedione androstenediol: testosterone: estrone=1.0mg 1.0mg 0.5mg 0.1mg: 5μg/tablet) and thyroid hormone (thyroid-sicca 7.5mg/tablet) preparation in a dose of 2 tablets/day.
    When the radial bone mineral density (RMD) before the treatment was taken as 100%, RMDs of each group at 6, 12, 18 and 24 months were 96.4±3.1%, 97.3±2.0%, 93.7±2.1% and 96.1±1.8% in Group 1, 100.8±2.8%, 106.4±2.1%, 101.3±3.4% and 108.8±2.9% in Group 2, 103.0±2.8%, 106.2±3.5%, 105.9±4.3% and 100.2±4.7% in Group 3, 105.3±2.2%, 104.7±2.3%, 112.6±6.4% and 112.1±6.7% in Group 4, respectively.
    Therefore, significant increases in RMD were observed in Groups 2, 3 (transient) and 4 when compared with Group 1.
    In Group 3, serum level of parathyroid hormone (PTH) was significantly (p<0.05) increased from 0.28±0.03ng/ml before the treatment to 0.55±0.15ng/ml at 24 months after the treatment. In Group 2, transient (6 months after the treatment) but significant (p<0.01) increase in urinary Ca/Creatinine ratio from 0.15±0.04 to 0.20±0.03 was found. Serum A1-P activities in Group 4 was shown to increase transiently from 131±10 IU to 151±12 IU (p<0.05) at 6 months and to 158±13 IU (p<0.01) at 12 months followed by subsequent decrease to 135±6 IU at 18 months and 133±10 IU at 24 months after the treatment. Serum level of calcium in Group 4 was decreased from 9.6±0.1mg/dl to 9.1±0.2mg/dl at 18 months after the treatment (p<0.05). These findings indicated the following possibilities. 1) Administration of 1 α-OHD3 and, sex hormones and thyroid hormone preparation are effective in increasing bone mineral density in senile osteoporosis. 2) Administration of a low dose of estrogen might increase bone mineral density in senile osteoporosis. However, this increment in bone mineral density is transient possibly because of the subsequent rise in serum level of PTH. 3) The mechanisms of these drugs in bone metabolism might be different.
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  • Yutaka TAKEZAWA, Yoshitatsu FUKABORI, Seijirou HONMA
    1991 Volume 67 Issue 2 Pages 96-110
    Published: February 20, 1991
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Estrogen formation from androst-4-ene-3,17-dione and its kinetics were studied using microsomes from rat hypothalamus.[4-14C] androst-4-ene-3, 17-dione and a homogenate of rat hypothalamus were incubated in the presence of NADPH at 37°C for 3 hrs. The estrogen fraction was extracted from the incubation mixture with ethyl acetate, purified by column chromatography on Sephadex LH-20 and Bond Elut C18, and separated into estrone and estradiol fractions by HPLC. In analysis of the trimethylsilyl (TMS) derivatives of each fraction by gas chromatography-mass spectrometry (GC-MS), the molecular ion peak of the estrone fraction appeared at m/z 344, within 2 amu of that for the TMS derivative of natural estrone. The retention time of the estrone fraction derivative was 11.6 min, the same as that of natural estrone.14C-estrone was thus concluded to be biosynthesized from [4-14C]-androst-4-ene-3,17-dione in rat hypothalamus.
    The kinetics of the aromatase of rat hypothalamic tissue was studied by measuring 3H2O released from [1β-3H]-androst-4-ene-3,17-dione and estrone as the estrogen product by measured gas chromatography selected ion monitoring (GC-SIM). High correlation was found between 3H2O release and estrone measured by GC-SIM (r=0.97). Aromatase activity was linear with respect to incubation time and quantity of tissue. Km and Vmax were 30.3nM and 7.98fmol estrogen/h/mg of wet tissue, respectively.
    4-hydroxyandrostenedione (4-OH-A) suppressed the activity of aromatase in both rat hypothalamic and human placental tissue in a concentration-dependent manner. Polyclonal IgG to human placental aromatase also suppressed aromatase activity of human placental tissue, but only slightly suppressed that of rat hypothalamus. The molecular structure of aromatase in rat hypothalamus was thus concluded to differ from that in human placenta.
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