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68 巻, 10 号
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片上 秀喜, 松倉 茂1992 年 68 巻 10 号 p. 1057-1072
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーGrowth hormone (GH)-releasing hormone (GRH) is a stimulatory hypothalamic hypophysiotropic hormone which, along with an inhibitory peptide, somatostatin (SRIF), regulates the synthesis and secretion of GH in anterior pituitary somatotrophs. Although GHRH genes in several species have been characterized, there is only a limited understanding of the neural and hormonal mechanisms regulating GRH biosynthesis and secretion. Recent progress in PCR and in situ hybridization techniques as well as hGRF-transgenic animal models have provided an opportunity to study the regulation of GRH gene expression and secretion as well as its metabolism. The difference in 5′-untranslated sequences in both mouse and rat GRH cDNAs from hypothalamus and placenta has also suggested tissue-specific regulation of the GRH gene.
GH excess has been shown to result in a decrease in hypothalamic GRH mRNA as well as GRH content and secretion while GH deficiency caused by hypophysectomy, hypothyroidism or genetic dwarfism causes an increase in GRH mRNA levels as tested by Northern blot analysis or in situ hybridization. Treatment of animals with GH or SRIF inhibits the increased GRH gene expression in the hypothalamic arcuate nucleus. Double immunocytochemistry for hypothalamic GRH and SRIF has shown both axo-perikaryal and axo-axonal connections between GRH-and SRIF-containing neurons. SRIF binding and GH receptor mRNA are demonstrated on a subpopulation of GRH-containing neurons in the hypothalamic arcuate nucleus. It is therefore possible to conclude that regulation of GRH gene expression, primarily related to inhibitory feedback effects of GH and IGFs on hypothalamic GRH gene expression, is mediated at least in part by SRIF or GH.
The single transcript of the human GRH gene encodes a 108 amino acid precursor, prepro-hGRH, which is cleaved into the signal peptide and the remaining peptide, pro-hGRH. The latter is further processed to yield two equipotent forms of the releasing hormone, hGRH (1-44)-NH2, hGRH (1-40)-OH, and a carboxyl-terminal peptide (hGCTP) of unknown function. Studies in transgenic mice demonstrate the processing of hGRH-prohormone into both mature forms of hGRH and hGCTP, and provide evidence that hGRH (1-40)-OH is derived from hGRH (1-44)-NH2. Since immunoreactive GRH has been found in extrahypothalamic sites and is rapidly degraded in the blood, the origin and molecular forms of circulating GRH in nomal human subjects have remained unanswered until the recent development of a highly sensitive enzyme immunoassay for plasma GRH, which demonstrates that hGRH in the peripheral blood is produced mainly by the gastrointestinal tract and pancreas in its three major molecular forms, hGRH (3-44) NH2, hGRH (1-44) NH2 and a hydrophobic, as yet unidentified, form of hGRH.抄録全体を表示PDF形式でダウンロード (2004K) -
肥塚 直美1992 年 68 巻 10 号 p. 1073-1081
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーInsulin-like growth factors bind to specific binding proteins (IGFBPs) in serum and tissues. At present, six different IGFBPs have been characterized. Recent studies suggest that IGFBPs act as a reservoir for IGFs but also modulate the bioavailability of IGFs. Binding protein for growth hormone (GH) in serum has been recognized recently. Interestingly, the high affinity GH binding protein (GHBP) is identical with the extracellular domain of GH receptor and is absent in patients with Laron-type dwarfism, suggesting that serum GHBP might serve as a marker for the GH receptor in tissue. In this short review, updated information on serum GHBP and IGFBP is presented.抄録全体を表示PDF形式でダウンロード (972K) -
田中 敏章1992 年 68 巻 10 号 p. 1082-1088
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーOne of the important aims of growth hormone (GH) treatment in GH deficient children is to allow them to grow to their full genetic potential. Usually, however, the final height of GH deficient children does not reach normal adult height and is below their target height. Furthermore, isolated GHD with spontaneous puberty is known to lead to a shorter adult height than that obtained in GHD associated with gonadotropin deficiency.
The height at the start of puberty is reported to be well correlated with final height in GHD. Therefore, when isolated GHD subjects treated with GH reached puberty while they were still shorter than normal, they ended up by being shorter than normal as adults. The trial to increase the GH dose during puberty did not seem to increase the final height. The gonadal suppression therapy combined with GH treatment significantly increased the final height in isolated GHD.
It is now the consensus that insufficient height at the onset of puberty leads to short final height and that early diagnosis of GHD is thus important to allow catch-up growth to optimal height before puberty. It may also be beneficial to treat GHD with higher doses to overcome the waning phenomenon with GH treatment.抄録全体を表示PDF形式でダウンロード (652K) -
石突 吉持, 広岡 良文, 村田 善晴, 谷川 俊一1992 年 68 巻 10 号 p. 1089-1095
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーWe reported a female case of painful thyroiditis occurring after hysterosalpingography and investigated whether the destructive thyroiditis was iodine-induced
The patient, aged 28, had TBG deficiency and the previous episode of thyrotoxicosis caused by Graves' disease. Lipiodol (containing 4.8g of iodide in 10ml solution) was administered via vagina for hysterosalpingography. One month after the radiography, serum inorganic iodide and Tg were elevated abnormally, but she was asymptomatic. After the subsequent 3 months she developed a painful and 3rd grade-sized goiter with concomitant marked elevation of thyroid hormones and inorganic iodide and also high titer of MCHA (3202X). A dramatic response was obtained with steroid. Thereafter she was treated with acupuncture on the thyroid gland, resulting in a sudden reappearance of tender goiter. This traumatic thyroiditis disappeared successfully in 2 weeks with steroid treatment. The painful thyroiditis subsided in 5 months throughout the course and she remained euthyroid for the ensuing 2 years. Aspiration biopsy was performed twice and revealed lymphocytic thyroiditis.
Values of serum Tg varied in good correlation with those of serum inorganic iodide or rT3 throughout the course, respectively (P<0.01, P<0.05). Significant correlations between FT4 and FT3, and also T4 and T3 were observed, respectively (P<0.01, P<0.05).Serum inorganic iodide was elevated to 316μg/dl at the symptomatic stage of the thyroiditis and decreased to 170μg/dl at the resolving phase 2 months after the inflammation. Iodide disappearance curve showed a diphasic slope. The BHL was calculated as 60.3 days during the symptomatic stage and 6.9 months in euthyroid state. Ten months after the administration of radiographic contrast media, serum inorganic iodide was 101.7μg/dl and the urinary excretion was 2974μg/day.
These findings suggested that this painful thyroiditis developed due to the administration of Lipiodol to a patient with underlying chronic thyroiditis.抄録全体を表示PDF形式でダウンロード (1016K) -
橋本 浩三, 西岡 達矢, 伊与田 孝一郎, 中山 富雄, 伊藤 裕之, 武田 京子, 高松 和永, 沼田 幸子, 小笠 貴司1992 年 68 巻 10 号 p. 1096-1111
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーTwo hundred and forty-one cases of isolated ACTH deficiency have been reported in Japan since 1969. Pituitary hormone responsiveness to stimulation tests before and after hydrocortisone supplementation was investigated in these cases.
Plasma ACTH level showed no or little change in response to lysine vasopressin, metyrapone, CRF or insulin-induced hypoglycemia in 97.3-100%of the cases. Serum GH level changed little or not at all in response to GRF, insulin-induced hypoglycemia, glucagon, 1-dopa and arginine in 26.9, 29.3, 40.0, 50.0 and 56.1%, respectively. Serum TSH and prolactin (PRL) levels showed hyperresponse to TRH in 34.7 and 35.6%, respectively. After hydrocortisone therapy, GH secretion was more responsive than before therapy in 78.9% of the cases. After supplementation, TSH level was less responsive to TRH stimulation than before therapy in 59.3% of the cases. After hydrocortisone supplementation, TSH response to TRH decreased in 75%of ACTH-deficient patients without primary hypothyroidism but did not decrease in more than half of those with primary hypothyroidism. TSH response to TRH decreased after supplementation in 76.5%of the patients with TSH hyperresponsiveness before therapy, and increased after therapy in 66.7%of those with normal TSH responses before therapy. After supplementation, PRL response to TRH was less than that before therapy in 43.5%of ACTH-deficient patients, and greater than that before therapy in 30.4%. PRL response to TRH decreased after therapy in 66.7%of the patients with PRL hyperresponsiveness before therapy, and increased in 63.6%of those with normal PRL response before therapy.
Primary hypothyroidism and Hashimoto's thyroiditis were complicated in 21.6 and 11.6%, respectively, of the 241 patients with isolated ACTH deficiency. In patients who had TSH hyperresponsiveness and/or high basal TSH levels and PRL hyperresponsiveness and/or high basal PRL levels, primary hypothyroidism was complicated in 58.4 and 42.3%, respectively. Hashimoto's thyroiditis was complicated in 29.8 and 20.5%, respectively, of these patients. Pituitary cell antibody (PCA) was detected in 36.6%of ACTH-deficient patients who were examined. Pituitary cell surface antibody (PCSA) to AtT-20 cells and GH3 cells was detected in 50.0 and 28.0%of the examined cases, respectively. The prevalence of PCA and PCSA did not differ between TSH-hyperresponsive patients and those with normal TSH basal levels and response, whereas PCA and PCSA were significantly more prevalent in PRL-hyperresponsive patients than in those with normal PRL levels and response. An empty sella was found in 30.2%of the examined case. The prevalence of empty sella was similar in patients with high or normal TSH levels and in those with high or normal PRL levels.
These results suggest that impaired GH response in ACTH-deficient patients is due mostly to hypocortisolism, and TSH hyperresponsiveness is caused by both hypocortisolism and primary hypothyroidism, while other factors are also responsible for PRL hyperresponsiveness in isolated ACTH deficiency.抄録全体を表示PDF形式でダウンロード (1650K) -
眞弓 克彦, 鈴木 晟時, 詫摩 哲郎, 五味 由加利, 近藤 弓子, 坂巻 隆男, 高慶 承平, 井上 健, 飯野 史郎1992 年 68 巻 10 号 p. 1112-1120
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーThe difference in the actute metabolic change in ketone bodies between patients with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) was investigated in this study. The subjects employed were 7 patients with IDDM losing residual insulin secretion and 7 patients with NIDDM matched to the former patients for age, body mass index, duration of diabetes, daily insulin dosage, fasting plasma glucose and HbA1c.
Blood samples were drawn at 3A. M. and 7A. M. on the same day, and plasma glucose, acetoacetic acid (AcAc), 3-β-hydroxybutylic acid (3-OHBA), free fatty acid (FFA), glycerol, cortisol and growth hormone (GH) concentrations were determined.
Plasma total ketone bodies (AcAc and 3-OHBA), 3-OHBA and FFA concentrations at 7A. M. were significantly higher in the patients with IDDM than in those with NIDDM (p<0.05), while there were no significant differences in any other parameters at 3A. M. between the patients with IDDM and those with NIDDM.
The ratios of 7A. M. value/3A. M. value of total ketone bodies, AcAc and 3-OHBA concentrations were also more significantly elevated in the patients with IDDM than in those with NIDDM. It was observed that the ratio of 3-OHBA was more than 2.0 in all of the patients with IDDM and less than 2.0 in all of the patients with NIDDM, the difference being significant with p<0.001. The reason why the concentration of total ketone bodies was elevated in the early morning only in the patients with IDDM but not in those with NIDDM was not certain, but it was thought that it is due to the absence of basal insulin secretion in the patients with IDDM.
These results indicate that 7A. M. value/3A. M. value ratio of plasma 3-OHBA will become one of the useful tools for differentiating IDDM from NIDDM.抄録全体を表示PDF形式でダウンロード (882K) -
原 秀雄, 伴 良雄, 佐藤 龍次, 石川 直文, 吉村 弘, 久岡 俊彦, 伊藤 國彦1992 年 68 巻 10 号 p. 1121-1129
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーWe evaluated the determination of serum G-CSF in the diagnosis of granulocytopenia due to methimazole (MMI) in 54 patients with Graves' disease, while they were being treated with MMI, by way of measuring WBC counts and serum levels of G-CSF, thyroid hormones, IgE, and interleukin-2. Serum TSH was measured by immunoradiometric assay, serum G-CSF was done by enzyme immunoassay, thyroid hormones and IgE were done by radioimmunoassay, and serum Interleukin-2 was done by enzyme-linked immunosorbent assay. The population whose G-CSF levels were higher than the minimum detectable level (30pg/ml) was 6 (30%) in normal subjects, 4 (22%) in patients with untreated Graves' disease, 2 (12%) in patients with treated euthyroid Graves' disease, 3 (23%) in patients with Graves' disease who had gone through agranulocytosis, and 2 (33%) in patients with Graves' disease complicated with granulocytopenia. There was no significant change in WBC counts for 4 weeks, but there was a significant difference between WBC counts before treatment and those at 8 weeks after treatment. We observed no significant change of serum G-CSF levels in patients with Graves' disease under treatment. However, there were significantly high levels of serum G-CSF and significantly low counts of WBC in patients with Graves' disease complicated with granulocytopenia induced by MMI, compared with those in normal subjects, patients with untreated Graves' disease, patients with treated euthyroid Graves' disease, and patients with euthyroid Graves' disease who had gone through agranulocytosis. We recognized a significant correlation between WBC counts (neutrophil counts) and G-CSF levels in the patients whose G-CSF levels were higher than the minimum detectable level.
We concluded that methimazole might influence the production of WBC in the bone marrow and serum G-CSF levels within 4 weeks during treatment, and that there was a feedback mechanism between G-CSF levels and WBC counts.抄録全体を表示PDF形式でダウンロード (747K) -
自験例副腎腺腫例1例と文献的考察中山 智祥, 相馬 正義, 久保 淳, 松岡 昌子, 阿部 好伸, 伊藤 みき, 渡辺 昌司, 渡辺 吉康, 泉 洋一, 八杉 忠男1992 年 68 巻 10 号 p. 1130-1149
発行日: 1992/10/20
公開日: 2012/09/24
ジャーナル フリーPregnancy in cases of Cushing's syndrome is rare. A pregnant patient with Cushing's syndrome due to an adrenal adenoma who was diagnosed in the third trimester is described. She underwent conservative treatment for Cushing's syndrome and delivered a normal infant by Caesarean section.
Currently, 121 pregnancies in 97 patients have been reported, but a principle for the treatment of the mother and fetus has not yet been established. We reviewed pregnancy in Cushing's syndrome based on the world literature and evaluated the choice of treatment to take. In the first trimester of pregnancy, therapeutic abortion or surgical treatment, such as adrenalectomy or resection of the pituitary tumor in Cushing's syndrome, is recommended for patients with severe hypercorticism (plasma cortisol?30μg/dl, urinary 17-OHCS≥15mg/day, urinary free cortisol?1000μg/day), while conservative treatment is recommended for patients with mild hypercorticism (plasma cortisol<30μg/dl, urinary 17-OHCS<15mg/day, urinary free cortisol<1000μg/day). In the second trimester of pregnancy, surgical treatment is recommended for patients with severe hypercorticism, while conservative treatment is recommended for patients with mild hypercorticism. In the third trimester of pregnancy, Caesarean section is recommended for most cases. Drug treatments such as with metyrapone should be limited to patients showing severe hypercorticism or a maternal high risk who have contraindications to surgical treatment.抄録全体を表示PDF形式でダウンロード (5261K)
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