Endocrinologia Japonica
Online ISSN : 2185-6370
Print ISSN : 0013-7219
ISSN-L : 0013-7219
26 巻, 1 号
選択された号の論文の19件中1~19を表示しています
  • YUKIO OCHI, TAKASHI HACHIYA, TADAYOSHI MIYAZAKI, YOSHIHIRO KAJITA, MAN ...
    1979 年 26 巻 1 号 p. 1-7
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    In an attempt to analyze thyroid stimulators in serum we developed an assay procedure using hTSH radioimmunoassay (RIA) in combination with receptor competition. The principle of this method is the determination by RIA of hTSH displaced by other thyroid stimulators from a thyroidal receptor preparation which previously bound unlabelled hTSH. Practically 4μU of hTSH were bound with human or bovine receptor, and then hTSH displaced by addition of test serum (0.1ml) or samples dissolved in serum (0.1ml) was measured by RIA.
    This assay can determine the thyroid stimulators other than hTSH in serum that has the displacement activity of 0.5-4.0μU of hTSH in the useful range, such as mU/ml level of bovine TSH ox rat TSH. Cholera toxin that has the thyroid stimulating activity like TSH also showed the displacement of the bound hTSH.
    This assay is not applicable for the human serum with more than 5μU/ml of TSH, because the assay value is over estimated by the free hTSH derived from the test serum. On the other hand, eighteen sera with high LATS activity and42sera with negative LATS activity from patients with untreated hyperthyroidism did not show any displacement. This might be due to the lower binding activity of LATS with hTSH receptor or the lower sensitivity of this assay method.
    Although it is difficult to use this assay clinically because of its low sensitivity, increased TSH in animal serum can be determined by this assay. The principle of this method may be also useful for examining the receptor binding of other peptide hormone that can be determined by an RIA method.
  • TETSUO NISHIKAWA, KEIJI MIKAMI, YASUSHI TAMURA, MASAHIRO YAMAMOTO, AKI ...
    1979 年 26 巻 1 号 p. 9-17
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The responses of the cylic AMP-generation system and corticosteroids biosynthesis to ACTH and angiotensin II and cholesterol and other lipid contents in adrenal tissues were estimated in the in vitro experiments in3cases of Cushing's syndrome due to ACTH-responsive and unresponsive adenomas, one case of Cushing's disease (diffuse hyperplasia), one case of primary aldosteronism and one normal subject.
    The responses of cAMP accumulation and corticosteroids production to ACTH in in vitro studies were quite in good agreement with the in vivo responses of plasma cortisol by ACTH infusion test. The adenylate cyclase activity decreased and the phosphodiesterase activity increased in the case of hyperplasia and in one case of ACTH-responsive adenoma, whereas the basal cyclic AMP content was slightly more in ACTH-responsive adenoma and maximal in hyperplasia compared with that of the normal adrenal tissue. The characteristic features observed in ACTH-unresponsive adenoma were the largest amount of the basal corticosteroids production and esterified cholesterol content, and the lowest content of cAMP. These results indicate that there was not always the consistent correlation between the cAMP-generation system, corticosteroids and aldosterone production, and conversion of cholesterol to pregnenolone by the stimulation of ACTH and angiotensin II in adrenal tumors.
  • TARO WASADA, TETURO SAKIMOTO, YOSHINORI ASO, KEN-ICHI KATO, HIROSHI IB ...
    1979 年 26 巻 1 号 p. 19-26
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    A case of a19-year-old, non-obese female with insulin resistant diabetes mellitus and polycystic ovary syndrome was reported. The maximal insulin requirement attained360units per day, but a satisfactory control of diabetes did not follow. The patient's serum contained not only anti-insulin antibodies, but also possible anti-insulin receptor antibodies which were demonstrated by the 125I-insulin binding test using insulin receptors derived from human placental plasma membrane. The insulin resistance in this case was assumed to be caused primarily by possible blocking antibodies to insulin receptors and partly by anti-insulin antibodies because of the following observations. First, high serum free insulin (165μU/ml) without hypoglycemia indicates the presence of insulin resistance due to other factors than antiinsulin antibodies. Second, the titer of 125 I-insulin binding capacity of serum was not unusually higher than those seen in chronically insulin-treated diabetics. Third, immunologically heterospecies insulin (fish insulin) was also ineffective.
    The clinical features such as absence of ketoacidosis and association with polycystic ovary syndrome resemble those of an unique diabetic syndrome reported previously though acanthosis nigricans and endogenous hyperinsulinemia were not found in this case.
    Her insulin resistance remitted spontaneously and over the next18months'observation, her diabetes remained regulated without insulin therapy.
  • NOBUHIKO TONOOKA
    1979 年 26 巻 1 号 p. 27-34
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Neonatal rats which had received a daily injection of 50μg of2, 4-dinitrophenol (DNP) or 30μg of L-thyroxine (T4) for7days beginning on the day of birth were compared as to the late effect of the hypothalamo-pituitary-thyroid axis with the neo saline control. Neo DNP rats and neo T4 rats revealed the retardation of growth compared with neo saline rats. The plasma level of TSH in both groups presented its low response following TRH administration. Furthermore, plasma TSH levels following the challenge of PTU were depressed in both neo DNP and neo T4 rats compared with neo saline control rats. A small dose of T4 injection, however, did not bring any difference on plasma TSH levels between neo T4 and neo saline control rats while neo DNP rats showed a little blunted response of pituitary compared with neo T4 and neo saline rats. Pituitary contents of TSH in neo T4 rats decreased, but not in neo DNP rats. These results suggest that neonatal hypermetabolism causes the hypofunction of pituitary-thyroid axis through adult life and that the alteration of hypothalamus may be more obvious in neo T4 rats than in neo DNP rats.
  • TSUNEO FUJITA, YOKO MATSUNARI, KOJI SATO, MUTSUKO HAYASHI, YUKICHI KOG ...
    1979 年 26 巻 1 号 p. 35-39
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Rats were given soybean trypsin inhibitor or repeatedly injected with pancreozymin (daily 40 I.D.U./kg) for 7 days, and the insulin and glucagon contents of the pancreas were measured. The insulin and glucagon contents were markedly increased after these treatments and this effect was especially conspicuous after injections of large doses (daily 120 I.D.U.) of depot-type pancreozymin. Insulin content thus reached 1.9times, and glucagon content 2.4times as much in control values. This result is compatible with our previous histological finding that not only the exocrine pancreas but also islet cells undergo the trophic effect of endogenous and exogenous pancreozymin.
  • MITSUYASU ITOH
    1979 年 26 巻 1 号 p. 41-58
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Effects of various hormonal and pharmacological manipulations on somatostatin distribution were investigated to elucidate the physiological significance of somatostatin in the hypothalamus and the other regions of the rat brain. Immunoreactive somatostatin (IRS) was measured by radioimmunoassay newly developed. Insulin induced an increase of hypothalamic IRS and a decrease of plasma RGH, while glucose administration resulted in the opposite responses, which were not significant.
    Insulin also increased IRS in the thalamus and the brain stem. The insulin-induced increase of hypothalamic IRS was reduced by hyperglycemia. Glucagon reduced IRS initially and then increased it with an elevation of plasma RGH. L-dopa did not affect hypothalamic IRS, although it decreased plasma RPRL. Phentolamine slightly increased plasma RGH and decreased IRS in most regions of the rat brain, while propranolol increased IRS in these regions. Pretreatment with propranolol significantly increased plasma RGH120min after insulin administration, and hypothalamic IRS decreased initially by pretreatment with propranolol, and then it increased significantly. When pretreated with propranolol, glucagon markedly increased plasma RGH and decreased IRS significantly. From these findings it is concluded that hypothalamic IRS may participate in the hormonal regulatory system in correlation to plasma RGH, as observed in studies on plasma GH and hypothalamic IRS following insulin, glucose, propranolol or phentolamine administration, but IRS in other regions of the brain may have some other actions as a neurotransmitter or a modulator, because of no significant correlation between plasma GH or PRL and IRS in these regions following various stimuli. In addition, glucose homeostasis and adrenergic mechanism may be important factors in regulating IRS in the rat brain.
  • RYOICHI TANAKA, TATSUO MATSUYAMA, KENJI SHIMA, NORIO SAWAZAKI, SEIICHI ...
    1979 年 26 巻 1 号 p. 59-63
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The composition, half life and hyperglycemic action of the porcine gastrointestinal glucagon-like immunoreactive materials were examined. Glucagon immunoreactivity (GI) measured using specific antiglucagon serum was more abundunt in the extract from the gastric fundus than in the one from the small intestine. When the extract from the gastric fundus was injected in dogs, the half life (T1/2) of total glucagonlike immunoreactivity (total GLI) measured using nonspecific antiglucagon serum was 9.5±1.1min (mean±SEM), which was longer than that of crystalline pancreatic glucagon, 3.4±0.2min, but shorter than that of the extract from the small intestine, 15.9±1.3min. On the other hand, T1/2 for GI from the gastric fundus was 5.1±0.9min, which was not significantly different from that of crystalline pancreatic glucagon. Blood sugar levels were significantly increased from the basal by 25±mg/100ml at 10min and 19±4mg/100ml at 15 min following an injection of the extract from the gastric fundus, but such a change in blood sugar levels was not demonstrated when the extract from the small intestine was injected. These results suggest that GI of the gastric fundus is close to pancreatic glucagon in respect of its metabolism and hyperglycemic activity.
  • HIROSHI KAJINUMA, YASUNORI KANAZAWA, HIROYUKI SANDO, MASAKI HAYASHI, S ...
    1979 年 26 巻 1 号 p. 65-73
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The correlation between plasma C-peptide immunoreactivity (CPR) and immunoreactive insulin (IRI) was investigated during the oral glucose tolerance test in 20 normals, 127 diabetics, and 39 non-diabetics with chronic liver or renal disorders. When all subjects were included, the increment of CPR 30 minutes after glucose load (4CPR) correlated well with that of IRI (ΔIRI)(r=0.66, p<0.001), but the return of CPR towards the basal level was delayed as compared with IRI. The positive correlation was also observed between the sum of 6 IRI and that of6CPR values during the glucose tolerance test in diabetics and controls (r=0.53, p<0.001).ΔCPR/ΔBS (30min.) was also well correlated with ΔIRI/ΔBS (30min.), and was specifically low in diabetics.
    Insulin-treated maturity-onset diabetics showed low but considerable CPR responses while no CPR responses were observed in insulin-treated juvenile diabetics.
    In each plasma sample, CPR always exceeded IRI on the molar basis. At fasting CPR/IRI ratio was 15.6±1.7 (mean±SE) in normals and 14.9±1.3-16.9±1.0 in diabetics. In chronic liver diseases IRI response was augmented while CPR response was not different from that of controls, and the molar ratio of CPR/IRI was significantly low (9.5±1.1). On the contrary, it exceeded that of normals in chronic renal diseases (35.7±14.9).
    It is concluded that, first, the plasma CPR response appears to be a valuable indicator of pancreatic B-cell function, and second, it is, nevertheless, modified in chronic liver or renal disorders.
  • NORIKO MURAKAMI, AKIO YOSHIDA, SHOGO ICHII
    1979 年 26 巻 1 号 p. 75-80
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    To examine the binding specificity of steroid hormone-cytoplasmic receptor complexes to nuclei, binding of 3H-dexamethasone (Dex)-liver, 3H-Dex-thymus and3Hdihydrotestosterone (DHT)-prostate receptor complexes to nuclei from liver, prostate, thymus, spleen and kidney was studied. It was observed that a significant amount of steroid-receptor complexes was bound to any nuclei used in the present study and the extent of the binding of receptor complexes to nuclei from homologous tissues was not always greater than that to nuclei from heterogenous tissues. However, a significant portion of the 3H-Dex-liver and 3H-DHT-prostate receptor complexes was not absorbed by nuclei from kidney, spleen and thymus, and the unabsorbed complexes were efficiently bound to liver and prostate nuclei. The results obtained indicate that two types of receptor complex with regard to nuclear binding were present in cytosols of liver and prostate one binds to nuclei from kidney, spleen, thymus, liver and prostate and the other does not bind to nuclei from kidney, spleen and thymus but does bind to nuclei of liver and prostate. The latter type of receptor complex was not observed in the cytosol from the thymus.
  • KOHEI YAMAGUCHI, HIDEO FUKUSHIMA, HARUO UZAWA
    1979 年 26 巻 1 号 p. 81-88
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Serum HGH, PRL and TSH responses to intravenous injection of 500μg of TRH were investigated in nine patients with liver cirrhosis and in patients of the same number with diabetes mellitus who served as controls. They were roughly matched in age, sex and body weight. The basal serum HGH levels in the cirrhotic group were significantly high with a value of 4.7±1.7ng/ml compared to the values of 1.5±0.9ng/ml in the control diabetic group. Serum HGH levels in the cirrhotic group at 15, 30, 60 and 90min intervals after TRH were significantly higher than the basal serum HGH levels. The control diabetic group showed no positive response. Similar responses were observed again in three subjects of the cirrhotic group after treatment for hepatic insufficiency. Two subjects of the cirrhotic group showed an elevation of serum HGH in response to TRH even under hyperglycemia induced by glucose administration. The basal serum PRL levels were identical in both groups. The serum PRL levels in both groups evidently increased in response to TRH with significantly higher response in the cirrhotic group than in the control diabetic group at15, 30 and 60min intervals after TRH. There was no significant difference in the basal levels of serum TSH or the levels after TRH between both groups. It was concluded that the serum HGH levels in cirrhotic patients were elevated by TRH. Since the response was independent of clinical severity, the possibility exists that it could be attributed to some basic metabolic abnormality of the underlying liver cirrhosis. Since the abnormal HGH response to TRH was not seen in the control diabetic group and was not altered by hyperglycemia in the cirrhotic group, an abnormality of the glucose metabolism was eliminated as a possible cause.
  • KENGO NAGAOKA, TAKEHIKO SAKURAMI, NOBORU NABEYA, HIROO IMURA, SHOTARO ...
    1979 年 26 巻 1 号 p. 89-95
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The leucocyte migration inhibition test (LMT) was performed by the agarose plate method with thyroid and pancreatic antigens in patients with insulin-dependent or independent diabetes mellitus. The mean migration indices with thyroglobulin, thyroid mitochondria and beef insulin were not significantly different in insulindependent diabetics from those in insulin-independent diabetics or normal controls.
    However, significant inhibition of leucocyte migration was observed in insulindependent diabetics when thyroid microsome or pancreatic extract was used as antigen. Although no significant difference was found in the percentages of T and B lymphocytes between insulin-dependent diabetics and insulin-independent diabetics or normal controls, the results of LMT strongly suggest the presence of cellular immunity against the thyroid and pancreas in insulin-dependent juvenile-onset diabetes.
  • HIDETOSHI YAMANAKA, MASANORI MATSUOKA, HISAKO YUASA, ATSUSHI KOYA, KYO ...
    1979 年 26 巻 1 号 p. 97-102
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Tne binding of 5α-dihydrotestosterone to the hypophyseal and hypothalamic cytosol macromolecules prepared from castrated male rats was observed. The effects of antiprostatic agents on 5α-dihydrotestosterone binding to both hypophyseal and hypothalamic cytosol macromolecules was examined. Cyproterone acetate and chlormadinone acetate Showed the significant inhibiting effects on 5α-dihydrotestosterone binding to 7-8 S macromolecules of cytosol from both hypophysis and hypothalamus. SCH 13521 and AA 560 did also affect 5α-dihydrotestosterone binding to 7-8 S macromolecules of cytosol from both tissues.
  • Kozo HASHIMOTO, SHO YUNOKI, JIRO TAKAHARA, TADASHI OFUJI
    1979 年 26 巻 1 号 p. 103-109
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HYCRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0, 0165 HE/ml and 0.5HE/ml. Relatively high doses of lysine-vasopressin showed a slight additive effect onl the release of ACTH induced by 0.1HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrottopin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, β-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and γ-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
  • MASAYOSHI YAMAGUCHI
    1979 年 26 巻 1 号 p. 111-115
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The effects of calcitonin (CT) and other hormones on the bile calcium excretion after a single intraperitoneal administration of calcium (4.0mg/100g BW) was investigated in thyroparathyroidectomized rats. Porcine, salmon, and synthetic eel CT (80MRCmU/100g BW, respectively) markedly increased the bile calcium excretion in comparison with that of calcium-administered rats. Tetragastrin (7.5μg/100g BW), and insulin (50mU/100g BW) did not alter significantly the bile calcium excretion, while epinephrine (100μg/100g BW), glucagon (50μg/100g BW), and parathyroid hormone (25U/100g BW) increased significantly. The increasable effect of CT on the bile calcium excretion was significantly prevented by epinephrine (10 and 100μg/100g BW). The present results suggest that the bile calcium excretion may be increased by the hormones which causes the elevation of cyclic AMP in the liver cells of rats.
  • TERUHIKO TAMAYA, NORIO FURUTA, YOUSUKE OHONO, NORIMASA IDE, TOSHIHIDE ...
    1979 年 26 巻 1 号 p. 117-122
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    This study was designed to investigate the chromatin transcription in vitro by progesterone-receptor complex in the estrogen-primed rabbit uterus. RNA synthesis by the uterine chromatin was stimulated when progesterone-uterine cytosol complex was bound to the chromatin and the stimulation was dependent upon the dose of the bound progesterone-cytosol 8S complex and upon the incubation time of the complex in the presence of the chromatin. Either norethindrone-or dydrogesteroneuterine cytosol complex also stimulated the uterine chromatin transcription but the extent was less than that of progesterone complex. These results indicate that progesterone as well as synthetic progestogens can directly regulate chromatin tran scription via progesterone receptor in the rabbit uterine cells.
  • KENICHI IMAGAWA, TOMOYOSHI NISHINO, SADAHITO SHIN, SHIGERU UEHATA, ETS ...
    1979 年 26 巻 1 号 p. 123-131
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The C-terminal region-specific anti-glucagon sera were raised in rabbits using as immunogen, a conjugate of BSA and a C-terminal fragment of pancreatic glucagon. The hapten was prepared by trypsin digestion of the glucagon, which was proved to be a 1: 3 mixture of glucagon (18-29) and (19-29). Six rabbits were immunized by subcutaneous injection of an emulsion of the conjugate with complete Freund's adjuvant and five of the rabbits produced antibodies to the glucagon (GC-1, GC-2, GC-3, GC-5 and GC-6). For comparison, rabbit antisera were also produced against glucagon polymer (GA-10) and syrupy glucagon fibrils (PGA-2). All these antisera as well as the pancreatic glucagon-specific antiserum 30K were characterized with dog gut-extract (gut-GLI) and glucagon-related peptide fragments in the radioimmunoassay systems. The assay systems utilized 125I-monosubstituted pancreatic glucagon as tracer and human mono-component glucagon as standard. All sera of the GCseries crossreacted with the dog gut-extract very weakly and antisera GC-5 and GC-6 exhibited the lowest crossreactivities with the extract, which were shown to be as low as that of 30k. Characterization of the antiserum GC-5 with purified glucagonrelated fragments indicated that the major antigenic determinant located exactly in the C-terminal region of glucagon. The present results clearly showed high efficiency of the use of the glucagon C-terminal fragment as haptenic immunogen in obtaining the C-terminal region-specific, i.e., pancreatic glucagon-specific antisera.
  • YOSHIAKI OKADA, KAZUO WATANABE, TORU TAKEUCHI, TOSHIO ONISHI, KIYOJI T ...
    1979 年 26 巻 1 号 p. 133-136
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The relation between height increment and food intake in 21 growth-hormonedeficient patients was studied in comparison with 10 normal and 13 constitutionally short children. Total calory of food intake and height increment were 64.6±18.6 Cal/kg/day and 7.31±2.53cm/year in normal children, 71.4±17.7Cal./kg/day and 6.13±1.52cm/year in constitutionally short children and 64.59±29.14Cal/kg/day and 5.29±1.11cm/year in HGH-deficient patients who were given HGH at a small dose ranging from 0.17 to 0.375 (0.248±0.064) IU/kg/week. Distribution of carbohydrate, protein and fat did not show any significant difference in relation to the total calory. A significant correlative relation between food intake and height increment was noted in normal children (r=0.748p<0.01) and in children with constitutionally short stature (r=0.7005p<0.005). Food intake by which to be able to expect normal prepubertal or pubertal growth is likely to be more than47.3Cal/kg/day. In a group of16HGH-deficient patients who had food intake ranging from 26.9 to 78 Cal/kg/day, a significant correlation between food intake and height increment was observed (r=0.473p<0.05), but in5patients who had food intake with more than 80 Cal/kg/day, height increment was not related to food intake but ranged from 5.4to 6.3cm/year. In a group of HGH-deficient patients who had food intake ranging from26.9 to 78 Cal/kg/day, the food intake of9responders to HGH (56.55±10.34 Cal/kg/day) was significantly more than that of 7 non-responders to HGH treatment (42.0±11.8Cal/kg/day), despite no statistically significant difference in HGH dose between responders and non-responders. These data suggest that the decreased food intake is one of the causative factors which induce unresponsiveness to HGH in HGH-deficient children who are treated with a small dose of HGH.
  • RITSUJI YAMADA, JIN SATO, EIZO KOMIYA
    1979 年 26 巻 1 号 p. 137-140
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    Considering that the determination of chromogranin levels in the blood for the diagnosis of pheochromocytoma will provide clinically useful information, an attempt was made to establish the serological assay system for blood chromogranin, and also chromogranin levels in the blood of normal subjects, patients with essential hypertension and a patient with pheochromocytoma were studied.
    Chromogranin was isolated and purified from the granular internal fluid of the catecholamine storing vesicles of the pig adrenal glands. The antibodies against chromogranin and the chromogranin-sensitized sheep red blood cells were prepared; and chromogranin levels in the blood were determined by the passive hemagglutination inhibition reaction (PHI), using the microtiter system.
    As it was observed in the determination of chromogranin levels in the blood by PHI that globulin fractions gave rise to nonspecific agglutination by this reaction system, the serum samples were pretreated by the salting-out method with ammonium sulfate into the albumin fraction, on which PHI was performed.
    Chromogranin levels in the blood of 41normal subjects and 12 patients with essential hypertension in terms of inhibition values of PHI were distributed chiefly in the range from 1: 20 to 1: 80. The level in the blood of one patient with pheochromocytoma was 1: 640, whose titer was obviously higher than the titers in the blood of normal subjects and patients with essential hypertension. These evidences suggest that the determination of chromogranin levels in the blood will provide useful information for the diagnosis of pheochromocytoma.
  • MICHIO MIYAZAKI, KAZUHIKO YASUMURA, SATOSHI II, YASUAKI TAKATA, TOSHIA ...
    1979 年 26 巻 1 号 p. 141-145
    発行日: 1979年
    公開日: 2011/01/25
    ジャーナル フリー
    The response of serum prolactin (PRL) to thyrotropin-releasing hormone (TRH) was evaluated by radioimmunoassay in 6 normal women and44breast cancer cases. They were divided into the following 5 groups: group 1:6 normal women; group 2:10 preoperative patients with early breast cancer; group 3:13 preoperative patients with advanced cancer; group 4:13 postoperative patients with no recurrence of cancer for more than 2 years; group 5:8 postoperative patients with cancer recurrence.
    The maximum increment of serum PRL levels following the administration of TRH was significantly higher in groups 2, 3 and 5 than in groups 1 and 4. These results indicate that patients with recurrent breast cancer have a higher PRL response to TRH than those without recurrence of cancer.
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