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59 巻, 3 号
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森本 妙子, 青山 正明, 後藤 英司, 塩之 入洋1983 年 59 巻 3 号 p. 215-229
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーSeveral methods for determination of angiotensin II (AII) in human plasma had been reported. Most popularized method was extraction method using Dowex (H+) resin. Direct method and extraction method using acetone-petroleum ether were also used. However these methods have several defects, such as intricate procedure, low sensitivity or low rate of extraction. Therefore we developed a new method for AII in human plasma which was used florisil adsorption and elution with acetone-hydrochrolic acid solution.
In our method compared with the method using acetone-petroleum ether or the direct method, the extraction rate was 84% and minimum detectable value was 0.75pg/tube (B/Bo 95% intercept value).
Reproducibility of intra-assay and inter-assay were 11.7% and 12.9%, respectively. This our method was more sensitive, specific and simple, and was useful for routin clinical investigation.
We studied the untreated 21 patients with essential hypertension (containing 11 males and 10 females, their averaged age was 41.5 years old, and blood pressure on admission was 175.8/112.5mmHg).
We measured plasma renin activity (PRA) and AII (florisil-method) in venous blood before and after intravenous injection of 20mg furosemide and oral administration of 25mg captopril. After the furosemide administration, All in venous blood significantly increased to 35.0 8.0pg/ml (Mean±SE) from 14.6±2.6pg/ml (p<0.001), and PRA also increased to 2.40 0.89ng/ml/hr from 0.92±0.21ng/ml/hr. Although after captopril administration PRA significantly increased to 2.56±1.02ng/ml/hr from 1.05±0.32ng/ml/hr (p<0.01), All decreased to 8.2±2.2pg/ml from 15.2±3.1pg/ml (p<0.001). Moreover, All levels in arterial and venous blood were 27.8±7.8pg/ml and 28.8±6.7pg/ml, respectively.抄録全体を表示PDF形式でダウンロード (908K) -
野津 和巳, 桜美 武彦, 平田 正名, 後藤 康生, 野手 信哉, 野津 吉友, 国司 博行, 遠藤 治郎1983 年 59 巻 3 号 p. 230-240
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーCirculating thyroid antibodies are important markers for detecting autoimmune thyroid diseases. A survey was conducted in Daiwa Village, Shimane Prefecture, to determine the incidence of significant asymptomatic autoimmune thyroiditis, in a rural population. One thousand two hundred and forty-two people were examined in the survey. The incidence of overt thyroid disorders was 3/570 males and 12/672 females. Eight were cases of hyperthyroidism and three were diffuse or nodular goiter. Three were postoperative cases of struma, including thyroid cancer, and the other one was that of overt hypothyroidism. We examined antithyroglobulin antibodies (TG) and thyroid microsomal antibodies (MS), excluding 15 patients with overt thyroid diseases. TG and MS were measured by the tanned red cell hemagglutination technique, using commercially available kits, Thyroid Test and Microsome Test (Fuzi Zoki, Tokyo). Eight of 567 (1.4%) males were positive for TG and 32 (5.6%) were positive for MS. Twenty-five of 660 (3.8%) females were positive for TG and 73 (11.1%) were positive for MS. The incidence of TG and/or MS was higher in females. Age-specific prevalence of antithyroid antibodies gradually increased in those over 40. We examined the serum cholesterol levels in subjects with thyroid autoantibodies and also in controls and we found no statistical significance. The serum TSH levels were also studied. 3.9pU/ml, which was the mean serum TSH level in subjects with thyroid autoantibodies, was significantly higher than 2.3μU/ml, such being the mean serum TSH level in controls matched according to sex and age (p<0.01). There was a correlation between the serum TSH levels and the titers of thyroid microsomal antibodies.
Four had high levels in the serum thyrotropin (>10/μU/ml), that is 20.1, 18.0, 15.7 and 10.8μU/ml. All were positive for MS and the only one of four was positive for TG. These patients were re-examined for clinical signs of thyroid disorders. We palpated a small goiter in one and tentative diagnosis of Hashimoto's thyroiditis was made. The other three seemed to be cases of significant asymptomatic autoimmune thyroiditis. We consider that detection of MS may be more pertinent than that of TG.抄録全体を表示PDF形式でダウンロード (998K) -
弓田 滋, 古川 洋太郎, 佐々木 厚, 孫 孝義, 海上 寛, 三浦 良, 吉永 馨1983 年 59 巻 3 号 p. 241-247
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーA 29-year-old man came to our hospital with tetany and sensorineural deafness. Routine laboratory testing revealed a serum calcium of 5.5mg/d1 and a serum phosphate of 6.1mg/d1. The level of circulating immunoreactive parathyroid hormone was undetectable, and he showed hyperresponsiveness to the exogenous parathyroid hormone (synthetic hPTH (1-34), 100U). Thus, he was diagnosed as having idiopathic hypoparathyroidism. The other endocrine functions were normal. The parathyroid antibody was negative and no moniliasis was found. On the examination of his family, it was found that his male sibling and one of his female siblings also had hypocalcemia (6.4mg/d1 and 6.0mg/d1) and undetectable levels of circulating immunoreactive parathyroid hormone, and all his siblings, his father and one of his nieces had sensorineural deafness, so he was diagnosed as having familial idiopathic hypoparathyroidism and familial progressive sensorineural deafness. In addition to this case, we have experienced two siblings of another family having the same combination of these disorders (unpublished observation). Since familial idiopathic hypoparathyroidism is not common, it seems that the present combination of these disorders is not a chance association抄録全体を表示PDF形式でダウンロード (614K) -
柳沼 健之, 橋本 重厚, 水野 兼志, 小川 さつき, 春山 和見, 福地 總逸1983 年 59 巻 3 号 p. 248-256
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーA male diabetic patient aged 53 years with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is described.
The patient had a seven-year history of diabetes mellitus, which was regulated with dialy injections of NPH insulin, 14 units, for six years. He was well until general fatigue and emaciation developed and he entered to our hospital.
On admission, he complained of general fatigue. His height was 163 cm and his weight was 37 kg. The 100 gram oral glucose tolerance test indicated a diabetic pattern (blood sugar; 0'; 205 mg/dl, 30'; 345 mg/dl, 60'; 410 mg/dl, 120'; 485 mg/dl). The funduscopic findings showed diabetic retinopathy (Scott II°). The direct and indirect light reflexes were slow in both eyes. The patellar and Achilles' tendon reflexes were weakened in both legs. The motor nerve conduction velocity of the right median nerve was 36 m/sec (normal range; 47-66 m/sec). These data indicated the presence of diabetic neuropathy.
The biochemical findings disclosed hyponatremia (110 mEq/l), hypochloremia (82 mEq/l), normokalemia (4.0 mEq/l), low serum osmolality (222 mOsm/l) and high urine osmolality (504 mOsm/l). The creatinine clearance was 80.3 ml/min and the P.S.P. test (15') was 25.5%. A high plasma antidiuretic hormone (ADH) level of 9.8 pg/ml was detected, in spite of low serum osmolality (250 mOsm/l). There was no relation between the serum osmolality and plasma ADH levels. In the water loading test (30 ml/kg), urine volume for 4 hours was only 19% of the loaded water (normal range; more than 80%), the free water clearance failed to rise and plasma ADH was not suppressed. In the water-ethanol loading test (water; 30 ml/kg, ethanol; 0.45 ml/kg), the urine volume for 4 hours was 64% of the loaded water, the free water clearance rose to +2.04 ml/min and plasma ADH fell to 2.5 pg/ ml from 8.4 pg/ml.
A low plasma renin activity of 0.1 ng/ml/h and increased circulating plasma volume of 62.9 ml/kg were detected. A chest X-ray and brain CT scan were normal.
The patient was diagnosed as having diabetes mellitus with idiopathic SIADH from the above findings. He was treated by the restriction of water intake to 800 ml/day for two months, besides diet-therapy (1200 Cal/day) and a daily injection of 18 units of soluble insulin. As a result, serum sodium rose to 141 mEq/1 and serum osmolality increased to 288 mOsm/l. The graded increase of water intake for three months did not decrease the serum sodium and the osmolality. Both the water loading test (urine volume for 4 hours; 94%, the free water clearance; +4.01 ml/min) and the motor nerve conduction velocity (47 m/sec) had improved, despite the free water intake for six months.
The clinical course and the biochemical findings of this patient suggest that the diabetic neuropathy induced SIADH through the impaired afferent nerves from the osmoreceptors.抄録全体を表示PDF形式でダウンロード (795K) -
人工膵島システムの応用菊池 幹雄1983 年 59 巻 3 号 p. 257-272
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーAn exaggerated rise in plasma glucagon (IRG) during stimulation by intravenous arginine infusion is one of the characteristic abnormalities in diabetes mellitus. Since the administration of insulin lowers the exaggerated IRG responses to arginine, this abnormality is thought to be secondary to insulin deficiency. However, in previous reports the doses and patterns of insulin administration were variable, and the normalization of glucose and plasma insulin profiles during arginine infusion was not achieved. Thus the effect of each factor to normalize exaggerated IRG responses has not been clarified.
In the artificial endocrine pancreas (AEP) that we originally developed, the perfect physiological normalization of blood glucose and plasma insulin profiles can be achieved in diabetes mellitus, and in addition, optimal glycemic clamp becomes possible with the operation of glucose infusion algorithm. To clarify whether the physiological blood glucose and plasma insulin profiles can normalize the exaggerated IRG responses and to qualify the effect of each of the glycemic excursions and insulin profiles, the following 4 investigations were conducted in each of 7 nonobese noninsulin-dependent diabetes mellitus (NIDDM) patients and 8 insulin-dependent diabetes mellitus (IDDM) patients with the aid of AEP.
Arginine was iv infused into both diabetic groups according to the following protocol : 1) in a hyperglycemic state without insulin infusion, 2) in perfect glycemic control by AEP, 3) in glycemic control by AEP with lower plasma insulin profiles (parameters of insulin in-fusion algorithm were made smaller than 2)), 4) in a hyperglycemic state with physiological plasma insulin profiles (blood glucose was clamped in the same way as 1) with glucose in fusion algorithm by AEP, and insulin infusion obtained in 2) was operated with a preprogrammable insulin infusion pump). The changes in plasma glucagon responses in each experiment were compared with those seen in healthy subjects.
It was revealed that IRG responses were completely normalized in 2) and 4) in both NIDDM and IDDM, of which plasma insulin profiles simulated those of healthy subjects whether hyperglycemia existed or not, but in 1) and 3), in which plasma insulin concentration was not detectable or low, marked hyperresponses of IRG were recognized.
In summary, it is clearly proven with this series of experiments that the exaggerated response of A-cell to arginine in insulin-deficient diabetes mellitus is secondary to insulin deficiency, and its normalization is dependent on physiological insulin concentrations whether hyperglycemia exists or not.抄録全体を表示PDF形式でダウンロード (1338K) -
ブドウ糖およびグルカゴン注入アルゴリズムの作成笹井 智令1983 年 59 巻 3 号 p. 273-286
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーTo accomplish an artificial endocrine pancreas system by adding a glucose and glucagon infusion mechanism in the artificial beta cell developed originally in the First Department of Medicine, Osaka University Medical School, glucose and glucagon infusion algorithms were invented.
The principle of glucose or glucagon infusion algorithm is determined as the proportional plus derivative modes of action to blood glucose concentration with a time delay constant, as follows :
GIR (t) = Cp [BGp - BG (t-T)] + Cd [-_??_BG (t-T)]
GnIR (t) = Gp [BGp - BG (t-T)] + Gd [-ABG (t-T)] + Gc where GIR (t) and GnIR (t) are the glucose infusion rate (mg·kg-1min 1) and glucagon infusion rate (ng.kg-1.min-1), respectively. BGp is the projected value of blood glucose concentration (mg/100ml), and BG (t) and _??_BG (t) are blood glucose concentration at time t (mg/ 100ml) and the rate of change in blood glucose concentration at time t (mg·100ml-1), respectively. Cp and Cd are coefficients for glucose infusion, and Gp and Gd are those for glucagon infusion. Gc is the constant for basal glucagon infusion supplementation. T (min) is the time delay constant for glucose and glucagon infusion.
The validation of these algorithms were attempted in depancreatized dogs. In dogs, hypoglycemias were induced by iv bolus insulin injections, then a counterregulatory system was operated according to each of these algorithms.
The following results were obtained :
1) When glucose was infused on the basis of the proportional action with a 20-min time delay (Cp/Cd/T = 0.2/0/20), the insulin-induced hypoglycemia in depancreatized dogs could be restored to normoglycemia in the same manner as seen in normal dogs.
2) A speedier and less fluctuating restoration to normoglycemia could be obtained when the glucose was infused on the basis of a proportional plus derivative mode of action with a 4-min time delay (Cp/Cd/T = 0.5/0.5/4).
3) In glucagon infusion algorithm, with the optimal parameters based on proportional plus derivative modes of action with a 10-min time delay (Gp/Gd/Gc/T = 0.2/0.4/0.4/10), both the blood glucose response curves and plasma glucagon profiles simulated perfectly those seen in normal dogs.
4) When glucagon was infused on the basis of proportional plus derivative modes of action without the time delay (Gp/Gd/Gc/T = 0.5/0.5/0.4/0), hypoglycemias rarely occurred in spite of iv insulin injections with the least glucagon infusion amount.
These results clearly indicate that an artificial endocrine pancreas system characterized with glucose or glucagon infusion algorithm constitutes a clinically useful device not only as a safety control against hypoglycemia, but it also enables adaptive and optimal glycemic controls. In addition, by applying these algorithms, an artificial endocrine pancreas system becomes a powerful research tool for such investigations as the dynamic property of the pancreatic a cell in glucagon secretion against blood glucose, the analysis of the effects of hormones on the glucoregulatory system and for the glucose clamp method.抄録全体を表示PDF形式でダウンロード (1337K) -
藤澤 由樹, 貴田 嘉一, 松田 博, 清水 達雄, 美濃 真, 鬼満 雅, 渡辺 鍾蔵, 川口 幸義1983 年 59 巻 3 号 p. 287-294
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーMyositis ossificans progressiva (MOP) is characterized by progressively developing ectopic ossification on the connective tissues of muscles and skin. Histologically, osteoblastic bone formation and osteoclastic bone resorption take plase on the affected connective tissues. No endocrine and metabolic disorders have been found to account for the ectopic ossification in MOP.
It is well established that vitamin D metabolites play a role in the regulation of the metabolism of bones, and therefore a disorder of vitamin D metabolism may cause metabolic bone disease. This study was performed to investigate the involvement of vitamin D metabolism in the development of MOP.
Five patients with MOP (MOP group) from six to sixteen years of age and fifty-one healthy subjects (control group) from five to nineteen years of age participated in this study after informed consent was obtained. Concentrations of 25-hydroxyvitamin D3 (25- (OH) Vit D3), lα, 25-dihydroxyvitamin D3 (la, 25- (OH) 2-Vit D3) and 24, 25-dihydroxyvitamin D3 (24, 25- (OH) 2 -Vit D3) in the blood were measured by competitive protein-binding assays and that of vitamin D binding protein (DBP) in the blood by a single radial immunodiffusion method.
The serum concentration of lα, 25- (OH) 2 -Vit D3 in MOP group was 68.9±5.2pg/ml, which was significantly higher than that of the control group which was 41.9± 2.1pg/ml (p<0.001). There were no significant differences in serum concentrations of 25- (OH) -Vit D3, 24, 25- (OH) 2-Vit D3 and DBP between the normal and MOP groups.
The serum level of phosphorus in the MOP group was 5.48± 0.32mg/dl and it was significantly high compared with that of the control group which was 4.28±0.12mg/dl (p<0.005), while the serum level of calcium did not show any significant difference between the normal and MOP groups. No changes in the parathyroid hormone and calcitonin in the blood were observed in the MOP patients.
These data indicate that the increased level of phosphorus in the blood, which might be resulted from the high concentration of 1α, 25- (OH) 2-Vit D3 in the blood, may have caused the ectopic ossification on the connective tissues with a sufficient supply of calcium. The reason why 1α, 25- (OH) 2 -Vit D3 in the blood is increased in patients with MOP and how it leads to the ossification of connective tissues still remains unknown.抄録全体を表示PDF形式でダウンロード (702K) -
高松 順太1983 年 59 巻 3 号 p. 295-303
発行日: 1983/03/20
公開日: 2012/09/24
ジャーナル フリーProlonged elevation of serum Triiodothyronine (T3) concentrations with normal serum Thyroxine (T4) levels are occasionally found during the course of drug therapy for Graves' disease; however, little is known regarding the preferential secretion of T3. In order to investigate the pathogenesis and clinical significance of the elevated T3 to T4 ratios, 42 patients who had persistently shown this phenomenon were studied. Some therapeutic methods were employed to observe the responses in these patients.
Following increase in doses of thionamides, serum T3 fell to normal levels; however, T4 levels simultaneously showed a decrease to levels which were lower than normal. As a result, the T3 to T4 ratios remained elevated. Changing the type of thionamide did not affect the elevated ratios. Addition of iodide to the therapy did not change the altered ratios. On the other hand, the patients who were subsequently treated by subtotal thyroidectomy showed normalization in the ratios.
The goiter size of these patients were significantly larger than those of the control group patients whose serum T3 to T4 ratios were within the normal range. Activities of TSH receptor antibodies in these patients were higher than those in the control group of Graves' disease. In addition, the serum T3 to T4 ratio and TSH receptor antibody activity showed a significant correlation.
Follow-up studies for two to four years of drug therapy revealed that prolonged remissions hardly occurred in patients whose serum ratios remained elevated. In all patients whose serum ratios fell to normal following subtotal thyroidectomy, remissions occurred and persisted.
These observations indicate that the prior site of preferential production of T3 is not in peripheral tissues but exists in the thyroid gland itself. Furthermore, the present study suggests that the T3 to T4 ratios may be utilized as a useful indicator in predicting the relapse after cessation of drug therapy and as a parameter in choosing optimal therapy for Graves' disease.抄録全体を表示PDF形式でダウンロード (812K)
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