摘要:

Growth hormone (GH) was measured in 215 short children (147 males and 68 females, 123 prepubertal, 92 at early pubertal stages), comparing GH responses to classical pharmacologic stimulation tests and spontaneous GH secretion during sleep. GH secretion during sleep, but not GH responses to stimuli, was higher in early pubertal than in prepubertal subjects. The patients were classified into five groups, according to the agreement between GH responses to stimuli and GH secretion during sleep: group I, normal GH-secreting children; group II, completely GH-deficient; group III, partially GH-deficient; group IV, with normal secretion during sleep and low responses to stimuli; group V, with the reverse situation. 30% of the patients were in groups IV and V, both at prepubertal and early pubertal stages. 46 patients of groups II-V were treated with extracted human GH( hGH). The growth rate was enhanced in groups IV and V, to the same extent as in groups II and III. Four points can be concluded: (1) the rise of GH secretion during sleep is an early event at the onset of puberty; (2) the discrepancy between the GH responses to classical stimuli and GH secretion during sleep are of pathological significance; (3) disturbances of GH secretion might be diagnosed by measuring GH secretion during sleep rather than by using conventional stimulation tests; (4) a trial course of hGH treatment could be proposed in patients with both kinds of discrepancies between GH responses to stimuli and GH secretion during sleep.

ISSN:1663-2818    

DOI:10.1159/000180989

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In 10 patients with idiopathic growth hormone (GH) deficiency (9 boys and 1 girl, aged 7.5–14.5 years, mean 12.1 ± 2.2 years), urinary 15N-balance studies were performed before and on recombinant hGH (2 × 3 IU/m2 of body surface area subcutaneously on consecutive days). Before and on the 2nd day of recombinant hGH, 99% 15N-labeled ammonium chloride (0.05 g/kg, divided in 3 doses per day, corresponding to 389 ± 30 mg/m2 of 15N) was administered and 24 h urine was collected. In urine, total nitrogen and the percentage of 15N were measured. From the ingested and excreted quantity, a urinary 15N balance was calculated. Mean 15N percentage from total N was 3.3 ± 0.5. In 9 patients, basal 15N balance was +79 ± 15 mg/m2 or +2.9 ± 0.4 mg/kg. On recombinant hGH, it was +166 ± 16 mg/m2 or +6.1 ± 0.6 mg/kg (p < 0.001). The recombinant hGH-induced positive 15N balance change was +87 ± 17 mg/m2 or +3.2 ± 0.6 mg/kg. 1 patient with a higher basal 15N balance (+196 mg/m2, +7.1 mg/kg) had no positive 15N balance change due to latent hypothalamic hypothyroidism. In previous similar studies with pituitary hGH, the change of 15N balance was +80 ± 27 mg/m2 or +2.8 ± 1.1 mg/kg. It is concluded that the acute nitrogen-retaining effect of recombinant hGH is at least equal to that of

ISSN:1663-2818    

DOI:10.1159/000180990

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Prostaglandins have been shown to modulate the secretion of several pituitary hormones, suggesting that therapeutic doses of nonsteroidal anti-inflammatory drugs may change basal hormone levels. In this study, plasma levels of prolactin, follicle stimulating hormone, luteinizing hormone, thyrotropin and beta-endorphin were determined in 6 healthy men after administration of diclofenac, a prostaglandin synthesis inhibitor. The subjects were given 75 mg intramuscularly and 50 mg orally at 08.00 h the first day, 50 mg orally at 08.00, 12.00 and 20.00 h the second day and an additional 50 mg orally at 08.00 h the third day. Blood samples were collected throughout these 3 days. Diclofenac resulted in a significant and sustained decrease in plasma level of prolactin (p < 0.005). The other hormones did not demonstrate significant change following diclofenac administration. These data suggest that administration of a prostaglandin synthesis inhibitor, such as diclofenac, selectively alters basal pituitary secretion of prolactin in humans without a detectable effect on plasma levels of other pituitary hormones. This study supports the hypothesis that prostaglandins are necessary for maintaining basal level of prolactin secretion in man.

ISSN:1663-2818    

DOI:10.1159/000180991

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Urinary aldosterone metabolites were measured before and after the administration of 1 g/day of kanamycin, a nonabsorbable antibiotic, for 7 days, in 6 normal volunteers and in 11 patients with liver cirrhosis. Urinary excretion of 21-deoxytetrahydroaldosterone (21-deoxy-THAldo) decreased by 40 and 86% from the control values in normal volunteers and in patients, respectively (p < 0.05), after kanamycin administration. Urinary excretion of 21-deoxyaldosterone (21-deoxy-Aldo) also fell by 48 and 89% in normal subjects and in patients, respectively, but the decrease was significant only in the normal subjects (p < 0.05). In normal volunteers, urinary free aldosterone and THAldo remained constant, whereas the ratio of 21-deoxy-Aldo to aldosterone and 21-deoxy-THAldo to THAldo decreased from 10.2 to 3.7 and 2.1 to 0.3, respectively (p < 0.01). These results indicate that intestinal bacteria participate in the metabolism of aldosterone during enterohepatic circulation in man.

ISSN:1663-2818    

DOI:10.1159/000180992

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Recent data suggest that adolescent individuals with growth hormone (GH) deficiency have subnormal levels of adrenal androgens (AA). In order to determine the developmental pattern of AA in GH deficiency and to assess whether AA levels can help identify children with GH deficiency, we measured plasma concentrations of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), Δ4-androstenedione (Δ4A), and cortisol in the basal state and during prolonged adrenocorticotropin (ACTH) infusion (8 h) in a group of 34 individuals, 26 males and 8 females, with short stature. Their chronological ages (CA) ranged from 1.75 to 17.5 years (median 10.35 years). The subjects were grouped into two categories according to the results of pituitary testing: group 1 = short, non-GH-deficient (n = 16), and group 2 = GH-deficient, ACTH-sufficient (n = 18). Patients in groups 1 and 2 had similar bone ages (BA: 7.2 ± 0.7 vs. 7.5 ± 1.0 years) and Z scores for height ( 3.0 ± 0.2 vs. – 3.2 ± 0.3 units) and height velocity (-2.5 ± 0.4 vs. -2.6 ± 0.2 units). For both groups there were significant increases from basal to peak levels for DHEA, DHEA-S, Δ4A and cortisol following prolonged ACTH infusion. Although both basal and peak levels of DHEA-S overlapped in groups 1 and 2 for all CA and BA, levels in group 2 tended to be lower, especially for BA greater than 10 years. Analysis of covariance showed a significant difference in the slopes of the regression lines of DHEA-S between groups 1 and 2 (basal vs. CA: F 4.9, p < 0.05; basal vs. BA: F 9.7, p < 0.005; peak vs. BA; F 8.7, p < 0.01). There were no differences noted between groups 1 and 2 for DHEA and Δ4 A, either in the basal state or after ACTH stimulation. Stimulated values of cortisol were similar for groups 1 and 2 (1,180 ± 40 vs. 1,300 ± 70 nmol/l). We conclude that, although differences in the overall pattern of DHEA-S between endocrinologically normal short individuals and those with GH deficiency were significant, measurements of AA in the age group studied are not helpful in the differential diagnosis of children with

ISSN:1663-2818    

DOI:10.1159/000180993

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Changes in rat and human testicular human chorionic gonadotropin (hCG) binding sites induced by hCG were estimated in vivo and in vitro. After a single administration of hCG, the specific 125I-hCG bindings were significantly reduced for 7 and 5 days in rat and human testes, respectively. Thereafter, 125I-hCG bindings had recovered to pretreatment values by the 14th day after the administration. Occupied hCG bindings accounted for about half of the reduced bindings on the day after administration of hCG. After this time, however, the occupancy did not contribute so much to the reduction of the bindings. In experiments in vitro using the organ culture technique, an exposure to hCG for 24 h induced a dose-related significant loss of the specific 125I-hCG bindings for 7 and 5 days in rat and human testes, respectively. Thereafter, the loss was gradually recovered. These patterns of changes in 125I-hCG bindings in vitro were similar to those in vivo. These findings suggest that the reduction in hCG binding sites by hCG is due to not only occupancy but also downregulation of the binding sites and that the testicular organ culture method used in the present study is useful to study hormonal regulation of testicular function, especially in human testes.

ISSN:1663-2818    

DOI:10.1159/000180994

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

A 59-year-old man developed Cushing’s syndrome with massive bilateral adrenal macronodular hyperplasia. Plasma ACTH levels were undetectable both peripherally and in the inferior petrosal sinus. Computed tomography scans of his pituitary were normal. Hypercortisolism was not suppressed by high doses of dexamethasone. His adrenal cells were successfully isolated and grown on bovine corneal extracellular matrix. The cultured cells displayed strikingly rapid growth and hypersecretion of cortisol during incubation with control serum. Addition of the patient’s serum to cultured fetal adrenal cells did not accelerate their growth. This was the first experience with our in vitro system in this rare clinical condition. The techniques described here may be used for future in vitro adrenal studies. These in vivo and in vitro data indicate that this patient’s bilateral adrenal hyperfunction and growth were independent of

ISSN:1663-2818    

DOI:10.1159/000180995

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

There is some controversy concerning a possible effect of diabetes mellitus on the sympathetic nervous system in humans with spontaneous diabetes mellitus and in animals with experimental diabetes mellitus. In this study we compared the tissue norepinephrine (NE) concentration of normal and diabetic Chinese hamsters in the untreated state and after treatment with insulin. Diabetes resulted in a 128% increase in the NE concentration of the kidney in female but not male hamsters. The NE concentration was increased in the liver (133%) and in the cerebral cortex (118%) of both male and female hamsters. There was no significant increase in the NE concentration of hypothalamus, acinar pancreas, pancreatic islets, or heart of diabetic hamsters. Three days of insulin therapy reduced the elevated NE concentration in kidney, liver and cerebral cortex of diabetic hamsters to the levels found in normal hamsters. However, insulin therapy of normal hamsters did not reduce the tissue NE concentration of the kidney, liver, and cerebral cortex below the normal levels found in these animals. Insulin therapy reduced the hypothalamic concentration of NE in both diabetic and normal hamsters. The increase in kidney NE concentration in female diabetic hamsters was not due to a reduction in renal size, for the kidneys of both female and male diabetic hamsters were larger than those of normal hamsters. When synthesis of NE was inhibited with α-methyltyrosine, there was a comparable rate of fall in the tissue NE concentration in the four experimental groups, suggesting that the increased tissue NE concentration in the tissues of diabetic hamsters was not due to a decreased rate of disappearance of this compound. We conclude that insulin deficiency in diabetes mellitus probably causes an increased rate of NE synthesis in some tissues of the Chinese hamster

ISSN:1663-2818    

DOI:10.1159/000180996

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:1663-2818    

DOI:10.1159/000180997

出版商:S. Karger AG    

年代:1988

数据来源: Karger