Modulation of Glucocorticoid Secretion by Growth Hormone

Chasalow, Fred I.; Blethen, Sandra L.

doi:10.1203/00006450-198508000-00009

Cited by 11 publications

(6 citation statements)

References 4 publications

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“…This is in agreement with several other reports which have also described nor mal cortisol responses in GH-deficient children follow ing both insulin hypoglycemia and short-term ACTH stimulation [3,22,23]. The slightly elevated baseline values of cortisol noted in our GH-deficient patients are probably stress-related and of doubtful physiologic sig nificance.…”

Section: Discussionsupporting

confidence: 82%

Adrenal Androgens in Children with Short Stature

et al. 1988

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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 short stature.

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Section: Discussionsupporting

confidence: 82%

Adrenal Androgens in Children with Short Stature

et al. 1988

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“…Nevertheless such changes do also occur. In humans, G H has been reported as having a significant effect on steroid biosynthesis in the adrenal cortex, modulating the adrenal response to ACTH by suppressing corticosterone secretion, without affecting cortisol secretion (Chasalow & Blethen, 1985). GH has a synergistic effect on ACTH action on the biosynthesis of cortisol in the adrenal (Castro-Magana et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

Growth hormone treatment in hypopituitary GH deficient adults reduces circulating cortisol levels during hydrocortisone replacement therapy

Rodriguez-Arnao

Perry

Besser

et al. 1996

Clinical Endocrinology

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These results suggest that GH therapy in GH deficient adults produces an alteration in the measured serum cortisol profile, with a reduction in concentration of total cortisol in blood after orally administered hydrocortisone. These changes in circulating cortisol probably depend primarily on the fall in CBG levels, as no changes were found in the levels of calculated unbound cortisol on and off GH. Our data show that when measuring circulating cortisol levels, the results should be interpreted with caution in GH deficient patients on GH replacement, and different criteria may have to be applied to the circulating cortisol profile of these patients. The results highlight the importance of ensuring adequate corticosteroid replacement in patients starting GH therapy.

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“…In humans, G H has been reported as having a significant effect on steroid biosynthesis in the adrenal cortex, modulating the adrenal response to ACTH by suppressing corticosterone secretion, without affecting cortisol secretion (Chasalow & Blethen, 1985). Nevertheless such changes do also occur.…”

Section: Discussionmentioning

confidence: 99%

Growth hormone treatment in hypopituitary GH deficient adults reduces circulating cortisol levels during hydrocortisone replacement therapy

guez-Arnao¹,

Perry²,

Besser³

et al. 1996

Clin Endocrinol

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OBJECTIVES Patlents wlth GH deficlency frequently have multiple hormone deficiencies and require hydrocortisone replacement. We have investigated whether GH treatment alters circulating cortisol levels in hypopituitary patients recelving stable replacement therapy. DESIGN SubJects were studied during 6 or 12 months of S.C. GH at a dose of 0.25 IUlkglweek (0.125 IUlkglweek for the first 4 weeks), and efter a wash-out period of at least 2 months off GH (range 2-5 months). PATIENTS Fourteen hypopituitary patients (2F:12M) receivlng stable hydrocortisone replacement and thyroxlne, gonadal steroids and bromocriptlne therapy as required. MEASUREMENTS Serum cortisol values were measured throughout the day over 105 hours. Thyrold hormones and cortlsol binding globulin (CBG) were measured in the baseline sample. Comparisons of the serum cortlsol peak after receiving the flrst dose of hydrocortlsone, the tlme when the serum cortlsol peak was obtained, the area under the curve (AUC) for the cortlsol values and the levels of unbound cortisol on and off OH therapy were made. The results are expressed as mean * SEM.Comparisons were carried out within lndivlduals, uslng the Wilcoxon signed rank test. A P-value less than 0.05 was consldered statistically signlflcant. RESULTS During OH therapy, there was a significant reductlon in the mean cortisol peak (662.2f 61.1 vs 848.0 f 58.6 nmol/l; P = 0.001), and In the AUC for cortisol t (185.3 f 18.3 vs 230 * 17.9 nmol/l/l0~5h; P = 0.03), but there was no signlflcant change in the tlme of the cortisol peak (55.7 f 7.6 vs 57.8 f 4.9 minutes; P = NS). Durlng GH therapy there was a significant reductlon In CBG levels (33.64 i 1-16 vs 40-86 f 1-34mg/l; P = 0.001); however, no changes were found In the levels of calculated unbound cortlsol on and off GH (2.87f0.38 vs 2.90 f 0.30 nmol/l; P = NS). Durlng OH therapy, there was a slgnificant increase In serum trilodothyronlne (T3) (1.88 f 0.15 vs 1-44 i 0.11 nmol/l; P = 0-Ol), and a significant decrease in thyroxlne (T4) levels (74.9 * 11.1 vs 97.6 + i 10.9 nmol/l; P = 0.02) but levels remained within the normal range. No change was observed in serum TSH levels (0.29 f 0.13 vs 0.83 & 0.71 mU/I;CONCLUSIONS These results suggest that OH therapy In GH deflclent adults produces an alteration in the measured serum cortisol proflle, with a reduction in concentration of total cortisol in blood after rrally admlnlstered hydrocortisone. These changes in circulatlng cortlsol probably depend primarily on the fall in CBG levels, as no changes were found in the levels of calculated unbound cortisol on and off GH. Our data show that when measuring circulating cortisol levels, the results should be interpreted with caution in OH deflclent patients on GH replacement, and different criteria may have to be applied to the circulating cortlsol profile of these patients. The results hlghllght the importance of ensuring adequate cortlcosteroid replacement in patients starilng GH therapy. P = NS).

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Modulation of Glucocorticoid Secretion by Growth Hormone

Cited by 11 publications

References 4 publications

Adrenal Androgens in Children with Short Stature

Adrenal Androgens in Children with Short Stature

Growth hormone treatment in hypopituitary GH deficient adults reduces circulating cortisol levels during hydrocortisone replacement therapy

Growth hormone treatment in hypopituitary GH deficient adults reduces circulating cortisol levels during hydrocortisone replacement therapy

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