Measurement of nocturnal urinary growth hormone values

1989 ◽  
Vol 121 (2) ◽  
pp. 290-296 ◽  
Author(s):  
Izumi Sukegawa ◽  
Naomi Hizuka ◽  
Kazue Takano ◽  
Kumiko Asakawa ◽  
Reiko Horikawa ◽  
...  

Abstract. Nocturnal urinary growth hormone values were measured by a sensitive enzyme immunoassay in normal adults, patients with GH deficiency, patients with Turner's syndrome, normal but short children who had normal plasma GH responses to provocative tests, and patients with acromegaly. The mean nocturnal urinary GH values in patients with acromegaly were significantly greater than those in normal adults (1582.3 ± 579.8 vs 53.5 ± 8.6 pmol/mmol creatinine (± sem); p < 0.05). In the normal but short children and patients with Turner's syndrome, the mean nocturnal urinary GH values were 83.1 ± 5.2 and 79.8 ± 29.5 pmol/mmol creatinine, respectively. In patients with GH deficiency, the nocturnal urinary GH values were undetectable (< 5.3 pmol/mmol creatinine) except in one patient where the value was 6.3 pmol/mmol creatinine. The nocturnal urinary GH values of the patients with GH deficiency were significantly lower than those of the other groups (p < 0.05). In normal but short children, the nocturnal urinary GH values correlated significantly with mean plasma nocturnal GH concentrations (r = 0.76, p < 0.001), and 24-hour urinary GH values (r = 0.84, p < 0.001), respectively. In 4 patients with GH deficiency who had circulating anti-hGH antibody, the urinary GH values were also undectable. These data indicate that nocturnal urinary GH value reflects endogenous GH secretion during collection time, and that measurement of the nocturnal urinary GH values is a useful method for screening of patients with GH deficiency and acromegaly.

1985 ◽  
Vol 110 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Naomi Hizuka ◽  
Kazue Takano ◽  
Kazuo Shizume ◽  
Izumi Tanaka ◽  
Noriko Honda ◽  
...  

Abstract. Pituitary growth hormone (GH) responses during a 10-h iv infusion of saline or human GH-releasing factor (hGRF-44) at 500 ng/kg/h, followed by an iv bolus injection of hGRF-44 at 2 μg/kg body weight, were studied in 10 patients with GH deficiency. During saline infusion in 4 patients, small plasma GH increase were observed in 2 patients. However, during hGRF infusion in 6 patients, up to 4 or 13 pulses of GH secretion were observed. The mean integrated GH pulse area during hGRF infusion was 22.5 ± 5.2 (se) ng/ml × h, which was greater than that obtained during saline infusion. Plasma somatomedin C levels did not increase after hGRF infusion. After saline or hGRF infusion all patients responded to an iv bolus injection of the peptide. These results indicate that hGRF infusion augments GH secretion by increasing the number and amplitude of GH pulses and that the infusion does not cause pituitary somatotrophs to lose their capacity to respond to hGRF subsequently.


1992 ◽  
Vol 127 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Jan M Wit ◽  
Albert A Massarano ◽  
Gerdine A Kamp ◽  
Peter C Hindmarsh ◽  
An van Es ◽  
...  

Twenty-four-hour growth hormone (GH) profiles in 26 girls with Turner's syndrome were compared with those of 26 normally growing short children and 24 slowly growing short children. All children were prepubertal and below 12 years of age. A subgroup of 13 girls was treated with ethinyl estradiol and a 24-h GH profile was reassessed. In an additional group of 45 girls with Turner's syndrome (aged 6.7–18.9 years) the effect of age, spontaneous breast development and ethinyl estradiol treatment was studied. The profiles were assessed by Fourier analysis. The oscillatory activity and the mean 24-h GH concentration were similar in children with Turner's syndrome and the normally growing short children, in contrast to lower levels in the slowly growing short children. The periodicity of GH secretion was similar in all groups. In the longitudinal study, ethinyl estradiol treatment resulted in a significant increase in pulse amplitude, but not in periodicity. In the cross-sectional study there was no significant difference between the subgroups of girls with either presence or absence of breast development or ethinyl estradiol treatment. GH secretion was not significantly related to age, height in standard deviation score or height velocity. These data imply that there is no abnormality in GH secretion in girls with Turner's syndrome.


1994 ◽  
Vol 131 (6) ◽  
pp. 598-601 ◽  
Author(s):  
Jaime Pineda ◽  
Pedro Martul ◽  
Felipe F Casanueva ◽  
Carlos Dieguez ◽  
Itxaso Rica ◽  
...  

Pineda J, Martul P, Casanueva FF, Dieguez C, Rica I, Loridan L. Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion. Eur J Endocrinol 1994;131:598–601. ISSN 0804–4643 Acute intravenous (iv) dexamethasone administration has been described recently as a new test for the diagnosis of growth hormone (GH) deficiency. In the present study, a new protocol of dexamethasone administration was evaluated. Twelve normal adults and 18 normal prepubertal children were studied. The dexamethasone iv test was performed in six adults at a dose of 4 mg and 12 children at a dose of 2 mg/m2. Blood samples were collected 15 min before, at time zero and every 15 or 30 min during 5 h, resulting in a total of 16 samples. In the remaining six adults and six children, 8 and 4 mg, respectively, of dexamethasone were administered orally at the subject's home, and blood sampling started 90 min later when they arrived at the hospital. Plasma GH was measured by radioimmunassay. The dexamethasone-induced GH response (mean ± sem, μg/1) to the iv or oral protocol did not differ in either the adults (iv 8.2 ± 2.1; oral 8.0 ± 1.6) or the children (iv 14.9 ± 1.3; oral 13.6 ± 1.8). It is concluded that the simpler protocol of acute oral dexamethasone administration hereby presented can be a safe and suitable test of GH secretion. J Pineda, Sección de Endocrinologia Pediátrica, Hospital de Cruces, 48903 Baracaldo (Vizcaya), Spain


1995 ◽  
Vol 132 (6) ◽  
pp. 712-715 ◽  
Author(s):  
A Leal-Cerro ◽  
E Garcia ◽  
R Astorga ◽  
FF Casanueva ◽  
C Dieguez

Leal-Cerro A, Garcia E, Astorga R, Casanueva FF, Dieguez C. Growth hormone (GH) responses to the combined administration of GH-releasing hormone plus GH-releasing peptide 6 in adults with GH deficiency. Eur J Endocrinol 1995;132:712–5. ISSN 0804–4643 In recent years the health problems of adults with growth hormone deficiency (GHD) and the benefits of GH replacement therapy have received considerable attention. However, the reliability of conventional GH tests in the assessment of pituitary GH reserve in this group of patients is still controversial. In this study, we assessed GH secretion after the combined administration of GH-releasing hormone (GHRH) (1 μg/kg iv) and GH-releasing peptide 6 (GHRP-6, 1 μg/kg iv) in adult patients diagnosed with GHD by conventional GH testing, and correlate this response with insulin-like growth factor I levels. Twenty-one subjects (13 male, 8 female) with long-standing diagnosis of GHD aged 21–54 years were studied. In 13 subjects GH responses to GHRH plus GHRP-6 were markedly reduced (peak GH response <10 mU/I), whereas in the remaining eight the response was greater (range 11–100 mU/l), In conclusion, our data show that combined administration of GHRH plus GHRP-6 elicited a significant increase in plasma GH levels in about 40% of patients diagnosed with GHD by conventional GH testing. C Dieguez, PO Box 563, 15700 Santiago de Compostela, Spain


1998 ◽  
Vol 83 (5) ◽  
pp. 1615-1618 ◽  
Author(s):  
G. Aimaretti ◽  
G. Corneli ◽  
P. Razzore ◽  
S. Bellone ◽  
C. Baffoni ◽  
...  

There is now wide consensus that, within an appropriate clinical context, GH deficiency (GHD) in adults must be shown biochemically by provocative testing of GH secretion and that appropriate cut-off limits have to be defined for each provocative test. Insulin-induced hypoglycemia (ITT) is indicated as the test of choice, and severe GHD, to be treated with recombinant human GH replacement, is defined by a GH peak response to ITT of less than 3 μg/L. GHRH + arginine (GHRH+ARG) is one of the most promising tests in alternative to ITT. In fact, it has been reported as a potent, reproducible, and age-independent test and that it is able to distinguish between GHD and normal adults. The aim of the present study was to compare the GH response to ITT and GHRH+ARG in a large group of hypopituitary adults (n = 40; 29 male and 11 female; age: 36.4 ± 2.1 yr). The third centile limit of the peak GH response to ITT has been reported as 5 μg/L, whereas in our lab, that to GHRH+ARG is 16.5 μg/L. In hypopituitary adults, the mean peak GH response to ITT (1.5 ± 0.2 μg/L, range: 0.1–8.5μ g/L) was lower (P &lt; 0.001) than that to GHRH+ARG (3.0 ± 0.4 μg/L, range 0.1–12.0 μg/L), though there was positive correlation (r = 0.61, P &lt; 0.001) between the GH responses to the 2 tests. The peak GH response to GHRH+ARG, but not that to ITT, was positively (though weakly) associated with insulin-like growth factor-I levels (r = 0.35, P &lt; 0.03). Childhood and adult onset GHD patients, as well as patients with single and multiple pituitary insufficiencies, had similar peak GH responses to ITT or GHRH+ARG. Analyzing individual GH responses, 4/40 (10%) of the hypopituitary patients had GH peaks higher than 5 μg/L after ITT; moreover, 3 other patients (7%) had GH peaks, after ITT, higher than 3 μg/L. On the other hand, after GHRH+ARG, all patients had GH peaks lower than 16.5 μg/L, whereas 21/40 (52.5%) had GH peaks higher than 3 μg/L. Because 3 μg/L is the arbitrary cut-off for ITT, the third centile limit of which is 5μ g/L, we arbitrarily considered 9 μg/L as the cut-off point for GHRH+ARG. It is noteworthy that 37/40 (92.5%) patients had a GH peak,. after GHRH+ARG, below this limit. In conclusion, our present results confirm that the ITT test is a reliable provocative test for the diagnosis of adult GHD, whereas they show that the GHRH+ARG test is, at least, as sensitive as the ITT test (provided that appropriate cut-off limits are considered). Note that even the arbitrary cut-off point below which severe GHD is demonstrated has to be appropriate to the potency of the test.


Author(s):  
J H Barth ◽  
J H Smith ◽  
P Clarkson

A comparison of three commercially available assays for growth hormone (Pharmacia hGH RIA, IDS Gamma-BCT GH and Delfia 22 kDa hGH) were used to measure growth hormone (GH) secretion in 26 short children after pharmacological stimulation. The IDS Gamma-BCT assay was compared with Pharmacia assay in 15 provocative tests (13 children; n = 94). The Pharmacia assay showed a strong positive proportional bias and this was particularly marked at GH > 20 mU/L; the mean difference between the assays at GH < 10 mU/L was 12%. The IDS Gamma-BCT assay was also compared with the Delfia 22 kDa assay in 18 provocative tests (13 children; n = 100). Results from the IDS assay was higher throughout the range 0−90mU/L with a mean difference of 11·4% in the range 10−90 mU/L; the mean difference between the assays at GH< 10 mU/L was −39%.


1976 ◽  
Vol 81 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Paul Saenger ◽  
Ernest Schwartz ◽  
Eckehart Wiedemann ◽  
Lenore S. Levine ◽  
Mary Tsai ◽  
...  

ABSTRACT Baseline somatomedin activity in seven of eight patients with Turner's syndrome was found to be within normal limits. Somatomedin activity readily suppressed with oestrogen administration. The overall mean serum somatomedin activity during oestrogen therapy (0.87 U/ml, sd 0.15) was significantly lower (P < 0.005) than the mean of the control serum somatomedin activities (1.09 U/ml, sd 0.24). During oestrogen therapy, suggestive elevations of fasting growth hormone levels were noted in five of eight patients. The data indicate that oestrogenic suppression of serum somatomedin was not due to decreased growth hormone secretion and suggest the existence of a negative feedback link between somatomedin and growth hormone.


1989 ◽  
Vol 120 (4) ◽  
pp. 442-446 ◽  
Author(s):  
E. Schober ◽  
H Frisch ◽  
F. Waldhauser ◽  
Ch. Bieglmayr

Abstract. The modulating effect of estrogen on GH secretion was studied in 22 patients with Turner's syndrome. Estrogen administration (0.5 μg/kg ethinylestradiol) for a period of 4 weeks resulted in a significant increase in basal GH concentrations (2.6 vs 4.8 μg/l, P< 0.01). The L-Dopa-stimulated GH concentrations were also significantly increased (P< 0.01), whereas no effect of estrogen substitution on GH responses to GHRH (1–44) and Sm-C levels was seen. Our findings demonstrate a priming effect of estrogen on GH secretion in patients with Turner's syndrome. These patients generally lack the puberty-associated rise in GH secretion, which might be due to ovarian failure and the concomitant estrogen deficiency.


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