0021-972X/90/7103-0770$02.00/0 Journal of Clinical Endocrinology and Metabolism Copyright© 1990 by The Endocrine Society
Vol. 71, No. 3 Printed in U.S.A.
Growth Hormone Secretion in Pubertal Age Patients with Turner's Syndrome ROBERTO LANES, SARA BRITO, MARIA SUNIAGA, GUSTAVO MONCADA, AND MARIETTA BORGES Department of Endocrinology, Hospital Central "Dr. Carlos Arvelo", Caracas, Venezuela
in the control group. Total GH output (205.4 ± 118.7 us. 251.4
ABSTRACT. GH levels were measured every 30 min during
± 122.0 U), total number of nocturnal GH pulses (2.4 ± 0.8 us.
sleep over 9 h in 10 patients with Turner's syndrome ranging in
age from 10.6-18.9 yr (mean, 15.0 ± 2.7 yr) and in 12 controls matched for bone age, all of whom had normal GH responses to an orally administered dose of clonidine. We found no significant difference in the mean 9-h overnight GH concentration between groups. The overnight GH concentration was 3.8 ± 2.2 Mg/L (mean ± SD) in Turner's syndrome patients and 4.5 ± 2.4 fig/L
T
2.9 ± 0.7), and mean peak GH response during nocturnal sampling (13.0 ± 7.4 vs. 13.2 ± 3.3 Mg/L) were not different in the children with Turner's syndrome and the controls. We conclude that pubertal age patients with Turner's syndrome secrete GH normally and do not have any abnormality in GH regulation. (J Clin Endocrinol Metab 7 1 : 770-772, 1990)
also obtained from 12 healthy normal female control subjects matched for bone age (mean bone age, 12.8 ± 0.7 yr) with an appropriate weight for height, who were in Tanner stage 2-3 of puberty and were growing normally between the 10th and 75th percentiles. Thyroid function was normal in all patients, and no other medical problems were present; none of them had evidence of spontaneous breast budding. Four patients had received low dose short term estrogen therapy (one quarter of a 0.625-mg tablet of conjugated estrogen, 0.156 mg daily) for several months, and two patients had received oxandrolone, but all had discontinued the medication at least 4 months before entering the study; no subject received any prior treatment with GH. The clinical data for our patients are presented in Table 1. Bone ages were determined according to the method of Greulich and Pyle (4). After an overnight fast all patients received a single oral dose of 100 ixg/m2 clonidine, and blood samples for GH determination were drawn while the subject was in a recumbent position at 0, 30, 60, 90, and 120 min. For the GH release studies during sleep, blood samples were drawn from an indwelling venous catheter every 30 min from 2100-0600 h on the day after clonidine testing. Patients were admitted 4 h before the overnight sampling and had a balanced dinner at 1800 h. An effort was made to avoid stress and to encourage normal activity during this period. Lights were turned off at 2100 h, and each patient's status was recorded as awake or asleep; all patients had a minimum of 7 h of observed sleep. Samples were stored at —20 C, and all samples from a 9-h GH study were analyzed in the same assay and determined in duplicate by the same laboratory technician using a commercial RIA kit (HGH, human GH double antibody RIA, Diagnostic Product Corp., Los Angeles, CA), as previously described (5).
HE MAJORITY of children with Turner's syndrome have a decreased growth velocity and short stature as adults. Several recent reports have suggested that diminished GH secretion, as determined by responses to secretagogues and 24-h or overnight GH sampling may contribute to the limited adult stature in Turner's syndrome (1-3); this reduced GH secretion has been primarily noted in patients with gonadal dysgenesis older than 9 yr of age (3). Having found that most of our previous patients with Turner's syndrome seemed to secrete GH normally, we decided to evaluate the GH secretory status of a group of older subjects with Turner's syndrome (>9 yr old) and compared their GH responses to those of a control population. Materials and Methods
Ten patients with Turner's syndrome, with a mean chronological age of 15.0 ± 2.7 yr (range, 10.6-18.9 yr) and a mean bone age of 12.5 ± 1.7 yr, were studied at the pediatric endocrine clinic of the Hospital Central "Dr. Carlos Arvelo", Caracas. They were selected randomly after parental informed consent and approval of the Department Research and Publications Committee had been obtained. The diagnosis of Turner's syndrome was confirmed by leukocyte karyotype in all cases; the karyotypes were 45,X in 9 patients, and in 1 subject a mosasic pattern was detected (45,X/46,X iso Xq). Serum samples were Received May 15,1989. Address all correspondence and requests for reprints to: Roberto Lanes, M.D., c/o Jet Cargo INTL, M-177, P.O. Box 020010, Miami, Florida 33102.
770
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COMMENTS
771
TABLE 1. Clinical data from our patients Patient
CA
BA
no.
(yr months)
(yr m o n t h 9 )
1 2 3 4 5 6 7 8 9 10
107/12 11712 17712 14712 15712 15712 17712
18n/12
10 10 14 12 13 13 14 15
14712 14712
12712 12712
Ht (cm)
Karyotype 45, X 45, X 45, X 45, X 45, X 45, X/46, X iso Xq 45, X 45.X 45, X 45, X
Wt
(kg) 23.1
129.9 116.8 134.3 132.3 128.4 119.2 133.5 138
123.2 128.8
Growth velocity (cm/yr) 3.2"
27
3
40.8 42.5 32.5 26.8 41.2 35.4 32.3 31.5
3.6° 3.4° 4
2.9° 3.6° 2.2" 2 2.5
CA, Chronological age; BA, bone age. Discontinued low dose estrogen or oxandrolone therapy at least 4 months before this study.
0
The intra- and interassay coefficients of variation were 1.55.9% and 3.4-8.3%, respectively. The lower limit of sensitivity for our assay was 0.5 ng/L. The pattern of pulses in the 9-h GH profile was analyzed using the Pulsar program developed by Merriam and Wachter. The program identifies secretory peaks by height and duration from a smoothed baseline, using the assay SD as a scale factor. The cut-off parameters G 1-5 of the Pulsar program were set at 3.98, 2.4, 1.7, 1.2, and 0.9 times the intraassay SD as a criteria for accepting peaks one, two, three, four, and five points wide, respectively. The smoothing time was set at half the total profile time. The integrated overnight GH concentration was determined by obtaining the mean of all GH measurements over 9 h. The area under the GH curve over 9 h was used as an index of total GH secretion. The area under the curve was estimated above the zero level. Comparison of integrated overnight GH concentrations of the population studied was accomplished by analysis of variance. Total GH output was estimated by measuring the area under the curve us. the 9-h time curve, and comparison of both groups was performed with Newman-Keuls and Mann-Whitney tests. Results are expressed as the mean ± SD.
Results All 10 patients with Turner's syndrome were able to increase their GH levels to 10 /ug/L or more after oral clonidine administration. Mean peak GH concentrations of 18.6 ± 6.3 and 20.0 ± 7.3 /xg/L were obtained by our patients and the control group, respectively, 60 min after clonidine ingestion. Mean 9-h overnight GH concentrations, total GH output, number of nocturnal GH pulses (including pulse amplitude, height, and length), and mean peak GH response during nocturnal sampling were not significantly different in the two groups (Table 2).
Discussion Studies of the GH secretory status of patients with gonadal dysgenesis have yielded conflicting results, with some studies reporting normal GH responses to provoc-
TABLE 2. GH levels during overnight GH sampling in individual patients with Turner's syndrome and in both controls and Turner syndrome patients as a group
Patient no.
Mean Mean Total basal Total peak overnight GH output nocturnal nocturnal (AUC ± SD/9 GH GH pulses GH h;U) (Mg/L) (/xg/L)
Turner syndrome patients 3.0 2.0 2.0 4.0 3.0
6.9 1.5 3.8 3.3
266.0 95.5 80.0 477.0 211.0 156.0 267.0 90.0 233.0 178.0
3.8 ± 2.2 4.5 ± 2.4
1 2 3 4 5
5.0 1.7
6
2.6
7 8 9 10
Mean±SD Controls
1.5
8.2 3.7
15.0 5.4 5.6 30.0
12.0
3.0
8.0
2.0 1.0 2.0 2.0
17.0 7.0 15.0 15.0
205.4 ± 118.7
2.4 + 0.8
13.0 ± 7.4
251.4 ± 122.0
2.9 ± 0.7
13.2 ± 3.3
AUC, Area under the curve.
ative testing, while others described a decreased response (1, 2, 6). The 24-h GH secretion of a group of patients with Turner's syndrome was recently evaluated (3) and found to be diminished in subjects older than 9 yr of age when compared to the response of normal girls. In our population of patients with Turner's syndrome, all older than 9 yr of age, we were unable to find any difference in the mean 9-h overnight GH concentration, total basal GH output, or mean peak GH level and their number of GH pulses during sleep compared to those of a control population. Our findings are similar to those very recently reported by Lin etal.il), who demonstrated no statistical difference in the mean levels of GH in normal children and those with Turner's syndrome. The
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772
COMMENTS
children in that study were relatively young, with a mean chronological age of 11.6 yr, but only one child was less than 9 yr of age and five children were 12 yr or older. Our patients were older than those of Lin, with a mean chronological age close to 15 yr, and they secreted GH normally. As puberty progresses in our control subjects, GH secretion may increase, and a difference between patients and controls may become apparent. The mechanisms postulated by Ross et al. (3) by which older patients with Turner's syndrome secrete less GH included a lack of estrogen secretion. A role for estrogen could be compatible with the observation that estrogen increases GH responsiveness to provocative testing (8, 9). However, this has not been a consistent finding, as we found no stimulatory effect of estrogen on GH release after exercise in a large population of prepubertal children (10), and Lin et al. (11) and Zadik et al. (12) found that endogenous GH secretion in prepubertal normal children did not differ from that in pubertal children at stages 2-4 of puberty. Growth-promoting factors other than sex hormones may be involved in the growth process of children undergoing puberty, and Merimee et al. (13) recently suggested that insulin-like growth factor-I may be the principal agent of accelerated pubertal growth. We did not measure insulin-like growth factor-I concentrations in our patients. Ross et al. (3) found that the somatomedin-C concentrations of their 6- to 12-yr-old girls with gonadal dysgenesis were significantly decreased compared with those in normal girls matched for both chronological and bone age at the same time that these patients had normal GH responses to arginineinsulin and those less than 9 yr old had normal 24-h GH secretion. While Ross et al. (3) measured spontaneous GH secretion over 24 h, we only evaluated overnight GH levels. The diagnostic validity of overnight GH sampling has, however, been recently confirmed (14) based on the excellent correlation between overnight and 24-h GH concentrations. Blood samples for GH measurement were taken every 20 min by Ross et al. (3), while sampling in our study was performed every 30 min. Analysis of 24h GH profiles in children led Albertsson-Wikland and Rosberg (15) to conclude that a 30-min sampling interval
JCE & M • 1990 Vol71«No3
was a valid compromise, since no difference was found between 20- and 40-min sampling. In conclusion, in this study we were unable to find a decrease in the GH levels of a group of pubertal aged patients with Turner's syndrome, as assessed by both provocative testing and overnight GH sampling.
Acknowledgment We thank Dr. Ronald Gugg of Kabi International, for providing us the Pulsar program.
References 1. Donaldson EL, Wegienka LE, Miller D, Forsham PH. Growth hormone studies in Turner's's syndrome. J Clin Endocrinol Metab. 1968;28:383-5. 2. Laczi F, Jucesz I, Janaky T, Laszlo FA. Growth hormone reserve capacity in Turner's's syndrome. Horm Metab Res. 1979;ll:664-9.
3. Ross JL, Long LM, Loriaux DL, Cutler GB. Growth hormone secretory dynamics in Turner's syndrome. J Pediatr. 1985;106:2026. 4. Greulich WW, Pyle SI. Radiographic atals of skeletal development of the hand and wrist. 2nd ed. Stanford: Stanford University Press; 1959. 5. Lanes R, Bohorquez L, Leal V, et al. Growth hormone secretion in patients with constitutional delay of growth and pubertal development. J Pediatr. 1986;109:781-3. 6. Tzagournis M. Response to long term administration of human growth hormone in Turner's's syndrome. JAMA. 1969;210:2373-7. 7. Lin TH, Kirkland JL, Kirkland RT. Growth hormone assessment and short term treatment with growth hormone in Turner's syndrome. J Pediatr. 1988;112:919-22. 8. Sperling MA, Kenny FM, Drash AL. Arginine-induced growth hormone responses in children: effect of age and puberty. J Pediatr. 1970;77:462-7. 9. Gourmelen M, Pham-Huu-Trung MT, Girrard F. Transient partial hGH deficiency in prepubertal children with delay of growth. Pediatr Res. 1979;13:221-7. 10. Lanes R, Lifshitz F, Sekaran C, Fort P, Recker B. Premarin priming does not alter growth hormone release following exercise. J Endocrinol Invest. 1986;9:443-6. 11. Lin TH, Kirkland RT, Sherman BM, Kirkland JL. Growth hormone testing in short children and their response to growth hormone therapy. J Pediatr. 1989;115:57-63. 12. Zadik Z, Chalew SA, McCarter RJ, Meistas M, Kowarski AA. The influence of age on the 24-hour integrated concentration of growth hormone in normal individuals. J Clin Endocrinol Metab. 1985;60:513-6. 13. Merimee TJ, Zapf J, Hewlett B, Cavalli-Sforza LL. Insulin like growth factors in pygmies. The role of puberty in determining final stature. N Engl J Med. 1987;316:906-ll. 14. Richards GE, Cavallo A, Meyer WJ. Diagnostic validity of 12 hour integrated concentration of growth hormone. AJDC 1987;141:5538. 15. Albertsson-Wikland K, Rosberg S. Analysis of 24 hour growth hormone profiles in children. J Clin Endocrinol Metab. 1988;67:493-540.
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Vol. 71, No. 3 Printed in U.S.A.
Growth Hormone Secretion in Pubertal Age Patients with Turner's Syndrome ROBERTO LANES, SARA BRITO, MARIA SUNIAGA, GUSTAVO MONCADA, AND MARIETTA BORGES Department of Endocrinology, Hospital Central "Dr. Carlos Arvelo", Caracas, Venezuela
in the control group. Total GH output (205.4 ± 118.7 us. 251.4
ABSTRACT. GH levels were measured every 30 min during
± 122.0 U), total number of nocturnal GH pulses (2.4 ± 0.8 us.
sleep over 9 h in 10 patients with Turner's syndrome ranging in
age from 10.6-18.9 yr (mean, 15.0 ± 2.7 yr) and in 12 controls matched for bone age, all of whom had normal GH responses to an orally administered dose of clonidine. We found no significant difference in the mean 9-h overnight GH concentration between groups. The overnight GH concentration was 3.8 ± 2.2 Mg/L (mean ± SD) in Turner's syndrome patients and 4.5 ± 2.4 fig/L
T
2.9 ± 0.7), and mean peak GH response during nocturnal sampling (13.0 ± 7.4 vs. 13.2 ± 3.3 Mg/L) were not different in the children with Turner's syndrome and the controls. We conclude that pubertal age patients with Turner's syndrome secrete GH normally and do not have any abnormality in GH regulation. (J Clin Endocrinol Metab 7 1 : 770-772, 1990)
also obtained from 12 healthy normal female control subjects matched for bone age (mean bone age, 12.8 ± 0.7 yr) with an appropriate weight for height, who were in Tanner stage 2-3 of puberty and were growing normally between the 10th and 75th percentiles. Thyroid function was normal in all patients, and no other medical problems were present; none of them had evidence of spontaneous breast budding. Four patients had received low dose short term estrogen therapy (one quarter of a 0.625-mg tablet of conjugated estrogen, 0.156 mg daily) for several months, and two patients had received oxandrolone, but all had discontinued the medication at least 4 months before entering the study; no subject received any prior treatment with GH. The clinical data for our patients are presented in Table 1. Bone ages were determined according to the method of Greulich and Pyle (4). After an overnight fast all patients received a single oral dose of 100 ixg/m2 clonidine, and blood samples for GH determination were drawn while the subject was in a recumbent position at 0, 30, 60, 90, and 120 min. For the GH release studies during sleep, blood samples were drawn from an indwelling venous catheter every 30 min from 2100-0600 h on the day after clonidine testing. Patients were admitted 4 h before the overnight sampling and had a balanced dinner at 1800 h. An effort was made to avoid stress and to encourage normal activity during this period. Lights were turned off at 2100 h, and each patient's status was recorded as awake or asleep; all patients had a minimum of 7 h of observed sleep. Samples were stored at —20 C, and all samples from a 9-h GH study were analyzed in the same assay and determined in duplicate by the same laboratory technician using a commercial RIA kit (HGH, human GH double antibody RIA, Diagnostic Product Corp., Los Angeles, CA), as previously described (5).
HE MAJORITY of children with Turner's syndrome have a decreased growth velocity and short stature as adults. Several recent reports have suggested that diminished GH secretion, as determined by responses to secretagogues and 24-h or overnight GH sampling may contribute to the limited adult stature in Turner's syndrome (1-3); this reduced GH secretion has been primarily noted in patients with gonadal dysgenesis older than 9 yr of age (3). Having found that most of our previous patients with Turner's syndrome seemed to secrete GH normally, we decided to evaluate the GH secretory status of a group of older subjects with Turner's syndrome (>9 yr old) and compared their GH responses to those of a control population. Materials and Methods
Ten patients with Turner's syndrome, with a mean chronological age of 15.0 ± 2.7 yr (range, 10.6-18.9 yr) and a mean bone age of 12.5 ± 1.7 yr, were studied at the pediatric endocrine clinic of the Hospital Central "Dr. Carlos Arvelo", Caracas. They were selected randomly after parental informed consent and approval of the Department Research and Publications Committee had been obtained. The diagnosis of Turner's syndrome was confirmed by leukocyte karyotype in all cases; the karyotypes were 45,X in 9 patients, and in 1 subject a mosasic pattern was detected (45,X/46,X iso Xq). Serum samples were Received May 15,1989. Address all correspondence and requests for reprints to: Roberto Lanes, M.D., c/o Jet Cargo INTL, M-177, P.O. Box 020010, Miami, Florida 33102.
770
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COMMENTS
771
TABLE 1. Clinical data from our patients Patient
CA
BA
no.
(yr months)
(yr m o n t h 9 )
1 2 3 4 5 6 7 8 9 10
107/12 11712 17712 14712 15712 15712 17712
18n/12
10 10 14 12 13 13 14 15
14712 14712
12712 12712
Ht (cm)
Karyotype 45, X 45, X 45, X 45, X 45, X 45, X/46, X iso Xq 45, X 45.X 45, X 45, X
Wt
(kg) 23.1
129.9 116.8 134.3 132.3 128.4 119.2 133.5 138
123.2 128.8
Growth velocity (cm/yr) 3.2"
27
3
40.8 42.5 32.5 26.8 41.2 35.4 32.3 31.5
3.6° 3.4° 4
2.9° 3.6° 2.2" 2 2.5
CA, Chronological age; BA, bone age. Discontinued low dose estrogen or oxandrolone therapy at least 4 months before this study.
0
The intra- and interassay coefficients of variation were 1.55.9% and 3.4-8.3%, respectively. The lower limit of sensitivity for our assay was 0.5 ng/L. The pattern of pulses in the 9-h GH profile was analyzed using the Pulsar program developed by Merriam and Wachter. The program identifies secretory peaks by height and duration from a smoothed baseline, using the assay SD as a scale factor. The cut-off parameters G 1-5 of the Pulsar program were set at 3.98, 2.4, 1.7, 1.2, and 0.9 times the intraassay SD as a criteria for accepting peaks one, two, three, four, and five points wide, respectively. The smoothing time was set at half the total profile time. The integrated overnight GH concentration was determined by obtaining the mean of all GH measurements over 9 h. The area under the GH curve over 9 h was used as an index of total GH secretion. The area under the curve was estimated above the zero level. Comparison of integrated overnight GH concentrations of the population studied was accomplished by analysis of variance. Total GH output was estimated by measuring the area under the curve us. the 9-h time curve, and comparison of both groups was performed with Newman-Keuls and Mann-Whitney tests. Results are expressed as the mean ± SD.
Results All 10 patients with Turner's syndrome were able to increase their GH levels to 10 /ug/L or more after oral clonidine administration. Mean peak GH concentrations of 18.6 ± 6.3 and 20.0 ± 7.3 /xg/L were obtained by our patients and the control group, respectively, 60 min after clonidine ingestion. Mean 9-h overnight GH concentrations, total GH output, number of nocturnal GH pulses (including pulse amplitude, height, and length), and mean peak GH response during nocturnal sampling were not significantly different in the two groups (Table 2).
Discussion Studies of the GH secretory status of patients with gonadal dysgenesis have yielded conflicting results, with some studies reporting normal GH responses to provoc-
TABLE 2. GH levels during overnight GH sampling in individual patients with Turner's syndrome and in both controls and Turner syndrome patients as a group
Patient no.
Mean Mean Total basal Total peak overnight GH output nocturnal nocturnal (AUC ± SD/9 GH GH pulses GH h;U) (Mg/L) (/xg/L)
Turner syndrome patients 3.0 2.0 2.0 4.0 3.0
6.9 1.5 3.8 3.3
266.0 95.5 80.0 477.0 211.0 156.0 267.0 90.0 233.0 178.0
3.8 ± 2.2 4.5 ± 2.4
1 2 3 4 5
5.0 1.7
6
2.6
7 8 9 10
Mean±SD Controls
1.5
8.2 3.7
15.0 5.4 5.6 30.0
12.0
3.0
8.0
2.0 1.0 2.0 2.0
17.0 7.0 15.0 15.0
205.4 ± 118.7
2.4 + 0.8
13.0 ± 7.4
251.4 ± 122.0
2.9 ± 0.7
13.2 ± 3.3
AUC, Area under the curve.
ative testing, while others described a decreased response (1, 2, 6). The 24-h GH secretion of a group of patients with Turner's syndrome was recently evaluated (3) and found to be diminished in subjects older than 9 yr of age when compared to the response of normal girls. In our population of patients with Turner's syndrome, all older than 9 yr of age, we were unable to find any difference in the mean 9-h overnight GH concentration, total basal GH output, or mean peak GH level and their number of GH pulses during sleep compared to those of a control population. Our findings are similar to those very recently reported by Lin etal.il), who demonstrated no statistical difference in the mean levels of GH in normal children and those with Turner's syndrome. The
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772
COMMENTS
children in that study were relatively young, with a mean chronological age of 11.6 yr, but only one child was less than 9 yr of age and five children were 12 yr or older. Our patients were older than those of Lin, with a mean chronological age close to 15 yr, and they secreted GH normally. As puberty progresses in our control subjects, GH secretion may increase, and a difference between patients and controls may become apparent. The mechanisms postulated by Ross et al. (3) by which older patients with Turner's syndrome secrete less GH included a lack of estrogen secretion. A role for estrogen could be compatible with the observation that estrogen increases GH responsiveness to provocative testing (8, 9). However, this has not been a consistent finding, as we found no stimulatory effect of estrogen on GH release after exercise in a large population of prepubertal children (10), and Lin et al. (11) and Zadik et al. (12) found that endogenous GH secretion in prepubertal normal children did not differ from that in pubertal children at stages 2-4 of puberty. Growth-promoting factors other than sex hormones may be involved in the growth process of children undergoing puberty, and Merimee et al. (13) recently suggested that insulin-like growth factor-I may be the principal agent of accelerated pubertal growth. We did not measure insulin-like growth factor-I concentrations in our patients. Ross et al. (3) found that the somatomedin-C concentrations of their 6- to 12-yr-old girls with gonadal dysgenesis were significantly decreased compared with those in normal girls matched for both chronological and bone age at the same time that these patients had normal GH responses to arginineinsulin and those less than 9 yr old had normal 24-h GH secretion. While Ross et al. (3) measured spontaneous GH secretion over 24 h, we only evaluated overnight GH levels. The diagnostic validity of overnight GH sampling has, however, been recently confirmed (14) based on the excellent correlation between overnight and 24-h GH concentrations. Blood samples for GH measurement were taken every 20 min by Ross et al. (3), while sampling in our study was performed every 30 min. Analysis of 24h GH profiles in children led Albertsson-Wikland and Rosberg (15) to conclude that a 30-min sampling interval
JCE & M • 1990 Vol71«No3
was a valid compromise, since no difference was found between 20- and 40-min sampling. In conclusion, in this study we were unable to find a decrease in the GH levels of a group of pubertal aged patients with Turner's syndrome, as assessed by both provocative testing and overnight GH sampling.
Acknowledgment We thank Dr. Ronald Gugg of Kabi International, for providing us the Pulsar program.
References 1. Donaldson EL, Wegienka LE, Miller D, Forsham PH. Growth hormone studies in Turner's's syndrome. J Clin Endocrinol Metab. 1968;28:383-5. 2. Laczi F, Jucesz I, Janaky T, Laszlo FA. Growth hormone reserve capacity in Turner's's syndrome. Horm Metab Res. 1979;ll:664-9.
3. Ross JL, Long LM, Loriaux DL, Cutler GB. Growth hormone secretory dynamics in Turner's syndrome. J Pediatr. 1985;106:2026. 4. Greulich WW, Pyle SI. Radiographic atals of skeletal development of the hand and wrist. 2nd ed. Stanford: Stanford University Press; 1959. 5. Lanes R, Bohorquez L, Leal V, et al. Growth hormone secretion in patients with constitutional delay of growth and pubertal development. J Pediatr. 1986;109:781-3. 6. Tzagournis M. Response to long term administration of human growth hormone in Turner's's syndrome. JAMA. 1969;210:2373-7. 7. Lin TH, Kirkland JL, Kirkland RT. Growth hormone assessment and short term treatment with growth hormone in Turner's syndrome. J Pediatr. 1988;112:919-22. 8. Sperling MA, Kenny FM, Drash AL. Arginine-induced growth hormone responses in children: effect of age and puberty. J Pediatr. 1970;77:462-7. 9. Gourmelen M, Pham-Huu-Trung MT, Girrard F. Transient partial hGH deficiency in prepubertal children with delay of growth. Pediatr Res. 1979;13:221-7. 10. Lanes R, Lifshitz F, Sekaran C, Fort P, Recker B. Premarin priming does not alter growth hormone release following exercise. J Endocrinol Invest. 1986;9:443-6. 11. Lin TH, Kirkland RT, Sherman BM, Kirkland JL. Growth hormone testing in short children and their response to growth hormone therapy. J Pediatr. 1989;115:57-63. 12. Zadik Z, Chalew SA, McCarter RJ, Meistas M, Kowarski AA. The influence of age on the 24-hour integrated concentration of growth hormone in normal individuals. J Clin Endocrinol Metab. 1985;60:513-6. 13. Merimee TJ, Zapf J, Hewlett B, Cavalli-Sforza LL. Insulin like growth factors in pygmies. The role of puberty in determining final stature. N Engl J Med. 1987;316:906-ll. 14. Richards GE, Cavallo A, Meyer WJ. Diagnostic validity of 12 hour integrated concentration of growth hormone. AJDC 1987;141:5538. 15. Albertsson-Wikland K, Rosberg S. Analysis of 24 hour growth hormone profiles in children. J Clin Endocrinol Metab. 1988;67:493-540.
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