J. Endocrinol. Invest. 15: 735-739,1992
Growth hormone therapy in normal short children induces a transitory decrease in plasma growth hormone releasing hormone levels and in human growth hormone responsiveness to exogenous growth hormone releasing hormone I, Gil-Ad*, B. Klinger*, A. Pertzelan*, B, Erster*, A. Silbergeld**, H. Talpaz*, and Z. Laron 1** *Institute of Pediatric and Adolescent Endocrinology, Beilinson Medical Center, Petah Tiqva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, and **ARO, Volcani Institute, Beit Oagan, Israel. tional hGH therapy induced an increase in serum IGF-I levels which lasted as long as therapy was continued. Plasma GHRH levels showed an early transitory decrease after five days of therapy, whereas plasma somatostatin levels were unaltered. A slight suppression in hGH responsiveness to exogenous GHRH was found at 2 but not at 90 days after termination of hGH therapy. It is concluded that nonconventional hGH treatment does not cause permanent changes in physiological hGH secretion.
ABSTRACT. A three-month study of the effect of growth hormone (hGH) therapy (0.1 U/kg/day sc) on plasma levels of GH releasing hormone (GHRH), somatostatin and insulin-like growth factor I (IGF-I) and on the hGH responsiveness to exogenous GHRH was carried out in 32 prepubertal short-stature children with normal GH secretion. Blood sampIes were collected prior to initiation of therapy, and at 5, 30 and 90 days of onset of therapy, as weil as 2 and 90 days after termination of therapy. The nonconvenINTRODUCTION
for the two hormones on the GH autofeedback axis (7, 9). The availability of synthetic hGH and the widespread nonconventional use of this preparation in children with short stature prompted us to perform a longitudinal study on the effect of hGH on plasma GHRH, somatostatin and IGF-I levels and also to assess the hGH responsiveness to GHRH before therapy and 90 days after termination of three months of a therapeutic course.
Growth hormone limits its own secretion by a complex feedback mechanism which involves several regulatory peptides, including insulin-like growth factor (IGF-I), somatostatin and growth hormone releasing hormone (GHRH) (1-3). Previous studies have shown that administration of hGH in man induces impairment of the hGH responsiveness to provocative stimuli, such as insulin-induced hypoglycemia (4) and clonidine (5), and diminishes the sleep-induced release of hGH (6). In addition, exogenous GH was reported to inhibit endogenous GH responsiveness to GHRH following both short term (3 hours) as weil as more prolonged (2-5 days) administration (7, 8). Since there is a lag between the appearance and clearance of IGF-I in serum following hGH therapy, a differential mechanism has been suggested
MATERIALS AND METHODS Participants included 32 healthy prepubertal, shortstature, non-obese children (26 males, 6 females) aged 5 to 11 yrs. Height was
Growth hormone therapy in normal short children induces a transitory decrease in plasma growth hormone releasing hormone levels and in human growth hormone responsiveness to exogenous growth hormone releasing hormone I, Gil-Ad*, B. Klinger*, A. Pertzelan*, B, Erster*, A. Silbergeld**, H. Talpaz*, and Z. Laron 1** *Institute of Pediatric and Adolescent Endocrinology, Beilinson Medical Center, Petah Tiqva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, and **ARO, Volcani Institute, Beit Oagan, Israel. tional hGH therapy induced an increase in serum IGF-I levels which lasted as long as therapy was continued. Plasma GHRH levels showed an early transitory decrease after five days of therapy, whereas plasma somatostatin levels were unaltered. A slight suppression in hGH responsiveness to exogenous GHRH was found at 2 but not at 90 days after termination of hGH therapy. It is concluded that nonconventional hGH treatment does not cause permanent changes in physiological hGH secretion.
ABSTRACT. A three-month study of the effect of growth hormone (hGH) therapy (0.1 U/kg/day sc) on plasma levels of GH releasing hormone (GHRH), somatostatin and insulin-like growth factor I (IGF-I) and on the hGH responsiveness to exogenous GHRH was carried out in 32 prepubertal short-stature children with normal GH secretion. Blood sampIes were collected prior to initiation of therapy, and at 5, 30 and 90 days of onset of therapy, as weil as 2 and 90 days after termination of therapy. The nonconvenINTRODUCTION
for the two hormones on the GH autofeedback axis (7, 9). The availability of synthetic hGH and the widespread nonconventional use of this preparation in children with short stature prompted us to perform a longitudinal study on the effect of hGH on plasma GHRH, somatostatin and IGF-I levels and also to assess the hGH responsiveness to GHRH before therapy and 90 days after termination of three months of a therapeutic course.
Growth hormone limits its own secretion by a complex feedback mechanism which involves several regulatory peptides, including insulin-like growth factor (IGF-I), somatostatin and growth hormone releasing hormone (GHRH) (1-3). Previous studies have shown that administration of hGH in man induces impairment of the hGH responsiveness to provocative stimuli, such as insulin-induced hypoglycemia (4) and clonidine (5), and diminishes the sleep-induced release of hGH (6). In addition, exogenous GH was reported to inhibit endogenous GH responsiveness to GHRH following both short term (3 hours) as weil as more prolonged (2-5 days) administration (7, 8). Since there is a lag between the appearance and clearance of IGF-I in serum following hGH therapy, a differential mechanism has been suggested
MATERIALS AND METHODS Participants included 32 healthy prepubertal, shortstature, non-obese children (26 males, 6 females) aged 5 to 11 yrs. Height was
