Factors Attenuating Growth Promoting Effect of Growth Hormone Therapy for Turner's Syndrome.

Sato, Tamotu; Miyamori, Chiaki; Kajiwara, Sohei; Miyagawa, Kazuhiko; Shimizu, Makoto

doi:10.1507/endocrj1954.35.725

Cited by 4 publications

(1 citation statement)

References 24 publications

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“…IGF-I levels in children with TS of "pubertal age", i.e. older than about 10 years in comparison to healthy controls (Cuttler et al, 1985;Ranke et al, 1987;Sato et al,, 1988;Schober et al, 1989). In agreement with these authors we could not find correlations of IGF-I levels with the chromosomal status, or with pubertal stages.…”

Section: Discussionsupporting

confidence: 83%

Somatomedin-C/IGF-I, Insulin and Prolactin Levels in Ullrich-Turner's Syndrome

Amendt

Hesse²,

Rohde³

2009

Exp Clin Endocrinol Diabetes

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To clarify the pathogenesis of growth retardation in patients with Ullrich-Turner's syndrome (TS) we have investigated basal SmC/IGF-I, insulin and prolactin concentrations. Compared with 56 age matched healthy controls basal SmC/IGF-I concentration in 51 patients with TS older than 9-11 years was significantly lower (age group 13-14 years; TS 273 +/- 47 and controls 479 +/- 114 ng/ml). Mean basal prolactin level in 43 patients with TS (406 +/- 211 microU/ml) was significantly higher (p less than 0.01) than in 192 female controls (age 3-11 years; 264 +/- 176 microU/ml). Basal insulin concentration in 28 TS patients in comparison to 20 healthy children of a control group was significant higher (TS 18 +/- 8 microU/ml; controls 9 +/- 4 microU/ml; p less than 0.01). It seems that neither insulin nor prolactin are relevant stimulators of Smc/IGF-I in man, especially in patients with gonadal dysgenesis. Considering these results we speculate that despite higher prolactin and higher insulin levels in TS, the lower SmC/IGF-I concentrations may be predominantly related to the abnormal sex steroid secretion.

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Section: Discussionsupporting

confidence: 83%

Somatomedin-C/IGF-I, Insulin and Prolactin Levels in Ullrich-Turner's Syndrome

Amendt

Hesse²,

Rohde³

2009

Exp Clin Endocrinol Diabetes

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Growth hormone secretion in Alzheimer's disease: 24-Hour profile of basal levels and response to stimulation and suppression studies

Heuser

Baronti

Marin

et al. 1992

Neurobiology of Aging

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Update on Growth Hormone Therapy for Turner's Syndrome

Rosenfeld

1989

Acta Paediatrica

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With the development of recombinant DNA technology and the ability to mass produce synthetic human growth hormone (hGH), critical evaluation of the efficacy of hGH in patients with Turner's syndrome has become possible. Table 1 summarizes the literature published to date on hGH studies in Turner's patients. Earlier trials were limited by the small numbers of patients studied, the generally low-dose regimens employed, and the short-term follow-up of subjects. However, several large scale studies from the USA, Japan and Europe are beginning to yield important data concerning the short-term and longer-term efficacy of hGH, both alone and in combination with anabolic steroids or oestrogens.While these studies all vary in their entry criteria, age of subjects, hGH preparations and regimens used, and dosages of androgens or oestrogens given, all clearly demonstrate that hGH, both alone and in combination with sex steroids, can stimulate growth over a period of 1 year. Given alone, hGH has resulted in an increment in annual growth rate of 2.7 cm/year (19), 2.4 cm/year (20-22), 3.8 cm/year (23), 1.5 cm/year (24), 3.6 cm/year (25), and 3.2 cm/year (26). Further review of the cumulative data from these studies points to the following cautious conclusions.hGH alone. Given alone, hGH results in a modest, but significant, increase in growth rate over the first year of administration. This increase is all the more noteworthy given that the natural history of growth in Turner's syndrome is one of progressive growth deceleration (30,31). In the Genentech Collaborative Study (20-22), annual growth rate (expressed as SDS for Turner's syndrome patients) was -0.1 for the control group and +3.1 for the hGH group during the first year of therapy (Table 2).High-dose hGH therapy. While careful dose-response studies have not yet been performed, it is noteworthy that many of the clinical trials employed relatively high doses of hGH, and that the results suggest an enhanced growth response at rhGH doses as high as 1.22-1.35 IU/kg/week' . Combination therapy with low-dose oestrogens. Data accumulated to date indicate that the addition of low-dose oestrogen preparations to optimal hGH regimens does not significantly augment the clinical response to hGH.Vanderschueren-Lodeweyckx et al. (26) have shown that the addition of ethinyloestradiol, 25 ngikglday, to hGH increased incremental growth from +3.6 to +4.9 cm/year (Table l), but this increase did not achieve statistical significance. Similarly Ross et al. (32) have demonstrated that while ethinyloestradiol, 50 ng/kg/day , enhanced the lower leg growth response to hGH, 0.09 IU/kg three times a week, larger doses of ethinyloestradiol (100 ng/kg/day) did not alter the response to hGH, 0.15 IU/kg three times a week. Furthermore, oestrogen administration may be associated with undesirable feminization, as well as advancement of skeletal maturation.Combination therapy with oxandrolone. The original observation by Rudman et at. (10) of a synergism between oxandrolone and hGH appears to be substanti...

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Factors Attenuating Growth Promoting Effect of Growth Hormone Therapy for Turner's Syndrome.

Cited by 4 publications

References 24 publications

Somatomedin-C/IGF-I, Insulin and Prolactin Levels in Ullrich-Turner's Syndrome

Somatomedin-C/IGF-I, Insulin and Prolactin Levels in Ullrich-Turner's Syndrome

Growth hormone secretion in Alzheimer's disease: 24-Hour profile of basal levels and response to stimulation and suppression studies

Update on Growth Hormone Therapy for Turner's Syndrome

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