We have studied 71 sexually immature growth hormone (GH) deficient patients treated for 1 yr with human growth hormone (hGH). Nineteen patients had growth hormone deficiency secondary to an organic lesion. In 52 there was no demonstrable underlying cause. Patients with organic disease received thyroxine 0.2 mg/ M 2 /24 hr, cortisone acetate 20 mg/M 2 /24 hr, and 2 units hGH 3 times weekly from either unembalmed or embalmed pituitaries. These 2 groups grew (in cm/yr, mean ± 1 SD) 5.4 ± 2.8 and 7.0 =fc 2.8, respectively. Patients with idiopathic disease received hGH from unembalmed pituitaries. One group was given thyroxine, cortisone acetate and hGH 2 units 3 times weekly, a second only hGH 2 units 3 times weekly, and a third only hGH 10 units 3 times weekly. These groups grew 7.3 ± 3.5, 9.3 ± 2.3 and 11.9 i t 2.5 cm/yr, respectively. Embalmed hGH was as effective as unembalmed. The underlying cause of GH deficiency did not influence the degree of response. While the addition of cortisone and thyroxine did not clearly affect the response to hGH, this combination therapy was associated with an acceleration of bone age in excess of the advance in height age. A significantly greater response was observed in patients receiving hGH 10 units 3 times weekly. The amount of growth correlated with pretreatment height and weight; a greater response was observed in smaller children. While 2/3 of the patients responded well, 1/3 failed to increase their growth rate to greater than 7 cm/yr and/or to double their pretreatment growth rate. (/ Clin Endocrinol Metab 35: 483, 1972) A LTHOUGH human growth hormone (hGH) had been isolated from pitu-
ExtractTwelve hypopituitary patients ranging in age from 58f2 to 15 ?fa years were treated for 12 months with a standardized dose of human growth hormone (HGH), 0.1 or 0.05 U/kg three times weekly). From the 7th to 12th month inclusive, fluoxymesterone, 2.5 mg/m2/24 hr per os was given in combination with the growth hormone. From the 12th to the 18th month, no therapy was given. Heights and weights were recorded every 1 or 2 months. Bone age films were assessed at the onset and again in the 6th, 12th, and 18th month of the study.In the first 6 months of HGH therapy, the mean growth rate (centimeters per year f SD) was 9.4 =t 2.3. During combined treatment with HGH and fluoxymesterone, the mean growth rate of 13.4 f 3 was significantly greater ( P < 0.001) than on HGH alone. Post-treatment mean growth rate from the 13th through 18th month, inclusive, was 2.7 =t 1.2. Weight gain (kilograms per year & SD) during combined treatment (13 =t 7) was significantly greater ( P < 0.001) than during HGH administration (3.4 =t 2.4). Mean advancement in bone maturation (months =t SD) during HGH (12 f 7.7) was not significantly different from the mean gain in bone age during combined treatment (12 =t 12). In the final 6 months without any therapy, the mean gain in bone age was 8.8 f 6.1. In the 18 months of study, the mean increase in bone age was 33 months, and the mean gain in height age (HA) was 23 months.Although final evaluation of this treatment program depends upon a longer period of observation, the immediate assessment suggests that the significant improvements in height, weight, and physical appearance were sufficient to compensate for the gains in bone maturation, especially since the patients who entered the study had markedly retarded bone ages.
SpeculationHGH and androgens interact synergistically. Androgens stimulate HGH secretion in intact animals. In the hypopituitary state, androgens require the addition of HGH for optimal promotion of optimal growth and secondary sexual development.
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