Abstract. A major problem in the androgen treatment of escessive height in boys is acceleration of growth velocity especially in the early stages of therapy. Oestrogen treatment in tall girls, in contrast, instantly decelerates growth velocity, probably by its plasma somatomedin lowering effect. As oestrogen administration in male subjects causes a similar somatomedin depression and immediate growth inhibition is also wanted in the treatment of excessive height in boys, the effect of short-term low dose oestrogen therapy (ethinyloestradiol, Ee, Lynoral®, 0.050 mg daily) on growth was studied in 10 constitutionally tall boys. During oestrogen therapy three week ulnar growth rate (TUG-rate) dropped instantly from 0.84 ± 0.42 to 0.33 ± 0.27 mm (P < 0.02) within 6 weeks. Three week body growth rate also changed significantly from 0.48 ± 0.23 to 0.12 ± 0.37 cm during oestrogen loading (P < 0.05). The magnitude of the latter changes, however, allows only evaluation of the whole group, whereas changes in TUG-rates far exceeded the limits of confidence in most individual boys. Growth deceleration during Ee was accompanied by a significant decrease in serum alkaline phosphatase activities (from 299 ± 72 U/l before to 240 ± 79 U/l during Ee, P < 0.01), plasma calcium (from 2.45 ± 0.06 to 2.35 ± 0.05 mmol/l during Ee, P < 0.05) and plasma testosterone levels (from 392 ± 128 ng/100 ml before to 27 ± 7 ng/100 ml during Ee, P < 0.005). Within 2 months after stopping Ee administration plasma testosterone levels were normal again (432 ± 282 ng/100 ml). Testicular size was not affected. Mild reversible gynaecomastia, however, was present in all boys. The results demonstrate an instant growth decelerating effect of low dose oestrogen administration in tall boys reminiscent to the findings in tall girls under the same low dose regimen. Furthermore these data provide a theoretical base for combining androgens and oestrogens in the early stages of treatment of excessive height in boys in order to antagonize the initial growth accelerating effect of androgens alone.
Using a simple non-invasive ulnar length measuring technique a 70 to 80% decrease in ulnar growth velocity was found during one interval of 9 weeks of low dose ethinyloestradiol administration (0.050 mg daily) in girls with tall stature. This decrease in ulnar growth velocity was found to be statistically significant within 6 and even 3 weeks after starting oestrogen loading whereas the change in body growth velocity was only significant after 9 weeks. After interrupting oestrogen administration, ulnar growth velocities increased again but to values tending to be lower than before ethinyloestradiol loading. Serum alkaline phosphatase activities and plasma inorganic phosphorus and calcium levels also decreased significantly during oestrogen therapy within 9 weeks. The results found illustrate that the measuring technique used enables evaluation of the short-term effect of hormonal treatment on growth and thereby related biochemical phenomena.
Using a sensitive measuring device, 3-day hCG administration (Pregnyl; 1500 IU daily) was shown to temporarily increase ulnar growth velocity from prepubertal (0.40 +/- 0.35 mm/3 weeks to pubertal values (1.1 +/- 0.64 mm/3 weeks) in 10 boys with delayed puberty. This growth-promoting effect of diagnostic hCG administration, which was demonstrable for 3--9 weeks, was associated with an overt rise in plasma testosterone from 129 +/- 126 to 818 +/- 419 ng/100 ml and an approximate doubling of the serum alkaline phosphatase activities from 193 +/- 46 to 376 +/- 115 U/liter, suggesting an initiated growth spurt.
SUMMARYUsing a non‐invasive sensitive technique measuring ulnar length, short‐term growth was studied in two groups of boys with constitutional delay in growth. In one (group A) a protocol of multiple hCG injections weekly was used (3 × 1500 iu), whereas the other (group B) received a single dose of hCG weekly (1 × 1500 iu), both during 6 weeks. The two hCG protocols appeared to be equally potent in stimulating 3‐week Ulnar Growth rates (TUG‐rates), tripling the growth velocities from prepubertal to pubertal levels. After stopping hCG treatment the mean TUG‐rate decreased again to a post‐treatment level that, taking both groups together, was significantly higher than the mean pretreatment TUG‐rate. During hCG administration mean body growth rates also rose significantly in the two groups. The extent of the changes, however, only allowed evaluation for the whole group in contrast to the changes in TUG‐rates which far exceeded the limits of confidence in all but one boy. Serum alkaline phosphatase activities (APA) increased significantly during hCG treatment and almost paralleled the increase in TUG‐rates. The APA response (ΔAPA) in group A, however, was unexpectedly higher than in group B. After stopping hCG treatment the mean APA significantly decreased taking both groups together to an almost pretreatment level. The results showed that a weekly single dose hCG regimen was as effective as the weekly multiple injection protocol in stimulating TUG‐rates to pubertal levels in the groups of constitutionally delayed boys studied.
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