Abstract

We have recently shown in normal children of both sexes, that serum SHBG decreases significantly from infancy to late pre-pubeity, and that serum non-SHBG-bound (bioavailable, 8) testosterone (T) and estradiol (E2) increase significantly with age. It was postulated that the increase in BT and E2 could produce maturation changes in the central nervous system triggering the onset of puberty. We have also shown an age-related delay in the decrease of serum SHBG and in the increase of BT in patients with growth hormone (GH) deficiency. It was proposed that this mechanism could play a role in the prepubertal delay of patients with GH deficiency. As another model of delayed puberty, serum SHBG and BT were determined in 8 boys with chronic renal failure (CRF) in chronic dialysis for 0.25 to 3 years mean chronological age (CA) 9.90±4.43 years. A significant decrease of serum SHBG with age was found, r=0.76, p<0.01. The negative slope was not significantly different from normal (Controls, C, n=31, CA 10.17±2.61 years). Serum SHBG was significantly higher (X̄±SD 125±77.72 nmol/l) and serum BT lower (0.16±0.12 nmol/1) than in c (66.22±34.87 and 0.240.12, p<0.01 and p<0.05 respectively). It is concluded that, similarly to the findings in GH deficiency, increments in SHBG and decrements in BT could play a role in the pubertal delay of boys with CRI.

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