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Somatomedin-C in accelerated growth of children with precocious puberty
Insights
Somatomedin-C (Sm-C) levels are elevated in children with precocious puberty but do not drive the growth spurt. Sex steroids, not Sm-C, correlate with growth rates in these patients.
Area of Science:
- Pediatric Endocrinology
- Growth Hormone Axis
- Puberty Disorders
Background:
- Central precocious puberty involves early onset of puberty, leading to accelerated growth.
- The role of somatomedin-C (Sm-C) in mediating the growth spurt of precocious puberty is not fully understood.
- Investigating Sm-C levels is crucial for understanding pubertal development and growth acceleration.
Purpose of the Study:
- To determine if somatomedin-C (Sm-C) mediates the growth spurt in children with central precocious puberty.
- To compare Sm-C levels in children with precocious puberty to normal age-matched and pubertal controls.
- To assess the impact of LHRH analogue treatment on Sm-C levels and growth rates.
Main Methods:
- Compared Sm-C levels in 40 children with central precocious puberty, 87 normal children, and 110 pubertal controls.
- Administered LHRH analogue (LHRHa) for 6 months to patients with precocious puberty.
- Monitored changes in secondary sexual characteristics, growth rate, gonadotropins, sex steroids, and Sm-C levels.
Main Results:
- Sm-C levels were significantly elevated in precocious puberty patients, similar to normal puberty.
- LHRHa treatment decreased sexual characteristics, growth rate, and hormone levels, including Sm-C.
- Growth rates correlated with estradiol (girls) and testosterone (boys), but not with Sm-C levels before or during treatment.
Conclusions:
- The growth spurt in central precocious puberty is not explained by plasma somatomedin-C levels.
- Sex steroids (estradiol and testosterone) are the primary drivers of growth in precocious puberty.
- Further research into the complex interplay of hormones in pubertal growth is warranted.
Abstract:
To assess the role of somatomedin-C as a possible mediator of the growth spurt in children with central precocious puberty, we compared Sm-C levels in 40 children with central precocious puberty, 87 age-matched normal children, and 110 normal pubertal controls. Somatomedin C levels were significantly elevated for age in the children with precocious puberty (P less than 0.01), and were similar to the levels observed during normal puberty. The patients with precocious puberty were given the luteinizing hormone releasing hormone analogue D-Trp6-Pro9-NEt-LHRH (LHRHa) for 6 months. Treatment caused a significant decrease in secondary sexual characteristics, growth rate, plasma gonadotropins, sex steroids (estradiol in the girls and testosterone in the boys), and Sm-C levels. Growth during LHRHa treatment returned to the age-appropriate rate, whereas plasma Sm-C levels, although lower than pretreatment levels, remained significantly elevated for age (P less than 0.002). In addition, growth rates before and during treatment did not correlate with the plasma somatomedin C levels, nor did the decreases in growth rate during LHRHa therapy correlate with the decreases in somatomedin C levels. Growth rates did correlate significantly, however, with plasma estradiol levels in the girls (P less than 0.0005) and with plasma testosterone levels in the boys (P less than 0.025). We conclude that the growth spurt in children with precocious puberty cannot be explained by the plasma level of somatomedin C.