All children receiving publicly funded GH therapy in New Zealand have applications processed centrally. Review by the Multiregion Ethics Committee (Wellington, New Zealand) determined that ethics approval of this comprehensive audit was not required.Īnonymised patient data was provided by PHARMAC, the New Zealand agency that administers the GH program, from a database extending back to 1975 8. As a secondary aim, we also evaluated the effect of bone age delay and GH treatment on change in predicted adult height. In this study we examined the hypothesis that constitutional delay of growth is positively related with response to GH treatment and evaluated the relationship between age at the start of treatment, ethnicity and sex on growth rate and increase in height in an unselected national cohort of New Zealand children and adolescents with short stature.
In New Zealand, GH treatment is publically funded for growth hormone sufficient children with short stature 8.
However, in children with ISS who are treated with GH, greater bone age delay has been associated with greater final height 7. Perhaps surprisingly the difference between bone age and chronological age has been reported to have little effect on the initial acceleration of growth during GH therapy 6. Healthy children with ISS tend to have a delayed bone age. In Australia, a retrospective study suggested that girls had a reduced response compared to boys when GH was begun before 6 years of age, for unclear reasons 4.Ĭonstitutional delay, defined as a biological age a year or more behind the child's chronological age, is a measure of the potential future growth of the child 7. Previous studies suggest that better growth is associated with younger age at the start of GH treatment, taller height at start of GH therapy, taller parents and greater response to GH in the first year 1, 4, 6. Not surprisingly in this heterogeneous group, the response to GH is highly variable and some patients show little or no apparent gain in height. There is evidence from controlled trials that recombinant human growth hormone (GH) can increase short term growth rates and that this increases final height by a mean of approximately 5.5 cm 1, 3, 4, 5. Idiopathic short stature (ISS) is a condition in which a child is short for unknown reasons and consistently grows at a below average rate for their demographic 1, 2. This study shows that greater bone age delay was associated with greater initial improvement in height but less improvement in predicted adult heights, suggesting that children with very delayed bone ages may show accelerated maturation during GH treatment. PAH-SDS increased with treatment (+0.94 (0.18, 1.5)) increased PAH-SDS was associated with less bone age delay and greater initial increase in HtSDS. The increase in HtSDS but not in GV-SDS was greatest with younger patients and greater bone age delay, with no effect of sex, BMI-SDS or baseline HtSDS.
Demographic and auxological data were prospectively collected and standard deviation scores (SDS) were calculated for height (HtSDS), yearly growth velocity (GV-SDS), body mass index (BMI-SDS) and predicted adult height (PAH-SDS) at time of the last available bone age. 70 patients were treated with 21 GH iu/m2/week from 1975 to 2013 throughout New Zealand. Patients with an organic cause for delay are given sex-steroid therapy to induce puberty and are most likely to require lifelong hormone replacement therapy after puberty is complete.In a retrospective, population based cohort study, we examined whether constitutional delay was associated with the growth response to growth hormone (GH) in children with short stature and normal GH responses. Sex-steroid treatment is reserved for those with psychosocial maladaptation, and consists of a short course of sex steroids to induce puberty. Patients with constitutional delay are typically observed. The distinction between organic gonadotrophin deficiency and constitutional delay of puberty is not easy and is often resolved only with time.
Most patients seek medical assistance because of slow growth rather than slow pubertal development.Ĭareful assessment of height and pubertal stage is crucial for evaluation of the underlying cause. May be functional (constitutional delay, underlying chronic disease, malnutrition, excessive exercise) or organic, due to either a lack of serum gonadotrophin production or action (hypogonadotrophic hypogonadism), or gonadal insufficiency with elevated gonadotrophins (hypergonadotrophic hypogonadism). Defined as the lack of any pubertal signs by the age of 13 years in girls and 14 years in boys.
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