Abstract: SAT 026

Catch-up Growth in Prepubertal Children Treated for Celiac Disease, Juvenile Hypothyroidism and Growth Hormone Deficiency Can be Modeled with a Monomolecular Function

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Abstract


The growth response to GH treatment in prepubertal children with GH deficiency (GHD) is commonly described by annual height velocities, but this approach has limitations. An alternative approach is to model the complete phase of catch-up growth (CUG), as developed for celiac disease (CD) (1): a monomolecular function of height SDS minus target height SDS (adj-HSDS) over time: A*(1-B*EXP(-k*t))– 5, with t=time in years (0=start of therapy), A-5 = adj-HSDS(end), A*(1-B)-5 = adj-HSDS(0), and k as rate constant. view more

The growth response to GH treatment in prepubertal children with GH deficiency (GHD) is commonly described by annual height velocities, but this approach has limitations. An alternative approach is to model the complete phase of catch-up growth (CUG), as developed for celiac disease (CD) (1): a monomolecular function of height SDS minus target height SDS (adj-HSDS) over time: A*(1-B*EXP(-k*t))– 5, with t=time in years (0=start of therapy), A-5 = adj-HSDS(end), A*(1-B)-5 = adj-HSDS(0), and k as rate constant. We hypothesized that this function also fits CUG in treated children with juvenile hypothyroidism (JHT) or GHD, and may better detect an influence of predictors of the growth response (CUG) to GH treatment, in comparison to conventional techniques. We modeled all available prepubertal adj-HSDS data with a mixed-effects model in a study on 20 children with JHT (2) and a dose-response study on 19 children with GHD (a low GH dose of 0.67 mg/m2.day (LD) vs a high dose (HD) of 1.33 mg/m2.day) (3) using two approaches. Model 1 was based on a national height reference with an age cut-off of 10 (girls) and 12 (boys) years, to prevent bias by increasing mean height and SD in adolescence in the population. For GHD, we also used adj-HSDS for infancy-childhood growth (ICP-model) (4), if age(0) was >3, with no upper age limit (Model 2). Linear regression analyses were performed to test the difference of the model’s parameters between groups. In 2 cases with JHT and 3 with GHD the data could not be modeled, because adj-HSDS decreased >0.15 SD after the 2nd or 3rh measurement. In JHT, adj-HSDS=4.62*(1 – 0.65*EXP(-0.76*t))-5), with a mean (SD) adj-HSDS(0) at age 5.1 (2.7) yrs and adj-HSDS(end) of -3.3 (1.1) and -0.4 (1.1). Compared with CD, adj-HSDS(0) was lower and k higher (p=0.02), but adj-HSDS(end) was equal. In GHD (model 1), adj-HSDS=5.14*(1–0.55*EXP(-0.60*t))-5), with a mean (SD) adj-HSDS(0) at age 6.7 (3.4) yrs of -2.5 (1.0) and -2.8 (1.9) in LD and HD, and an adj-HSDS(end) of -0.1 (0.7) and 0.5 (1.2) (NS). k was lower than for CD (p<0.01) but similar to JHT, while adj-HSDS(0)and adj-HSDS(end) were similar to CD and JHT. With model 2, the function was adj-HSDS=5.83*(1 – 0.56*EXP(-0.58*t))-5), with a mean (SD) adj-HSDS(0) of -2.3 (1.0) and -2.6 (SD=1.8) in LD and HD, and adj-HSDS(end) was 0.6 (0.6) and 1.2 (1.0) (NS); k tended to be higher for HD (p=0.058). For both GHD groups, k and adj-HSDS(end) were lower than for CD (p<0.01). In comparison with JHT, LD had higher adj-HSDS(0), lower k (p=0.003), but higher adj-HSDS(end) (p=0.008); HD showed similar k, but higher adj-HSDS(end) in comparison to JHT (p=0.003).
In conclusion, CUG of prepubertal children with CD, JHT or GHD can be modeled with a monomolecular function. This can be used for assessing the adequacy of CUG and the influence of pretreatment variables and GH dose on the growth response to GH in prepubertal GHD children.

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