ESPE Abstracts

Introduction: Of any pituitary dysfunction following brain injury, growth hormone (GH) deficiency (GHD) is the most prevalent. The cut-point for defining GHD has been placed at 7 ng/mL representing optimum test performance. We hypothesised this cut-off may be set too low for genetically taller children with acquired brain injury, notably brain tumours, who demonstrate severe growth failure but repeatedly fail to meet diagnostic thresholds for GH replacement until several centiles have been crossed downward over time; this treatment delay may ultimately compromise metabolic status and post injury wellbeing. We reviewed the possibility this cut-off, and its undifferentiated applicability to a broad variety of taller children with clear longitudinal growth failure of different target heights, height predictions and BMIs, requires re-consideration for this cohort.

Methods: We reviewed retrospectively the parental heights, longitudinal growth records and charts of 50 children from diagnosis of a brain tumour (47) or traumatic (3) brain injury, and noted, at intervals, height, weight, Tanner stage and peak GH (pkGH) at first onset of growth failure and at any subsequent testing for persistent growth failure. BMI, BMI SDS, height SDS and midparental height SDS (MPHSDS) were calculated.

Results: After a period of Initial growth exceeding MPHSDS, 42/50 (≙ 84%) fell to the midparental centile and were assessed for GHD. 26/42 (≙ 61.9%) did not meet diagnostic criteria for GHD. Despite ‘persisting’ growth failure and little change in BMISDS, a median 24.7 (range 11.0; 53.1) months later, 10/26 again failed to meet GH treatment criteria and one additionally failed a third GH assessment 11.8 months later. In total, patients took a median 10.7 (range 0; 57.7) months to meet GH treatment criteria from first onset of growth failure, with an overall median −0.14 (range −1.21; 0.96) decrement in HTSDS and little change in BMISDS.

Conclusion: Our pre treatment data do not suggest a MPHSDS above average or an increment of BMISDS impairs diagnostic validity of current pkGH and may be a physiological ‘catch-down growth’ towards MPHSDS, not requiring immediate GH treatment. Severe GHD may ensue which requires continuous monitoring after recanalisation into the mid-parental centile and at onset of puberty. Post treatment review is still required to ensure that these children achieve their innate growth potential without compromise.