Article Text
Abstract
Growth failure occurs in up to 85% of children newly diagnosed with Crohn’s Disease (CD) and persists in up to 40% throughout their disease course.1 Undernutrition and chronic inflammation appear to be the main driving factors behind growth failure and poor bone health.2 3 Adequate disease control and good nutritional status contribute to achieving growth target potential and minimising the long-term implications related to bone health.
To explore correlations between CD characteristics, bone health and growth parameters at diagnosis and during follow-up (figure 1A) and assess ways to optimise these parameters.
Retrospective data were collected from children (age at diagnosis < 18 years) newly diagnosed with CD between January 2018 and December 2019, from the Electronic Patient Records at our Institution. Baseline information surrounding CD (including age of diagnosis, disease location and severity score), bone health (including bone age, densitometry scan (DXA) Z-scores for bone mineral density (BMD) and bone mineral concentration (BMC), Vitamin D level) and growth (including height and weight centiles, BMI and pubertal status) was retrieved. Growth parameters were reassessed at follow-up to understand the changes in anthropometric measurements over time. Growth delay (Paris classification G1) was defined as involuntary stable weight or weight loss of 10% or more over the previous 6 months, and/or a decrease in height by ≥ 1 centile or a decrease in height velocity by ≥ 1 standard deviations (SD). Inferential statistical analyses performed using IBM SPSS Statistics v28.0 and R Bioconductor, included Pearson’s Chi Squared test, Bonferroni correction for multiple testing, Fishers Exact Test, Spearman’s Rank Correlation Coefficient, linear and multiple regression.
Seventy-six children were included (53 males (69.7%); age at diagnosis: mean 12.8 years, median 13.7, range 4.05–17.2; disease location (Paris classification): 28 L1, 12 L2, 36 L3; follow-up duration: mean 3.2 years, median 3.4, range 1–4.3). Thirty-one (81%) children had a DXA scan at diagnosis while only 2 children had a repeat scan during follow-up. Children with poorer DXA Z-scores had a younger age at diagnosis (P=0.021), more severe disease (P=0.074 for BMD, P=0.017 for BMC) and a lower BMI (P=0.002) at diagnosis (figure 1B and 1C). Seventeen (22.4%) children had growth delay at diagnosis, and at follow-up 44% of these children continued to have growth delay. Five children had bone fractures during the follow-up (2 had growth delay at diagnosis and 4 received one or more courses of steroids). Multivariate regression analysis demonstrated an older age of diagnosis to be a significant predictor of a lower height velocity at follow-up.
Disease severity and age of diagnosis are important CD-related factors that influence bone health and growth (figure 1D and 1E). These factors are closely related and impact on each other, therefore monitoring and optimising each aspect is pivotal to support children towards achievement of their growth and bone health potential. Monitoring should include repeat DXA scans during the disease course and optimisation of calcium and vitamin D intake throughout follow-up.
References
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