Corneal thickness in children with growth hormone deficiency: the effect of GH treatment
A Ciresi1, R Morreale2, S Radellini1
1Biomedical Department of Internal and Specialistic Medicine (DIBIMIS), Section of Endocrinology, Diabetology and Metabolism, University of Palermo, Palermo, Italy.
Insights
Growth hormone (GH) treatment in children with GH deficiency (GHD) increases central corneal thickness (CCT) and intraocular pressure (IOP). Ocular monitoring is recommended during GH therapy to prevent potential side effects.
Area of Science:
- Pediatric Endocrinology
- Ophthalmology
- Growth Hormone Therapy
Background:
- The eye is a target for growth hormone (GH) action, but data in GH deficiency (GHD) are limited.
- Evaluating ocular parameters in GHD children is crucial for understanding GH's role.
Purpose of the Study:
- To assess central corneal thickness (CCT) and intraocular pressure (IOP) in children with GHD.
- To determine the impact of GHD and GH treatment on CCT and IOP.
Main Methods:
- Measured CCT and IOP in 74 prepubertal GHD children before and after 12 months of GH treatment.
- Compared measurements with 50 age, gender, and BMI-matched healthy children.
- Analyzed correlations with auxological and biochemical data.
Main Results:
- No significant baseline differences in CCT and IOP between GHD children and controls.
- GH treatment significantly increased CCT and IOP in GHD children after 12 months.
- No correlation found between ocular changes and auxological/biochemical parameters.
Conclusions:
- GH treatment in GHD children significantly affects CCT and IOP.
- Suggests the need for careful ocular evaluation during GH therapy follow-up.
- Highlights potential for undesirable ocular side effects during treatment.
Objective:
The eye represents a target site for GH action, although few data are available in patients with GH deficiency (GHD). Our aim was to evaluate central corneal thickness (CCT) and intraocular pressure (IOP) values in GHD children to assess the role played by GHD or GH treatment on these parameters.
Design:
In 74 prepubertal GHD children (51M, 23F, aged 10.4±2.4years) we measured CCT and IOP before and after 12months of treatment. A baseline evaluation was also made in 50 healthy children matched for age, gender and body mass index. The study outcome considered CCT and IOP during treatment and their correlations with biochemical and auxological data.
Results:
No difference in CCT and IOP between GHD children at baseline and controls was found (all p>0.005). GHD children after 12months of therapy showed greater CCT (564.7±13.1μm) than both baseline values (535.7±17μm; p<0.001) and control subjects (536.2±12.5μm; p<0.001), with a concomitantly higher corrected mean IOP (15.6±0.7mmHg; p<0.001) than both baseline (12.5±0.8mmHg; p<0.001) and controls (12.3±0.5mmHg; p<0.001), without correlation with auxological and biochemical parameters.
Conclusions:
12months of GH treatment in children with GHD, regardless of auxological and biochemical data, affect CCT and IOP. Our findings suggest careful ocular evaluation in these patients to prevent undesirable side effects during the follow-up.
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