Central corneal thickness in children with growth hormone deficiency

Abstract

Acta Ophthalmol. 2010: 88: 692–694 Abstract. Purpose: To evaluate central corneal thickness (CCT), intraocular pressure (IOP) and eye refraction in patients with congenital growth hormone (GH) deficiency. Methods: Retrospective case series. Forty‐five patients with growth defect treated with recombinant GH and 45 healthy children underwent ophthalmological examination, including CCT measurements, applanation tonometry and cycloplaegic refraction. Results: The average CCT in the GH deficiency group was 570.6 μm [standard deviation (SD) 37.4]. In the control group, it was 546.0 (SD 24.9). The average IOP in the GH deficiency group was 18.2 mmHg (SD 3.4). In the control group, it was 14.6 (SD 2.0). The mean refractive error (spherical equivalent) in the GH deficiency group was 0.59 D (SD 1.9). In the control group, it was 0.11 (SD 2.1). Conclusion: GH and insulin‐like growth factor 1 are involved in ocular growth by influencing the synthesis of the extracellular matrix of the sclera. Children with congenital GH deficiency or insensitivity have a mean hyperopic defect related to a shorter axial length. A number of studies have demonstrated that CCT in newborns is significantly greater than in adults; a decrease in CCT is closely correlated with an increase in corneal diameter. This finding suggests that the growth of the eye, with possible remodelling and stretching of collagen fibres, may play an important role in the reduction of corneal thickness in the first years of life. Therefore, we conclude that a greater CCT can represent a sign of a delayed growth of the eye in patients with GH deficiency. Finally, our study confirms the influence of corneal thickness on IOP measures, and the prevalence of hyperopia among children with growth defect.

Ocular biometry and central corneal thickness in children: a hospital-based study

“…Parentin et al hypothesized that this decrease took place during the first and second years of life. They claimed that rearrangements in collagen bundles and remodeling occurred in the early years of life (24) . Hussein et al studied children between the ages of 7 months and 14 years and reported that CCT was 538 µm in children under 2 years old, 546 µm in children between 2 and 4 years, 565 µm between 5 and 9 years, and 555 µm between 10 and 14 years old.…”

Human Growth Hormone Promotes Corneal Epithelial Cell Migration in Vitro

“…4 HGH is known to act on a variety of target organs and tissues, but little is known about its possible action on the cornea. Recently several human studies have shown alterations in the thickness and biomechanics of the cornea in acromegalic patients and GH deficient children, 5-7 suggesting a role of GH in the cornea. GH exerts its effect by binding to pre-dimerized GH receptors (GHRs) located on cell plasma membranes, leading to activation of intracellular Janus-kinase 2 (JAK2).…”

Novel Therapy to Treat Corneal Epithelial Defects: A Hypothesis with Growth Hormone

“…87 Recently, human studies have shown altered thickness and biomechanics of the cornea in acromegalic patients and GH-deficient children. 88–90 These findings suggest a role of GH in the cornea. We hypothesize that HGH can promote corneal wound healing and that it does so by activating phospho-STAT5 ( p-STAT5 ) signaling and promoting corneal epithelial and fibroblast proliferation and/or migration.…”