Growth hormone deficiency is a type of growth disorder caused by a partial or complete deficiency of growth hormone synthesized and secreted by the pituitary gland, abnormal molecular structure of growth hormone, or defects in receptors.
Growth hormone can promote the growth and development of the body by promoting protein synthesis, liver glycogen and fat decomposition, increasing the reproduction of muscle, tissue and organ cells, and can also promote the growth of height by promoting the proliferation of epiphyseal chondrocytes, bone deposition, epiphyseal plate thickening and longitudinal growth of osteogenesis.
Studies have found that growth hormone deficiency can not only lead to short stature in children, but also lead to cardiovascular diseases in children, impaired glucose and lipid metabolism in children, obesity, and delayed sexual development. Studies have shown that growth hormone can act on the eyes in an endocrine, autocrine and paracrine manner to promote the growth and development of the eye.
It can be assumed that growth hormone plays an important role in the development of the eyeball. Many scholars have also found that congenital abnormalities of the eyeball are associated with growth hormone deficiency. Growth hormone also plays an important role in the development of the refractive system of the eye, and the refractive status of the eye is mainly taken from the three main variables of the eye axis, cornea, and lens and the interaction between them.
After the birth of the newborn, although the eye axis continues to grow, the cornea and lens also undergo corresponding changes at the same time, and by the age of 7 years, the refractive state of the eye is dominated by farsightedness. From the age of 8 to 14 years, the axial length of the eye further increases, and the refractive state develops in the direction of emmetropia and myopia.
Previous studies have shown that short axial length, shallow anterior chamber, increased curvature of the anterior surface of the lens and small cornea are high-risk factors for primary open-angle glaucoma, and the eye axis of children with growth hormone deficiency is significantly shorter than that of normal children, making the eyeball of children with growth hormone deficiency smaller than that of normal children of the same age, and the narrowing of the eyeball is easy to cause shallow anterior chamber depth and anterior chamber stenosis.
Some scholars have found that children with growth hormone deficiency have thickened corneas and increased intraocular pressure compared with normal children, which is considered to be an important marker of growth hormone deficiency leading to eye development retardation. In the subsequent growth process, it may further lead to the occurrence of glaucoma, which is a highly insidious, rapidly developing eye disease that is extremely harmful to all parts of the eye and visual function.
At present, it is believed that children with growth hormone deficiency have a variety of problems with poor development of ocular parameters. There are a large number of children with growth hormone deficiency, and there is a lack of research on the comparison of axial length, refraction, cornea, and lens with normal children.
1. The effect of growth hormone deficiency on meibomian glands
Studies on human meibomian gland epithelial cells have shown that IGF-1 assists meibomian gland epithelial cell reproduction and lipid synthesis by stimulating the expression of binding proteins in the cell cycle. The lipids secreted by the meibomian glands, also called meibomian gland lipids, are a mixture of several lipids.
Meibomian lipids constitute the lipid layer of the tear film and have important physiological functions, including making the eyelid margin hydrophobic to prevent tears from overflowing, delaying the evaporation of tear film water, preventing sebaceous gland secretions from moving inward and destroying the tear film, providing a smooth and flat optical interface, reducing the surface tension of tears so that the liquid can be stored in the tear film, and forming a watertight layer between the eyelids.
Growth hormone deficiency can affect the loss of meibomian glands and the secretion of glands, and in severe cases, it can lead to a decrease in meibomian gland function. Meibomian gland dysfunction is a common chronic inflammation of the ocular surface with abnormal tear film and ocular irritation as the main manifestations in ophthalmology, which can lead to lipid deficiency, decreased tear film stability, and increased tear evaporation, which is an important cause of hyperevaporative dry eye.
2. The effect of growth hormone deficiency on the cornea
Studies have shown that a decrease in corneal thickness is closely related to an increase in corneal diameter, suggesting that eye growth and remodeling and stretching of collagen fibers play an important role in the reduction of central corneal thickness in the first years of life.
Studies have shown that children with growth hormone deficiency often exhibit corneal thickness that is different from that of normally developing children, and that the corneal thickness of children with growth hormone deficiency is higher than that of normal children, and the corneal thickness is significantly lower after growth hormone therapy.
Thus, in patients with growth hormone deficiency, a higher CCT associated with a shorter eye axis may represent a sign of eye retardation in children with growth hormone deficiency.
3. The effect of growth hormone deficiency on the eye axis
From birth to adolescence, the refractive state changes as the eye grows and develops. The previously reported pattern of ocular development in school-age children is that the eye axis becomes longer, the anterior chamber depth deepens, and the radius of corneal curvature changes more or less smoothly with age.
Growth hormone has a local or endocrine role in ocular tissue, and both ocular development and axial elongation are thought to be mediated by the regulation of angiogenesis and extracellular matrix, which plays an important role in the production of blood vessels and the regulation of the extracellular matrix.
It is well known that the refraction of the eye depends on three variables and their interactions: corneal refraction, lens refraction, and axial length. Although these variables have changed, the human eye gains emmetropia at a young age.
The eye grows rapidly in the first year of life: in the first 6 weeks, the cornea flattens from an average of 51 to 44 days, and the refractive power of the lens decreases from 34 days at birth to 26 days at 18 months. In the seventh year after birth, the main changes in refraction depend on the increase in the axial length. These morphological changes are associated with changes in the refractive power of the eye.
From birth to the end of the seventh year, hyperopia predominates and can increase slightly in general, and from 8 to 14 years of age, the refractive index moves rapidly towards myopia as the eye axis increases. Congenital growth hormone deficiency may interfere with the role of IGF on scleral growth, limiting eye development after birth.
4. The effect of growth hormone on the lens
The process of lens differentiation and maturation is regulated by many genes, forming a precise regulatory network. Abnormalities in any of these regulatory links may cause changes in the lens.
It is well known that the refraction of the eye depends on the interaction between three variables: corneal refraction, lens refraction, and axial length. During the first year of life, the cornea and lens show significant changes, after which the main changes in refraction depend on the increase in the axial eye.
The human eye is programmed to acquire emmetropic eyes at a young age. This process of confrontization is the result of both active and passive processes. The active mechanism is related to feedback from the retina on image focal formation and subsequent adjustment of axial length.
Growth hormone and other related growth factors can play an important role in this active mechanism. The passive process involves the proportional growth of the eye, which is associated with a proportional decrease in the diopter of the diopter system with an increased axial length.
5. Effect of growth hormone on diopter
The refractive development of the human eye is a dynamic development process, from birth to adulthood, the refractive parameters change accordingly, and the refractive state also changes. The development of the eye is often described as an emmetropic process. After the 7th year of life, the main change in refractive status depends on the increase in the axial eye.
From birth to the end of the 7th year, hyperopia predominates and can increase slightly, and from 8 to 14 years of age, the refractive state is secondary to an increase in the axial length and rapidly develops in the direction of myopia. The relationship between height and diopter has been pointed out in studies that show that taller children have longer eye axes and tend to be nearsighted in refractive states, suggesting that growth hormone may play an indirect role in the development of refractive errors.
The shorter axial lengths found in children with growth defects may explain the prevalence of hyperopia defects in these patients. It has been shown that the GH/IGF axis has an effect on the synthesis and coagulation of collagen fibers in the outer layer of the sclera, and that the growth of scleral cells may require local effects of IGF-II, and conversely, the cessation of IGF-II and type II IGF receptor expression may occur simultaneously with the terminal differentiation of scleral cells.
6. The effect of growth hormone on the choroid
The choroid, which is between the sclera and the Bruch membrane, is responsible for transporting oxygen and nutrients, and secretes growth factors, which has the role of nourishing the outer layer of the retina and ensuring the normal function of the retina, which occupies most of the blood flow in the eye and supplies the outer layer of the retina, including the choroidal layer and the vascular layer.
In recent years, many studies have shown that the subfoveal choroidal thickness of the macula is negatively correlated with the axial length, and the rate of choroidal thickness thinning varies among researchers, and the subfoveal choroidal thickness of the macula decreases by 13.55~79.33μm for every 1mm increase in axial length.
In patients with growth hormone deficiency, the choroidal thickness is thinner than that of healthy subjects, and this study also suggests that the choroid may be the route for growth hormone to reach the retina, and it may also be the site of action of growth hormone.
7. The effect of growth hormone on the retina
As one of the most important tissues for visual formation, the retina has a delicate and complex structure. The retina develops from the optic cup formed by the neuroectoderm during the embryonic period. The blood supply to the inner layer of the retina comes from the central retinal artery, while the choroidal vasovascular nutrition of the outer layer of the retina.
The junctional complex between retinal vascular endothelial cells forms a blood-intraretinal barrier, thereby blocking the entry of blood components and macromolecules into the retina in the retinal vessels and choroidal vessels. Therefore, the development of retinal blood vessels plays an important role in vision.
After birth, the retina has little or no vascularization, and most retinal vascularization occurs during the fetal period. Growth hormone has been shown to have angiogenic effects, and retinal cells are known as a domain of local growth factors, including insulin-like growth factor-1.
In clinical studies, the effect of growth hormone deficiency on retinal vascularization has been manifested by a decrease in vascular branch points and a decrease in retinal angiogenesis. In immunochemical studies, growth hormone and growth hormone receptors have also been found in retinal ganglion cells. In patients with growth hormone deficiency, decreased retinal vascularization and optic nerve hypoplasia are well described in the literature.
8. Conclusion
In summary, growth hormone plays an extremely important role in the structure and function of the eyeball through insulin-like growth factor-1 mediation. At present, there is a consensus that children with growth hormone deficiency need to be treated aggressively.
At present, the research on the evaluation of treatment efficacy mainly focuses on systemic indicators such as bone development and height. The effect of recombinant human growth hormone therapy in 97 children with growth hormone deficiency was observed, and it was found that about 89.58% of the children could reach the normal standard of final height.
Recombinant human growth hormone provides a new treatment for eye development abnormalities in children with growth hormone deficiency, but there are relatively few studies on the changes of multiple parameters of the eye in children with growth hormone deficiency after standardized treatment, and the safety, efficacy and practicability of long-term use of recombinant human growth hormone for eye development need to be further studied and confirmed.
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