Evaluation of axial length to identify the effects of monocular 0.125% atropine treatment for pediatric anisometropia.

The aim of the study is to determine the effects of monocular 0.125% atropine daily treatment on the longer axial length (AL) eyes in children with pediatric anisometropia. This was a retrospective cohort study. The charts of children with anisometropia (aged 6-15 years) who had a > 0.2-mm difference in AL between the two eyes were reviewed. Children who received monocular treatment of 0.125% atropine in the eye with longer AL were included for final analysis. The main outcome measure was the difference in AL between the two eyes after treatment. Regression analysis was used to model the changes in AL according to the time of treatment in both eyes. Finally, forty eyes in 20 patients (mean age 10.2 years) were included in the analyses. During the treatment period, AL was controlled in the treated eyes (p = 0.389) but elongated significantly in the untreated eyes (p < 0.001). The difference in AL between the treated and untreated eyes decreased from 0.57 to 0.22 mm (p < 0.001) after the 1-year treatment period. In the regression model, the best fit for the relationship between changes in AL and time during the treatment period in the treated eyes was the quadratic regression model with a concave function. In conclusion, these data suggest that 0.125% atropine daily is an effective treatment to reduce the interocular difference of AL in eyes with axial anisometropia. This pilot study provides useful information for future prospective and larger studies of atropine for the treatment of pediatric axial anisometropia.

Risk factors for rapid axial length elongation with low concentration atropine for myopia control.

Three hundred and twenty-eight myopic children, randomized to use either 0.01% (N = 166) or 0.02% (N = 162) atropine were enrolled in this study. Gender, age, body mass index(BMI), parental myopia status, atropine concentration used, pupil diameter, amplitude of accommodation, spherical equivalent refractive error (SER), anterior chamber depth (ACD) and axial length (AL) were collected at baseline and 1 year after using atropine. Rapid AL elongation was defined as > 0.36 mm growth per year. Univariate analyses showed that children with rapid AL elongation tend to be younger, have a smaller BMI, use of 0.01% atropine, narrow ACD, lower SER, shorter AL, smaller change in pupil diameter between 1 year and baseline (all P < 0.05). Multivariate logistic regression analyses confirmed that rapid AL elongation was associated with children that were younger at baseline (P < 0.0001), use of 0.01% atropine (P = 0.04), a shorter baseline AL (P = 0.03) and a smaller change in pupil diameter between 1 year and baseline (P = 0.04). Younger children with shorter AL at baseline, less change in their pupil diameter with atropine treatment and using the lower of the two atropine concentrations may undergo rapid AL elongation over a 12 months myopia control treatment period.

Topically instilled caffeine selectively alters emmetropizing responses in infant rhesus monkeys.

Oral administration of the adenosine receptor (ADOR) antagonist, 7-methylxanthine (7-MX), reduces both form-deprivation and lens-induced myopia in mammalian animal models. We investigated whether topically instilled caffeine, another non-selective ADOR antagonist, retards vision-induced axial elongation in monkeys. Beginning at 24 days of age, a 1.4% caffeine solution was instilled in both eyes of 14 rhesus monkeys twice each day until the age of 135 days. Concurrent with the caffeine regimen, the monkeys were fitted with helmets that held either -3 D (-3D/pl caffeine, n = 8) or +3 D spectacle lenses (+3D/pl caffeine, n = 6) in front of their lens-treated eyes and zero-powered lenses in front of their fellow-control eyes. Refractive errors and ocular dimensions were measured at baseline and periodically throughout the lens-rearing period. Control data were obtained from 8 vehicle-treated animals also reared with monocular -3 D spectacles (-3D/pl vehicle). In addition, historical comparison data were available for otherwise untreated lens-reared controls (-3D/pl controls, n = 20; +3D/pl controls, n = 9) and 41 normal monkeys. The vehicle controls and the untreated lens-reared controls consistently developed compensating axial anisometropias (-3D/pl vehicle = -1.44 ± 1.04 D; -3D/pl controls = -1.85 ± 1.20 D; +3D/pl controls = +1.92 ± 0.56 D). The caffeine regime did not interfere with hyperopic compensation in response to +3 D of anisometropia (+1.93 ± 0.82 D), however, it reduced the likelihood that animals would compensate for -3 D of anisometropia (+0.58 ± 1.82 D). The caffeine regimen also promoted hyperopic shifts in both the lens-treated and fellow-control eyes; 26 of the 28 caffeine-treated eyes became more hyperopic than the median normal monkey (mean (±SD) relative hyperopia = +2.27 ± 1.65 D; range = +0.31 to +6.37 D). The effects of topical caffeine on refractive development, which were qualitatively similar to those produced by oral administration of 7-MX, indicate that ADOR antagonists have potential in treatment strategies for preventing and/or reducing myopia progression.

A comparative study of orthokeratology and low-dose atropine for the treatment of anisomyopia in children.

Myopic anisometropia (anisomyopia) is a specific type of refractive error that may cause fusion impairment, asthenopia, and aniseikonia. It is sometimes severe enough to reduce the quality of life. Several studies have investigated the treatment effects of orthokeratology (Ortho-K) and topical atropine on anisomyopia control. However, no study has compared these two interventions simultaneously until now. The cohort of this retrospective study included 124 children with anisomyopia who were treated with binocular Ortho-K lenses, 0.01% atropine, or 0.05% atropine. After a 2-year follow-up, the inter-eye difference in axial length (AL) significantly decreased in the Ortho-K group (P = 0.015) and remained stable in the two atropine groups. When comparing the myopia control effect, the use of Ortho-K lenses resulted in an obviously smaller change in AL than the use of 0.01% and 0.05% atropine (P < 0.01). Ortho-K treatment may reduce the degree of anisomyopia and stabilise the progression of myopia. Hence, Ortho-K might be a better choice for anisomyopic children.

Blockade of epidermal growth factor and its receptor and axial elongation in experimental myopia.

To examine the influence of epidermal growth factor (EGF) and its receptor (EGFR) on axial ocular elongation, we intraocularly injected an EGF antibody and an EGFR antibody into young guinea pigs with lens-induced axial elongation (myopization). Mean axial elongation was reduced in the eyes injected with the EGF/EGFR-antibody compared with the contralateral control eyes injected with PBS (phosphate-buffered solution) (0.43 ± 0.13 mm vs 0.53 ± 0.13 mm; P < .001). The intereye difference in axial length increased (P = .005) as the doses of the EGF antibody and EGFR antibody increased. As a corollary, the thickness of the retina at the posterior pole was dose-dependently increased in the injected eyes compared to the contralateral control eyes. Immunohistochemical staining for EGF and the relative mRNA expression of EGF and EGFR were the highest in eyes not injected with the EGF antibody or EGFR antibody and decreased (P < .05) as the dose of EGF antibody or EGFR antibody increased. In an in vitro study, EGF had a stimulating effect and the EGF antibody had an inhibitory effect on the proliferation and migration of RPE cells. The findings showed that the intravitreal application of an EGF antibody and EGFR antibody is associated with a dose-dependent reduction in lens-induced axial elongation in young guinea pigs. The EGFR family may play a role in axial elongation of the eye and in the development of myopia.

Effect of chronic topical latanoprost on the sclera and lamina cribrosa of form-deprived myopic Guinea pigs.

The purpose of this study was to investigate the effects of latanoprost, an ocular hypotensive prostaglandin analog, on scleral collagen fibers and laminar pores in myopic guinea pigs. Young guinea pigs underwent monocular form deprivation (FD; white plastic diffusers) from 14-days of age for 10-weeks. After the first week, FD eyes also received daily topical A) latanoprost (Lat, 0.005%, n = 5) or B) artificial tears (AT; n = 5). At the end of the treatment period, animals were sacrificed, eyes enucleated and optic nerve heads (ONH) excised to include a 4 mm diameter ring of surrounding sclera for scanning electron microscopy (SEM), and an additional 6 mm ring of sclera surrounding the ONH was excised for transmission electron microscopy (TEM). For SEM, ONH samples were first immersed in 0.2M NaOH for 30 h to isolate the collagenous structures. All samples were stained with osmium tetroxide, dried through an ethanol series and finally subjected to critical point drying before imaging. Image J was used to analyze the dimensions of laminar pores (SEM images) and scleral collagen fibers (TEM images). As previously reported in a related study, latanoprost was effective in inhibiting myopia progression in FD eyes of the guinea pigs. The scleral fibers of FD myopic eyes treated with AT were smaller and more variable in cross-sectional areas compared to untreated (fellow) eyes (mean areas: 0.0059 ±â€¯0.0013 vs. 0.0085 ±â€¯0.002 µm2; p < 0.001), consistent with scleral changes reported for human myopia. In contrast, the scleral fibers of the Lat-treated FD eyes were similar to those of fellow eyes (0.0083 ±â€¯0.002 vs. 0.0078 ±â€¯0.0014 µm2). However, laminar pore size appeared unaffected by either the FD or drug treatments, with no significant difference found between FD eyes and their fellows, for either treatment group. That daily topical latanoprost appeared to protect against myopia-related changes in scleral collagen, rather than exaggerating them, as might be predicted from its known action on the uveoscleral extracellular matrix, lends further support its use for myopia control. In this guinea pig myopia model, the lamina cribrosa appeared unaffected.

Effects of Monocular Atropinization on Refractive Error and Eye Growth in Infant New World Monkeys.

Purpose: To explore the effect of topical atropine on axial eye growth and emmetropization in infant marmosets. Methods: Atropine was applied to one eye from the age of 7 to 56 days in two dose regimens, High (0.1-1% twice daily, increasing with age) or moderate (Mod) (0.1% once daily). Both eyes of the marmosets were refracted, and axial dimensions were measured ultrasonically, at 14, 28, 42, 49, 56, 70, 105, 168, and 279 days of age. The time course of each measured variable was analyzed using multilevel mixed-effects modeling realized in R. Results: The logistic growth curves fitted to anterior segment depth (ASD) did not differ significantly between the dose regimens, but xmid, the age at which growth was half-maximal, and scal, the time constant of the exponential term in the logistic growth curve equation, differed significantly between the ASD of atropinized and untreated eyes (P = 0.03 and P < 0.0001, respectively), with the ASD of atropinized eyes shorter than that of untreated eyes. The splines fitted to lens thickness did not vary significantly with dose, but differed significantly (P < 0.0001) between the atropinized and untreated eyes, with the atropinized lenses thicker. Vitreous chamber depth (VCD) was not significantly different, but the variance of VCD was significantly greater (P < 0.001) in the atropinized compared with the untreated eyes. Refractive error (RE) became relatively myopic in atropinized eyes. The variance of RE in atropinized eyes was significantly greater (P < 0.0001) than in untreated eyes. Conclusions: Atropine caused the infant marmoset lens to move forward and thicken, a relative myopia, and increases in the between-animals variance in VCD, which could be considered a failure of emmetropization.

Optical biometry-based axial length alterations after intravitreal dexamethasone implant / Alterações do comprimento axial com base na biometria óptica após o implante de dexametasona intravítrea

ABSTRACT Purpose: To investigate changes in axial length after intravitreal dexamethasone implantation in patients with macular edema. Methods: We performed a prospective comparative study of 46 patients with unilateral macular edema, due to diabetic retinopathy, retinal vein occlusion, and non-infectious uveitis, who underwent dexamethasone implantation. The fellow eyes of the patients were considered the control group. The central macular thickness was measured by spectral-domain optical coherence tomography, and axial length was measured by IOLMaster 700 optical coherence biometry. We compared axial length and central macular thickness values within the groups. Results: In the study group, the baseline central macular thickness was 460.19 ± 128.64 mm, significantly decreasing to 324.00 ± 79.84 mm after dexamethasone implantation (p=0.000). No significant change in central macular thickness measurements was seen in the control group (p=0.244). In the study group, the baseline axial length was 23.16 ± 0.68 mm, significantly increasing to 23.22 ± 0.65 mm after dexamethasone implantation (p=0.039). However, the control group exhibited no significant change in axial length (p=0.123). Conclusions: In addition to significantly reducing central macular thickness measurements, intravitreal dexamethasone implantation also significantly changes optical biometry-based axial length measurements.

RESUMO Objetivo: Investigar alterações no comprimento axial após implante de dexametasona intravítrea em pacientes com edema macular. Métodos: Foi realizado um estudo prospectivo e comparativo de 46 pacientes com edema macular unilateral, devido à retinopatia diabética, oclusão da veia retiniana e uveíte não infecciosa, que foram submetidos ao implante de dexametasona. Os olhos contralateral de cada paciente foram considerados o grupo controle. A espessura macular central foi medida por tomografia de coerência óptica de domínio espectral, e o comprimento axial foi medido por meio de biometria de coerência óptica de domínio espectral e o comprimento axial foi medido pela biometria de coerência óptica com IOLMaster 700. Comparamos o comprimento axial e os valores da espessura macular central dentro dos grupos. Resultados: No grupo de estudo, a espessura macular basal foi de 460,19 ± 128,64 mm, diminuindo significativamente para 324,00 ± 79,84 mm após o implante de dexametasona (p=0,000). Nenhuma mudança significativa nas medidas da espessura macular central foi observada no grupo controle (p=0,244). No grupo de estudo, o comprimento axial basal foi de 23,16 ± 0,68 mm, aumentando significativamente para 23,22 ± 0,65 mm após o implante de dexametasona (p=0,039). No entanto, o grupo controle não apresentou alteração significativa no comprimento axial (p=0,123). Conclusões: Além de reduzir significativamente as medidas da espessura macular central, o implante de dexametasona intravítrea também altera significativamente as medidas de comprimento axial baseadas na biometria óptica.

Amphiregulin and ocular axial length.

PURPOSE: To assess the potential role of amphiregulin as messenger molecule in ocular axial elongation. METHODS: The experimental study included guinea pigs (total n = 78) (age: 3-4 weeks) which underwent bilateral lens-induced myopization and received 15 days later three intraocular injections in weekly intervals of amphiregulin antibody (doses:5 µg, 10 µg, 20 µg) into their right eyes, and three phosphate-buffered saline injections into their left eyes; and guinea pigs without lens-induced myopization and which received three unilateral intraocular injections of amphiregulin antibody (dose: 20 µg) or amphiregulin (doses: 1 ng; 10 ng; 20 ng) into their right eyes, and three phosphate-buffered saline injections into their left eyes. Seven days later, the animals were sacrificed. Intravitally, we performed biometry, and histology and immunohistochemistry post-mortem. RESULTS: In animals with bilateral lens-induced myopization, the right eyes receiving amphiregulin antibody showed reduced axial elongation in a dose-dependent manner (dose: 5 µg: side difference: 0.14 ± 0.05 mm;10 µg: 0.22 ± 0.06 mm; 20 µg: 0.32 ± 0.06 mm; p < 0.001), thicker sclera (all p < 0.05) and higher cell density in the retinal nuclear layers and retinal pigment epithelium (RPE) (all p < 0.05). In animals without lens-induced myopia, the right eyes with amphiregulin antibody application (20 µg) showed reduced axial elongation (p = 0.04), and the right eyes with amphiregulin injections experienced increased (p = 0.02) axial elongation in a dose-dependent manner (1 ng: 0.04 ± 0.06 mm; 10 ng: 0.10 ± 0.05 mm; 20 ng: 0.11 ± 0.06 mm). Eyes with lens-induced axial elongation as compared to eyes without lens-induced axial elongation revealed an increased visualization of amphiregulin upon immunohistochemistry and higher expression of mRNA of endogenous amphiregulin and epidermal growth factor receptor, in particular in the outer part of the retinal inner nuclear layer and in the RPE. CONCLUSION: Amphiregulin may be associated with axial elongation in young guinea pigs.

Optical biometry-based axial length alterations after intravitreal dexamethasone implant.

PURPOSE: To investigate changes in axial length after intravitreal dexamethasone implantation in patients with macular edema. METHODS: We performed a prospective comparative study of 46 patients with unilateral macular edema, due to diabetic retinopathy, retinal vein occlusion, and non-infectious uveitis, who underwent dexamethasone implantation. The fellow eyes of the patients were considered the control group. The central macular thickness was measured by spectral-domain optical coherence tomography, and axial length was measured by IOLMaster 700 optical coherence biometry. We compared axial length and central macular thickness values within the groups. RESULTS: In the study group, the baseline central macular thickness was 460.19 ± 128.64 mm, significantly decreasing to 324.00 ± 79.84 mm after dexamethasone implantation (p=0.000). No significant change in central macular thickness measurements was seen in the control group (p=0.244). In the study group, the baseline axial length was 23.16 ± 0.68 mm, significantly increasing to 23.22 ± 0.65 mm after dexamethasone implantation (p=0.039). However, the control group exhibited no significant change in axial length (p=0.123). CONCLUSIONS: In addition to significantly reducing central macular thickness measurements, intravitreal dexamethasone implantation also significantly changes optical biometry-based axial length measurements.

Alpha2 -adrenoceptor agonists inhibit form-deprivation myopia in the chick.

BACKGROUND: The putative myopia-controlling receptor is thought to be muscarinic acetylcholine receptor subtype M4 , because mamba toxin-3 can inhibit form-deprivation myopia in chicks at a far lower concentration than atropine. However, mamba toxin-3 is equally potent at the human α1A -, α1D -, and α2A -adrenoceptors. To test the hypothesis that α-adrenoceptors might be involved in regulation of eye growth, the treatment effects of α2 -adrenoceptor agonists brimonidine, clonidine, and guanfacine, and antagonist yohimbine, on form-deprivation myopia in the chick were measured. METHODS: Right eyes of White Leghorn chicks were goggled with diffusers to induce form-deprivation myopia; left eyes were left open as controls. Goggled eyes were injected intravitreally with 20 µL of vehicle, or 2, 20, or 200 nmol of brimonidine, clonidine, guanfacine, or yohimbine, 24, 72, and 120 hours after goggle application. Alternatively, myopia was inhibited physiologically by goggle removal for two hours, and the α2 -adrenoceptor antagonist, yohimbine, was injected to test whether it could block this type of myopia inhibition. One day after the last injection, refractive error and axial length were measured. RESULTS: Brimonidine (20 and 200 nmol) and clonidine (200 nmol) effectively inhibited experimentally induced increases in negative refractive error and axial elongation. All doses of guanfacine significantly inhibited induced negative refractive error, but only 20 and 200 nmol significantly inhibited axial elongation. Yohimbine had no effect on form-deprivation myopia, but 200 nmol reduced the myopia-inhibiting effect of goggle removal. CONCLUSION: High concentrations of α2 -adrenoceptor agonists, similar to those required by atropine, inhibited chick form-deprivation myopia; antagonism by yohimbine had no effect. High-concentration yohimbine partially interfered with emmetropisation in form-deprived chicks experiencing normal vision for two hours per day. These data support the hypothesis that treatment with high concentrations of adrenergic drugs can affect experimentally induced myopia and normal visual processes.

Adjunctive effect of orthokeratology and low dose atropine on axial elongation in fast-progressing myopic children-A preliminary retrospective study.

PURPOSE: To investigate the adjunctive effect of orthokeratology (ortho-k) and low-dose atropine eye drops on axial length elongation in fast-progressing myopic children. METHODS: Axial elongation in 60 eyes of 60 subjects who completed two years of ortho-k treatment was retrospectively reviewed. They were aged between 5.6-11.6 (mean, 8.3 ± 1.5) years old when they started ortho-k treatment. During their first year of ortho-k treatment (Phase One), they all demonstrated a faster than 0.25 mm/yr axial elongation rate. They were then treated with nightly 0.01% atropine in addition to ortho-k treatment for another year (Phase Two). Annual axial elongation rates before and after atropine treatment were compared. RESULTS: Baseline spherical equivalent refractive error was -2.65 ± 1.08 DS and axial length was 24.34 ± 0.92 mm for the study cohort. The mean axial elongation rate was 0.46 ± 0.16 mm/yr during Phase One, being significantly faster in younger children (t = -4.920, P < 0.001). When atropine was added, annual axial elongation rate significantly decreased to 0.14 ± 0.14 mm/yr (t = -11.988, P < 0.001), and those who were fast progressors in Phase One had a greater reduction in the rate of axial elongation during Phase Two (t = -8.052, P < 0.001). CONCLUSIONS: Axial elongation rate is faster in younger children undergoing ortho-k treatment. For fast myopia progressors, low dose atropine may significantly slow axial elongation in addition to ortho-k's treatment effect. Those who have faster axial elongation after ortho-k treatment will benefit more from the addition of low dose atropine, regardless of their refractive error and age.

Scleral Cross-Linking Using Glyceraldehyde for the Prevention of Axial Elongation in the Rabbit: Blocked Axial Elongation and Altered Scleral Microstructure.

BACKGROUND: This study aims to assess the efficacy of the scleral collagen cross-linking method using glyceraldehyde solution for prevention of lens-induced axial elongation in New Zealand rabbits and investigate the biochemical and microstructural changes that occur. METHODS: The right eyes of New Zealand rabbits aged seven weeks were randomly divided into three groups: the cross-linking group (n = 6), non-crosslinking group (n = 5), and untreated control group (n = 5). Eyes in cross-linking and non-crosslinking groups were treated with a -8.00 Diopter spherical lens over the course of two weeks. The cross-linking effects were achieved by a sub-Tenon's injection of 0.15 ml 0.5 M glyceraldehyde to eyes in the CL group. Ocular parameters were measured on the 1st, 7th, and 14th days. Biomechanical testing, light and electronic microscopy were used. RESULTS: Following the cross-linking treatment, eyes in the cross-linking group had a shorter axial length compared to those in the non-crosslinking group (p = 0.006). Collagen fibrils larger than 240 nm were observed in the scleral stroma of cross-linking group, which were absent in the scleral stroma of the non-crosslinking and untreated control group. The mean ultimate stress and Young's modulus was significantly greater in the cross-linking group compared to those in the non-crosslinking and untreated control group (p < 0.05). No histological damage observed in the retina or choroid. CONCLUSIONS: This study demonstrates that lens-induced axial elongation in rabbits can be effectively blocked by cross-linking using glyceraldehyde, with anatomical and mechanical modification and no deleterious effects.

Axial elongation measured by long scan depth optical coherence tomography during pilocarpine-induced accommodation in intraocular lens-implanted eyes.

We used an ultra-long scan depth optical coherence tomography (UL-OCT) system to investigate changes in axial biometry of pseudophakic eyes during pilocarpine- induced accommodation. The right eyes from 25 healthy subjects (age range 49 to 84 years) with an intraocular lens (IOL) were imaged twice in the non-accommodative and the accommodative states. A custom-built UL-OCT instrument imaged the whole eye. Then accommodation was induced by two drops of 0.5% pilocarpine hydrochloride separated by a 5-minute interval. Following the same protocol, images were acquired again 30 minutes after the first drop. The central corneal thickness (CCT), anterior chamber depth (ACD), IOL thickness (IOLT), and vitreous length (VL) were obtained using custom automated software. The axial length (AL) was calculated by summing the CCT, ACD, IOLT, and VL. With accommodation, ACD increased by +0.08 ± 0.09 mm, while the VL decreased by -0.04 ± 0.09 mm (paired t-test each, P<0.05). CCT and IOLT remained constant during accommodation (P > 0.05). The non-accommodative AL was 23.47 ± 0.93 mm, and it increased by +0.04 ± 0.04 mm after accommodation (P<0.01). The AL increased and the IOL moved backward during pilocarpine-induced accommodation in pseudophakic eyes.

[Atropine for the Prevention of Progression in Myopia - Data, Side Effects, Practical Guidelines]. / Atropin zur Prävention der Myopieprogression ­ Datenlage, Nebenwirkungen, praktische Empfehlungen.

The prevalence of myopia has increased worldwide in recent decades. In East Asia's metropolises ≥ 80% of young adults are affected. This dramatic increase is mainly caused by changes in lifestyle and behaviour. Atropine has been used for more than 100 years to arrest myopia progression. It has become an evidence-based treatment regimen in the last decade, although the exact mechanism of the effect of treatment is still unknown. Atropine eye drops can slow myopia progression by an average of - 0.54 dioptres (D)/year in Asian children and - 0.35 D/year in Caucasian children. However, a non-response rate of about 10% has been found. Treatment should be established in schoolchildren only (age ≥ 6 years) with myopia ≤ - 2 D (spherical equivalent, cycoplegic refraction) and with documented myopic progression of - 0.5 D in the preceding year. 0.01% eyedrops should be instilled into the lower fornix at bedtime. Atropine 0.01% therapy is well tolerated. Atropine is usually administered for 2 years since efficacy is somewhat better in the second year. During treatment, a 6-month follow-up with cycoplegic refraction and axial length measurement is recommended. After the 2-year period, atropine withdrawal is justified if progression is less than - 0.25 D/year in the second year. Even after atropine has been stopped, follow-up examinations are needed to detect any rebound. Atropine-therapy is resumed if progression is again higher than - 0.5 D/year. Topical atropine is used off-label.

Riboflavin and ultraviolet A irradiation for the prevention of progressive myopia in a guinea pig model.

In this study, we evaluated the effect of oral administration of riboflavin combined with whole-body ultraviolet A (UVA) irradiation on the biochemical and biomechanical properties of sclera in a guinea pig model to control the progression of myopia. Experimental groups were administered 0.1% riboflavin solution with or without vitamin C by gavage from 3 days before myopic modeling and during the modeling process. Guinea pigs underwent 30 min of whole-body UVA irradiation after each gavage for 2 weeks. For control groups, guinea pigs were administered vitamin C and underwent either whole-body UVA irradiation without 0.1% riboflavin solution or whole-body fluorescent lamp irradiation with or without 0.1% riboflavin solution. Resultantly, myopia models were established with an increased axial length and myopic diopter. Compared with myopic eyes in the control groups, the net increase in axial length, diopter and strain assessment decreased significantly, and the net decrease in sclera thickness, ultimate load, and stress assessment decreased significantly in experimental groups. MMP-2 expression showed a lower net increase, while TIMP-2 expression showed a lower net decrease. In addition, hyperplasia of scleral fibroblasts was more active in myopic eyes of experimental groups. Overall, our results showed that oral administration of riboflavin with whole-body UVA irradiation could increase the strength and stiffness of sclera by altering the biochemical and biomechanical properties, and decreases in axial elongation and myopic diopter are greater in the guinea pig myopic model.

Atropine 0.5% eyedrops for the treatment of children with low myopia: A randomized controlled trial.

BACKGROUND: This study aimed to assess the efficacy and safety of atropine 0.5% eyedrops (ATE) for the treatment of children with low myopia (LM). METHODS: In this study, a total of 126 children with LM were randomly divided into an intervention group (administered 0.5% ATE) and a control group (administered a placebo), with 63 children in each group. The outcome measurements were changes in the spherical equivalent (SE), and axial length (AL), as well as adverse events (AEs). RESULTS: Compared with placebo, administration of 0.5% ATE led to less progression in LM, as measured by SE, and less increase in AL (P < .01). In addition, no serious AEs occurred in both the groups. CONCLUSION: About 0.5% ATE was efficacious and safe for controlling myopia in children with LM.

Changes in Ocular Parameters and Intraocular Lens Powers in Aging Cycloplegic Eyes.

PURPOSE: Age-related changes in lens elasticity and ciliary muscle contractility can affect how ocular parameters respond to cycloplegia, and therefore intraocular lens (IOL) power measurements calculated by formulas using anterior chamber depth (ACD), lens thickness (LT), or white-to-white (WtW) for effective lens position prediction can vary. In response, using swept-source optical biometry in prepresbyopic and presbyopic eyes, we investigated changes in ocular parameters and IOL power calculations attributable to cycloplegia. DESIGN: Cross-sectional study. METHODS: In 38 prepresbyopic and 42 presbyopic eyes, we measured pupil diameter, radius of corneal curvature values, central corneal thickness, WtW, ACD, LT, and axial length both before and after cycloplegia. We determined IOL power calculations with the Sanders-Retzlaff-Kraff/theoretical, Holladay 2, and Haigis formulas. To pinpoint the effect of cycloplegia, we recorded refractive predictions in pre- and postdilation conditions according to the same IOL power calculations, even if postdilation IOL power calculations had changed. RESULTS: With cycloplegia, pupil diameter changed significantly more in presbyopic eyes (P < .001). Central corneal thickness decreased in prepresbyopic eyes (P = .048), whereas WtW increased in presbyopic eyes (P = .02). In both groups, ACD and LT changed significantly (P < .001). IOL power calculations according to the Holladay 2 formula differed in prepresbyopic eyes (P = .042), and refractive predictions with the Holladay 2 and Haigis formulas differed significantly in prepresbyopic eyes (P = .043 and P = .022, respectively). CONCLUSION: Surgeons should consider the effect of cycloplegia on refractive prediction errors and IOL power calculations determined with Haigis and Holladay 2 formulas, especially in prepresbyopic ages.

Effect of pharmacological pupil dilation on measurements and iol power calculation made using the new swept-source optical coherence tomography-based optical biometer.

PURPOSE: To determine whether pupil dilation affects biometric measurements and intraocular lens (IOL) power calculation made using the new swept-source optical coherence tomography-based optical biometer (IOLMaster 700©; Carl Zeiss Meditec, Jena, Germany). PROCEDURES: Eighty-one eyes of 81 patients evaluated for cataract surgery were prospectively examined using the IOLMaster 700© before and after pupil dilation with tropicamide 1%. The measurements made were: axial length (AL), central corneal thickness (CCT), aqueous chamber depth (ACD), lens thickness (LT), mean keratometry (MK), white-to-white distance (WTW) and pupil diameter (PD). Holladay II and SRK/T formulas were used to calculate IOL power. Agreement between measurement modes (with and without dilation) was assessed through intraclass correlation coefficients (ICC) and Bland-Altman plots. RESULTS: Mean patient age was 75.17±7.54 years (range: 57-92). Of the variables determined, CCT, ACD, LT and WTW varied significantly according to pupil dilation. Excellent intraobserver correlation was observed between measurements made before and after pupil dilation. Mean IOL power calculation using the Holladay 2 and SRK/T formulas were unmodified by pupil dilation. CONCLUSIONS: The use of pupil dilation produces statistical yet not clinically significant differences in some IOLMaster 700© measurements. However, it does not affect mean IOL power calculation.

Scleral Cross-linking Using Riboflavin and Ultraviolet-A Radiation for Prevention of Axial Myopia in a Rabbit Model.

Myopic individuals, especially those with severe myopia, are at higher-than-normal risk of cataract, glaucoma, retinal detachment and chorioretinal abnormalities. In addition, pathological myopia is a common irreversible cause of visual impairment and blindness. Our study demonstrates the effect of scleral crosslinking using riboflavin and ultraviolet-A radiation on the development of axial myopia in a rabbit model. The axial length of the eyeball was measured by A-scan ultrasound in New Zealand white rabbits aged 13 days (male and female). The eye then underwent 360° conjunctival peritomy with scleral crosslinking, followed by tarsorrhaphy. Axial elongation was induced in 13 day-old New Zealand rabbits by suturing their right eye eyelids (tarsorrhaphy). The eyes were divided into quadrants, and every quadrant had two scleral irradiation zones, each with an area of 0.2 cm² and a radius of 4 mm. Crosslinking was performed by dropping 0.1% dextran-free riboflavin-5-phosphate onto the irradiation zones 20 sec before ultraviolet-A irradiation and every 20 sec during the 200 sec irradiation time. UVA radiation (370 nm) was applied perpendicular to the sclera at 57 mW/cm² (total UVA light dose, 57 J/cm²). Tarsorrhaphies were removed on day 55, followed by repeated axial length measurements. This study demonstrates that scleral crosslinking with riboflavin and ultraviolet-A radiation effectively prevents occlusion-induced axial elongation in a rabbit model.