ABSTRACT
Objective:To evaluate the clinical effect of Toric design orthokeratology in myopic teenagers with mild-to-moderate astigmatism.Methods:A non-randomized controlled clinical study was conducted.Eighty juvenile myopia patients (160 eyes) diagnosed with mild to moderate astigmatism with myopia after mydriatic computer optometry and received the treatment of orthokeratology at Zhejiang Rongjun Hospital from January 2016 to June 2017 were enrolled.The patients were divided into regular spherical design orthokeratology group and Toric design orthokeratology group, with 80 eyes (40 cases) in each group.The patients wore orthokeratology for 8 to 10 hours every night and were re-examined at 1 day, 1 week and 1, 3, 6, 12 and 18 months after wearing, respectively.The visual acuity, refraction, corneal health status and central deviation of the treatment area in the corneal topography map were measured and recorded during the 18-month treatment.The complications during treatment were recorded.After 12-month wearing, the uncorrected visual acuity and the center deviation of the treatment area were compared between the two groups.After 18-month wearing, patients in the two groups stopped wearing the orthokeratology lens for 1 month, and then the refraction examination, IOLMaster and corneal topography were performed to compare the spherical equivalent, axial length and degree of astigmatism.This study protocol adhered to the Declaration of Helsinki and was approved by an Ethics Committee of Zhejiang Rongjun Hospital (No.2020-10). Written informed consent was obtained from guardians prior to any medical examination.Results:After 12-month wearing, the center deviation of the shaping treatment area was (0.86±0.23)mm in the Toric design orthokeratology group, which was significantly lower than (1.16±0.44)mm in the regular spherical design orthokeratology group ( t=5.404, P<0.001). After 12-month wearing, the uncorrected visual acuity was (0.03±0.08) LogMAR in the Toric design orthokeratology group, which was significantly higher than (0.09±0.10) LogMAR in the regular spherical design orthokeratology group ( t=2.963, P=0.004). The spherical equivalent and the axial length of Toric design orthokeratology group were significantly smaller than those of the regular spherical design orthokeratology group ( t=2.542, 2.107; both at P<0.05), and there was no statistically significant difference in the degree of astigmatism between the two groups ( t=0.821, P=0.413). During the 18-month follow-up, the adverse reaction, punctate corneal epithelial opacity, occurred in 18 eyes.The incidence of adverse effect was 6.26%(5/80) in the Toric design orthokeratology group, which was significantly lower than the 16.25% (13/80) in the regular spherical design orthokeratology group ( χ2=3.897, P=0.048). Conclusions:The Toric design orthokeratology shows better efficacy in myopia control as well as reducing the adverse reaction rate in juvenile myopia, and it can better solve the deviation in corneal shaping in the use of regular spherical design orthokeratology.
ABSTRACT
ObjectiveTo investigate the effects of lipopolysaccharide (LPS) on mRNA expression of iron metabolism related genes. Methods Ten male mice (2 months) were injected intraperitoneally with lipopolysaccharide(0.5 μg/g). After 6 hours, mice were sacrificed and then sera, liver and spleen were collected. The mice blood routine was measured. The serum iron and total iron binding capacity (TIBC) were determined with reagent kit. The quasi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was performed for mRNA of hepatic hepcidin(HP), ferroportin1(Fpn1), transferrin receptor 1(TfR1) and spleenic HP, Fpn1 and interleukin-6(IL-6). Results The serum iron and TIBC were reduced in mice injected LPS, which exhibited mild anemia(P＜0.05) . LPS can increase the expression of hepatic hepcidin and decrease Fpn1 and TfR1 in liver after LPS administration 6 hours(P＜0.05). In spleen, IL-6 was upregulated and Fpn1 downregulated(P＜0.05). Conclusion LPS can influence serum iron through regulating the mRNA expression of hepatic and spleenic iron metabolism related genes, such as HP, Fpn1 and TfR1.