中华眼视光学与视觉科学杂志
中華眼視光學與視覺科學雜誌
중화안시광학여시각과학잡지
CHINESE JOURNAL OF OPTOMETRY OPHTHALMOLOGY AND VISUAL SCIENCE
2013年
11期
671-674
,共4页
张钰%陈跃国%夏英杰%齐虹
張鈺%陳躍國%夏英傑%齊虹
장옥%진약국%하영걸%제홍
角膜磨镶术,激光原位%近视%炎症因子%泪液
角膜磨鑲術,激光原位%近視%炎癥因子%淚液
각막마양술,격광원위%근시%염증인자%루액
Keratomileusis,laser in situ%Myopia%Inflammatory cytokine%Tear
目的 研究去瓣机械法准分子激光上皮瓣下角膜磨镶术(Epi-LASIK)眼与留瓣Epi-LASIK眼术后泪液中炎症因子释放率及临床结果的差异,并探讨导致差异的可能原因.方法 前瞻性随机双盲对照研究.18名近视患者纳入本研究,一眼接受去瓣Epi-LASIK(去瓣组),对侧眼接受传统Epi-LASIK(留瓣组).术前、术后2h、术后1d、术后5d分别收集每只眼的泪液.采用多通道免疫微珠分析测定泪液中IL-1β、IL-6、IL-8及肿瘤坏死因子α(TNFα)的浓度,并以浓度乘上泪液流量计算炎症因子的释放率.评估患者的裸眼视力、屈光状态、最佳矫正视力、角膜haze分级、角膜上皮愈合百分比.数据采用配对t检验、Wilcoxon秩和检验及卡方检验进行比较.结果 与留瓣组相比,去瓣组在术后第5天裸眼视力更好(t=--4.832,P<0.01),角膜上皮愈合百分比更高(Z=5.861,P<0.01);术后1个月角膜haze程度更轻(U=6.045,P<0.05).术前,2组泪液中各个炎症因子的释放率差异均无统计学意义;术后2h,去瓣组泪液中IL-8和TNFα的平均释放率显著低于留瓣组(Z=-1.965、-2.145,P<0.05),术后1d和5d2组泪液炎症因子差异无统计学意义.结论 去瓣Epi-LASIK术后角膜上皮愈合及视力恢复更快,角膜haze程度更轻.去瓣组术后2h泪液IL-8和TNFα释放率较低可能是2组存在临床差异的原因之一.
目的 研究去瓣機械法準分子激光上皮瓣下角膜磨鑲術(Epi-LASIK)眼與留瓣Epi-LASIK眼術後淚液中炎癥因子釋放率及臨床結果的差異,併探討導緻差異的可能原因.方法 前瞻性隨機雙盲對照研究.18名近視患者納入本研究,一眼接受去瓣Epi-LASIK(去瓣組),對側眼接受傳統Epi-LASIK(留瓣組).術前、術後2h、術後1d、術後5d分彆收集每隻眼的淚液.採用多通道免疫微珠分析測定淚液中IL-1β、IL-6、IL-8及腫瘤壞死因子α(TNFα)的濃度,併以濃度乘上淚液流量計算炎癥因子的釋放率.評估患者的裸眼視力、屈光狀態、最佳矯正視力、角膜haze分級、角膜上皮愈閤百分比.數據採用配對t檢驗、Wilcoxon秩和檢驗及卡方檢驗進行比較.結果 與留瓣組相比,去瓣組在術後第5天裸眼視力更好(t=--4.832,P<0.01),角膜上皮愈閤百分比更高(Z=5.861,P<0.01);術後1箇月角膜haze程度更輕(U=6.045,P<0.05).術前,2組淚液中各箇炎癥因子的釋放率差異均無統計學意義;術後2h,去瓣組淚液中IL-8和TNFα的平均釋放率顯著低于留瓣組(Z=-1.965、-2.145,P<0.05),術後1d和5d2組淚液炎癥因子差異無統計學意義.結論 去瓣Epi-LASIK術後角膜上皮愈閤及視力恢複更快,角膜haze程度更輕.去瓣組術後2h淚液IL-8和TNFα釋放率較低可能是2組存在臨床差異的原因之一.
목적 연구거판궤계법준분자격광상피판하각막마양술(Epi-LASIK)안여류판Epi-LASIK안술후루액중염증인자석방솔급림상결과적차이,병탐토도치차이적가능원인.방법 전첨성수궤쌍맹대조연구.18명근시환자납입본연구,일안접수거판Epi-LASIK(거판조),대측안접수전통Epi-LASIK(류판조).술전、술후2h、술후1d、술후5d분별수집매지안적루액.채용다통도면역미주분석측정루액중IL-1β、IL-6、IL-8급종류배사인자α(TNFα)적농도,병이농도승상루액류량계산염증인자적석방솔.평고환자적라안시력、굴광상태、최가교정시력、각막haze분급、각막상피유합백분비.수거채용배대t검험、Wilcoxon질화검험급잡방검험진행비교.결과 여류판조상비,거판조재술후제5천라안시력경호(t=--4.832,P<0.01),각막상피유합백분비경고(Z=5.861,P<0.01);술후1개월각막haze정도경경(U=6.045,P<0.05).술전,2조루액중각개염증인자적석방솔차이균무통계학의의;술후2h,거판조루액중IL-8화TNFα적평균석방솔현저저우류판조(Z=-1.965、-2.145,P<0.05),술후1d화5d2조루액염증인자차이무통계학의의.결론 거판Epi-LASIK술후각막상피유합급시력회복경쾌,각막haze정도경경.거판조술후2h루액IL-8화TNFα석방솔교저가능시2조존재림상차이적원인지일.
Objective To compare the release rate of inflammatory cytokines in tears and the clinical outcomes for off-flap epi-LASIK eyes and the contralateral on-flap Epi-LASIK eyes; to explore the possible mechanisms for the clinical differences.Methods This prospective and randomized study enrolled 18 myopic patients who underwent off-flap Epi-LASIK in one eye (off-flap group) and on-flap Epi-LASIK in the contralateral eye (on-flap group).Tears were collected from each eye preoperatively and 2 hours,1 day and 5 days postoperatively.Concentrations of intedeukin-lβ (IL-1β),IL-6,IL-8 and tumor necrosis factor α (TNFα) were measured by a multiplex immunobead assay.The release rate (tear fluid flow-corrected concentration) was calculated by multiplying the concentration by tear fluid flow.Uncorrected visual acuity (UCVA),refraction,best-corrected visual acuity,haze score,and percentage of corneal epithelial healing were also evaluated.Data were analyzed using a paired t test,Wilcoxon rank sum test,and a chi-square test.Results Compared with the on-flap group,the off-flap group had better UCVA outcomes (t=-4.832,P<0.01) and higher percentages of epithelial healing (Z=5.861,P<0.01) at 5 days after surgery,and lower levels of haze at 1 month after surgery (U=6.045,P<0.05).Preoperatively,there were no significant differences in the release rate of all tear cytokines between the two groups.At 2 hours postoperatively,the mean release rates of IL-8 and TNFα in the off-flap group were significantly lower than those in the on-flap group (Z=-1.965,-2.145,P<0.05).On postoperative days 1 and 5,no significant differences were observed in the release rate of all cytokines between the 2 groups.Conclusion Off-flap Epi-LASIK offers faster corneal epithelial healing and visual recovery,and temporarily less haze than from on-flap Epi-LASIK.The lower tear levels of IL-8 and TNFα in the off-flap group 2 hours after surgery may suggest a possible mechanism for the clinical differences.