非缺血型视网膜分支静脉阻塞黄斑水肿抗VEGF治疗的疗效研究

目的：探究雷珠单抗与康柏西普治疗非缺血型视网膜分支静脉阻塞黄斑水肿的疗效及安全性。

方法：选取我院于2014-03/2018-05收治的非缺血型视网膜分支静脉阻塞黄斑水肿患者80例80眼,随机分为A组(40例)和B组(40例),分别行玻璃体腔内注射雷珠单抗和康柏西普治疗。随访3mo,比较治疗前后两组患者的眼压、CMT、黄斑中心体积(CMV)、BCVA、玻璃体腔注射次数和并发症发生情况。

结果：治疗后2wk,1、2、3mo,B组患者CMT、CMV、BCVA均明显优于A组(P<0.05)。随访3mo,B组患者视力提高比例显著高于A组(65% vs 38%,P<0.05),玻璃体腔注射次数显著低于A组(P<0.05),但两组患者并发症发生情况(5% vs 0%)无明显差异(P=0.999)。

结论：与雷珠单抗比较,康柏西普治疗非缺血型视网膜分支静脉阻塞黄斑水肿在改善视力,降低CMT和CMV,减少玻璃体腔注射次数方面具有一定优势。     

双通道客观视觉质量分析系统评估多焦点人工晶状体植入术后视觉质量

目的：应用双通道客观视觉质量分析系统(OQAS)测量区域折射型(SBL-3)和衍射折射型(SN6AD1)多焦点人工晶状体(MIOL)植入术后患者的视觉质量。

方法：选取2017-03/2018-04在我院行白内障超声乳化吸除联合人工晶状体植入术的年龄相关性白内障患者47例47眼。根据植入MIOL的不同分为SBL-3组(22例22眼)和SN6AD1组(25例25眼)。术后随访3mo,比较两组患者的裸眼及矫正远、中、近视力,并采用OQAS检查客观视觉质量。

结果：术后3mo,SBL-3组患者裸眼中视力优于SN6AD1组\〖0.14(0.04,0.26)vs 0.26(0.12,0.40),P<0.05\〗,客观散射指数\〖2.52(2.35,3.86)vs 1.89(1.39,2.28)\〗和人工晶状体眼伪调节力(2.47±0.88D vs 1.25±0.70D)均显著高于SN6AD1组,MTF-cut/off、SR及模拟对比度视力均显著低于SN6AD1组(P<0.01)。

结论：SBL-3和SN6AD1 MIOL植入术后患者均能够获得较好的主观视觉质量,但OQAS系统能够反映二者产生的客观视觉质量差异。     

伴有面转代偿头位的先天性下直肌麻痹临床特征与手术治疗

目的：描述伴有面转代偿头位的先天性单纯下直肌麻痹患者的临床表现,并分析其手术治疗效果。

方法：回顾性分析2014-05/2018-07伴有明显面转代偿头位的先天性下直肌麻痹患者,手术前后患者面转程度的变化借助骨科量角器来检查,垂直、水平斜视度变化通过三棱镜交替遮盖试验来测量,旋转斜视度变化通过眼底对眼球客观旋转状态评估。下直肌缩短术是主要治疗方案。

结果：在15例研究对象中,有13例行下直肌缩短术或者联合上直肌后徙术术后疗效好,下直肌运动不足明显改善,眼球运动协调,以面转为主的代偿头位消失,垂直、水平、旋转斜视得到矫正; 并得出：每缩短1 mm下直肌可矫正1.54±0.93°内旋斜视。而行下斜肌断腱术治疗的垂直斜视度小的患者,面转改善不理想,仍遗留眼球运动不协调。

结论：先天性单纯的下直肌麻痹以面转代偿头位为主,下直肌缩短术治疗效果好,轻度的过矫及欠矫不影响手术疗效。     

三种角膜屈光手术对近视患者角膜内皮细胞的影响

目的：对比角膜板层刀制瓣的前弹力层下准分子激光角膜磨镶术(SBK)、飞秒激光制瓣的SBK术(FS-SBK)与飞秒激光小切口角膜基质透镜取出术(SMILE)对近视中央角膜内皮细胞的短期及长期影响。

方法：我院近视34例34眼行SBK术; 41例41眼行FS-SBK术; 49例49眼行SMILE术,术前和术后1wk,1a利用SP-1P型非接触角膜内皮显微镜检查角膜内皮细胞,统计分析各组中央角膜内皮细胞密度(ECD)、内皮细胞面积的变异系数(CV)和六边形内皮细胞百分比。

结果：三组间术前、术后1wk,1a裸眼视力及屈光度均无差异(P>0.05)。术后1wk三组中央ECD均较术前减少(P<0.01),术后1a各组均较术前无差异(P>0.05); 术前及术后各随访时间点,三组间中央角膜内皮细胞面积CV及六边形内皮细胞百分比均无差异(P>0.05); 不同组内,术前及术后各随访时间点结果均无差异(P>0.05)。

结论：SBK、FS-SBK和SMILE手术对近视内皮细胞的安全性确切,术后早期各组中央角膜ECD均轻度降低,1a后恢复; 术后各组中央角膜内皮细胞面积CV及六边形内皮细胞百分比较术前无明显改变。     

Gatifloxacin inducing apoptosis of stromal fibroblasts through cross-talk between caspase-dependent extrinsic and intrinsic pathways

AIM: To reveal the cytotoxicity and related mechanisms of gatifloxacin (GFX) to stromal fibroblasts (SFs) in vitro. METHODS: SFs were treated with GFX at different concentrations (0.009375%-0.3%), and their viability was detected by MTT method. The cell morphology was observed using light/transmission electron microscope. The plasma membrane permeability was measured by AO/EB double-staining. Then cell cycle, phosphatidylserine (PS) externalization, and mitochondrial transmembrane potential (MTP) were analyzed by flow cytometry. DNA damage was analyzed by electrophoresis and immunostaining. ELISA was used to evaluate the caspase-3/-8/-9 activation. Finally, Western blotting was applied for detecting the expressions of apoptosis-related proteins. RESULTS: Morphological changes and reduced viability of GFX-treated SFs demonstrated that GFX above 0.009375% had cytotoxicity to SFs with dependence of concentration and time. GFX-treating cells also showed G1 phase arrest, increased membrane permeability, PS externalization and DNA damage, which indicated that GFX induced apoptosis of SFs. Additionally, GFX could activate the caspase-8, caspase-9, and caspase-3, induce MTP disruption, downregulate B-cell leukemia-2 (Bcl-2) and B-cell leukemia-XL (Bcl-XL), and upregulate Bcl-2 assaciated X protein (Bax), Bcl-2-associated death promoter (Bad), Bcl-2 interacting domain (Bid) and cytoplasmic cytochrome C in SFs, suggesting that caspase-dependent extrinsic and intrinsic pathways were related to GFX-contributed apoptosis of SFs. CONCLUSION: The cytotoxicity of GFX induces apoptosis of SFs through triggering the caspase-dependent extrinsic and intrinsic pathways.     

Scleral buckling combined with internal cyclopexy for severe traumatic cyclodialysis cleft in open globe injuries

This study aimed to evaluate the effect of scleral buckling combined with internal cyclopexy on the treatment of severe traumatic cyclodialysis cleft in open globe injuries (OGIS). This retrospective study recruited 10 patients of 10 eyes. With our surgical intervention, all the 10 eyes achieved retinal and ciliary body anatomic re-attachment. The choroidal ruptures in nine eyes were closed with complete choroidal reattachment. Postoperative best-corrected visual acuity of nine eyes had various improvements. The mean intraocular pressure was increased from 8.9±2.6 mm Hg to 13.4±4.4 mm Hg. Eventually, six eyes underwent silicone oil (SO) removal without complications, two eyes still had SO tamponade and two eyes became SO-dependent eyes. The result shows that internal direct cyclopexy combined with scleral buckling is an effective treatment for severe traumatic cyclodialysis cleft in OGIS.     

联合激光与传统药物治疗原发性闭角型青光眼急性发作期的临床研究

目的评价激光周边虹膜成形术联合激光瞳孔成形术与传统降眼压药物治疗原发性闭角型青光眼急性发作的有效性和安全性。 方法收集2014年1月至2015年7月于邯郸市眼科医院(邯郸市第三医院)就诊的62例(68只眼)确诊为原发性闭角型青光眼首次急性发作并未做降眼压治疗患者的病例资料。其中,男性15例(17只眼),女性47例(51只眼),平均年龄(67.5±8.5)岁,所有患者眼压升高≥40 mmHg(1 mmHg＝0.133 kPa)。将入选患者采用数字表法随机分为激光组和药物组。激光组给予激光周边虹膜成形术联合激光瞳孔成形术治疗,药物组给予传统降眼压药物治疗。采用TA03型Icare眼压计测量治疗前、治疗后1 h和2 h的眼压,记录两组角膜及前房情况。以治疗后2 h眼压降至30 mmHg及以下为抢救成功,反之则为治疗失败。激光组和药物组年龄、就诊时眼压和发作时间等资料的描述采用均数±标准差表示,组间比较使用独立样本t检验;两组治疗成功率的描述采用眼数和百分比,比较采用χ²检验;两组治疗前、治疗后1 h和2 h眼压的比较采用两因素重复测量方差分析。 结果治疗后1 h激光组14只眼抢救成功,成功率为41.2%;药物组15只眼抢救成功,成功率为44.2%。治疗后2 h激光组18只眼抢救成功,成功率为52.9%;药物组20只眼抢救成功,成功率为58.2%。治疗后1 h与2 h两组间成功率无统计学意义( χ²＝0.06,0.24;P>0.05)。激光组治疗前视力为光感至0.4,治疗后1 h视力为眼前手动至0.6,治疗后2 h视力为眼前手动至0.6。药物组治疗前视力为光感至0.4,治疗后1 h视力为光感至0.8,治疗后2 h视力为光感至0.8。两组主要并发症为前房内炎症反应和角膜内皮皱褶,无眼内感染和脉络膜下暴发性出血等严重并发症。激光组治疗前、治疗后1 h和2 h平均眼压分别为(56.9±8.7)mmHg、(37.9±16.2)mmHg和(32.9±16.4)mmHg,治疗后眼压下降,与治疗前的比较差异有统计学意义(t＝6.02,7.76;P<0.05)。药物组治疗前、治疗后1 h和2 h平均眼压分别为(55.8±9.5)mmHg、(37.6±17.7)mmHg和(30.6±18.2)mmHg,治疗后眼压下降,与治疗前的比较差异有统计学意义(t＝5.28,7.16;P<0.05)。但两组各时间点的眼压比较均无统计学意义(t＝0.89,0.58,0.85;P>0.05)。 结论激光周边虹膜成形术联合激光瞳孔成形术和传统的降眼压药物治疗均能快速降低原发性闭角型青光眼急性发作期的眼压,但激光治疗安全、有效,可避免药物治疗给机体带来的副作用,是治疗原发性闭角型青光眼急性发作期的重要辅助措施。     

PSTPIP1‐associated myeloid‐related proteinemia inflammatory syndrome: A rare cause of childhood neutropenia associated with systemic inflammation and hyperzincemia

Neutropenia in pediatric patients can be due to a variety of disorders. We describe two patients who underwent extensive evaluation over many years for arthralgias and moderate neutropenia of unclear etiology. Genetic testing identified a pathogenic variant in PSTPIP1 (proline‐serine‐threonine phosphatase‐interacting protein 1) in both patients. Markedly elevated inflammatory markers and zinc levels confirmed the rare diagnosis of PSTPIP1‐associated myeloid‐related proteinemia inflammatory (PAMI) syndrome, tailoring treatment. Neutropenia is common in patients with PAMI syndrome. Unique mutations seen in PAMI syndrome may account for the specific phenotypic features of this disorder.