翼状胬肉切除联合自体角膜缘干细胞移植术治疗翼状胬肉临床观察

目的观察翼状胬肉切除联合自体角膜缘干细胞移植术治疗翼状胬肉的疗效。方法采用翼状胬肉切除联合自体角膜缘干细胞移植术方法治疗翼状胬肉【】50例(52只眼)观察术后角膜情况进行术前术后对比,并随访半年。结果 50例(52只眼)手术中、术后无严重并发症,随访半年,只有1例复发。结论翼状胬肉联合自体角膜缘干细胞移植术,疗效满意,大大降低术后复发率。     

Pilot study of transepithelial， very high fluence accelerated corneal collagen cross-linking in primary keratoconus

Objective Evaluate the safety and effectiveness of transepithelial, very high fluence accelerated corneal collagen cross-linking （A-CXL） in primary keratoconus. Methods Self-control study. Thirteen primary keratoconus eyes of 13 patients were treated with transepthelial, very high fluence A-CXL with a UVA intensity of 45 mW/cm2, an irradiation time of 2 min 40 s, and a total energy of 7.2 J/cm2. Routine ophthalmologic examination, UCVA, BCVA, refractive error, corneal keratometry, anterior and posterior elevation （AE and PE）, index of vertical asymmetry （IVA）, minimum corneal thickness （CT）, compensated intraocular pressure （IOPcc）, endothelial cell density （ECD） were evaluated pre-operatively and 7-day, 1-month, 3-month, 6-month, 12-month post-operatively. Results The UCVA （F=6.111, P＜0.01） and BCVA （F=9.734, P＜0.01） showed a statistically significant improvement by 12-month post-operatively. The decrease in spherical lens （F=5.871, P＜0.05）, steeper K-value （F=19.651, P＜0.05）, Kmax （F=3.253, P＜0.05）, AE （F=23.958, P＜0.01）, PE （F=20.832, P＜0.01） and IVA （F=4.068, P＜0.05） were statistically significant. CT （F=4.180, P＞0.05）, ECD （F=1.812, P＞0.05） and IOPcc （F=0.332, P＞0.05） were without significant change. Conclusion Transepithelial, very high fluence A-CXL is safe and effective in treating primary keratoconus.     

冠状动脉扩张症患者的临床特征及新分型指导介入治疗的效果观察

目的:总结51例冠状动脉扩张症(CAE)患者新分型临床特点及指导介入治疗的临床疗效。方法:回顾性分析我院2015年1月至2019年1月出院诊断含CAE且冠状动脉造影结果均符合CAE诊断标准患者51例。收集临床资料,按CAE新分型分类,随访主要不良心血管事件(MACE),其定义为全因死亡、心原性死亡、心肌梗死、血运重建的复合终点。结果:51例CAE患者中,36例(70.6%)临床表现为急性冠状动脉综合征,11例(21.6%)有CAE相关陈旧性心肌梗死。共69处冠状动脉扩张病变。CAE新分型结果如下:Ⅰ型:0例患者;Ⅱ型:1例(2.0%),1处(1.4%)冠状动脉扩张病变;Ⅲ型:20例(39.2%),36处(52.2%)冠状动脉扩张病变;Ⅳ型:14例(27.5%),14处(20.3%)冠状动脉扩张病变;Ⅴ型:16例(31.4%),18处(26.1%)冠状动脉扩张病变。依据CAE新分型指导介入治疗60处(87.0%),药物治疗9处(13.0%),手术成功率100%。中位随访时间13(6,36)个月,随访期间发生MACE 7例(13.7%),其中心肌梗死2例(3.9%),血运重建治疗5例(9.8%),均为非靶血管相关事件。结论:CAE患者多以急性冠状动脉综合征为主要表现,CAE新分型中Ⅲ型发病率较高,新分型指导CAE介入治疗临床效果满意。     

以猪角膜脱细胞基质为载体培养人脐静脉内皮细胞构建实验性角膜后板层

 目的： 探讨以异种后弹力膜/基质为载体诱导人脐静脉内皮细胞向角膜内皮细胞分化的可行性及移植术后在活体的生理功能。方法：体外分离培养脐静脉内皮细胞作为诱导移植的种子细胞;取当地质检合格的猪眼球以直径6.2 mm、厚100 μm、冷冻脱水进行角膜深板层载体的制备;接种经CM-DiI荧光标记的第2~3代人脐静脉内皮细胞于载体的后弹力层面,体外培养7~10 d行细胞形态、密度、组织学和扫描电镜观察,待细胞与后弹力层面融合形成单层后,用于兔角膜移植。受眼：正常健康新西兰大白兔24只（24眼）,实验组（人脐静脉内皮细胞移植组）12眼,对照组（单纯猪角膜深板层移植组）12眼,全角膜范围去除术眼内皮细胞,实施移植手术。结果：人脐静脉内皮细胞在猪后弹力膜/基质载体上贴附生长,形成紧密连接的单层,形态近似六角形,呈铺路石状分布,具有正常兔角膜内皮细胞的超微结构。术后8周实验组角膜基本透明,周边角膜略有水肿。对照组单纯猪角膜深板层移植后,移植角膜明显水肿、混浊。结论：以异种角膜后弹力膜/基质为载体培养的人脐静脉内皮细胞,行异种异体移植后,能够在活体上成活,并能维持角膜透明,具有正常角膜内皮细胞的生物学功能。深板层角膜内皮移植术是体外培养血管内皮细胞移植的一种有效术式。     

早期圆锥角膜与近视的Orbscan II角膜地形图对比分析

目的：探讨早期圆锥角膜的Orbscan II角膜地形图特点及敏感指标。方法应用Orbscan II研究23例（43只眼）早期圆锥角膜患者和25例（50只眼）近视患者角膜地形图的参数改变特点,并进行统计分析。结果患者年龄、近视度数、散光度数均无统计学差异（P ＞0．05）。角膜地形图参数中：角膜最薄点厚度、角膜前表面高度、角膜后表面高度、3．0 mm区不规则性（3．0 mm Zone Irreg）、5．0 mm区不规则性（5．0 mm Zone Irreg）在两组之间均有统计学差异（ P＜0．05）。结论角膜最薄点厚度、角膜前表面高度、角膜后表面高度、3．0 mm区不规则性有助于区分早期圆锥角膜和近视患者,是诊断早期圆锥角膜的敏感地形图指标。     

Comprehensive analysis of dural ectasia in 150 patients with a causative FBN1 mutation

The purpose of this study was to perform a comprehensive study of dural ectasia (DE) related to FBN1 mutations. We performed a database analysis of two German metropolitan regions of 150 patients (68 men, 82 women; mean age 35 ± 16 years). All patients had a FBN1 mutation and underwent dural magnetic resonance imaging. Age was <16 years in 20, 16–25 in 27, 26–35 in 67, and >35 in 36 patients. Prevalence of dural ectasia was 89% with criteria of Oosterhof and Habermann, 83% with Fattori, 78% with Lundby, and 59% with Ahn. DE was less frequent in patients <16 years with Ahn and Fattori. DE related to skeletal manifestations with all criteria, to aortic Z‐scores and mitral valve prolapse with criteria of Habermann and Lundby, and to age with criteria of Fattori. The Fattori‐grade of DE increased with age, aortic Z‐scores, and skeletal score points. There was no consistent relationship of DE with any type of FBN1 mutation. DE is frequent in patients with FBN1 mutations irrespective of age and its severity increases during life. Criteria of Oosterhof and Habermann yielded most consistent diagnostic results. DE relates to skeletal involvement, aortic Z‐scores, and mitral valve prolapse.     

A comparative study on endothelial cell loss in nanophthalmic eyes undergoing cataract surgery by phacoemulsification

Purpose:The purpose of this study is to compare the endothelial cell loss (ECL) in nanophthalmic eyes and age-matched controls undergoing cataract surgery by phacoemulsification and also to identify the risk factors influencing the endothelial cell density (ECD). This was a prospective comparative interventional case series.Methods:We enrolled 19 nanophthalmic eyes (study group) and 42 age-matched cataract controls (control group) undergoing phacoemulsification after meeting the inclusion criteria. Ocular parameters like best-corrected visual acuity, intraocular pressure, pachymetry, specular microscopy, and slit lamp findings were noted preoperatively and at month 1 and 3 postsurgery. All nanophthalmic eyes underwent cataract surgery with concomitant prophylactic posterior sclerostomy.Results:The median percentage endothelial loss in nanophthalmic eyes was 4.0 (IQR 0–23.5), 7.4 (IQR 1.0–-22.4) at 1 and 3 months postoperatively compared to 6.3 (IQR 1.7–14.1) and 6.4 (IQR 2.6–-12.1) in age controlled normal eyes (P = 0.94, P = 0.46, respectively). Linear regression analysis showed increasing age as the only variable influencing the percentage decrease in corneal ECD in the study group (P = 0.001). Nanophthalmic eyes with ACD <2.5 mm had a significantly greater reduction in ECD at 3 months postcataract surgery compared to baseline (P = 0.039). Visual outcomes and IOP reduction in the study group with ACD >2.5 mm were significantly better postcataract surgery (P = 0.02 and P = 0.002, respectively).Conclusion:The percentage of ECL in nanophthalmic eyes undergoing phacoemulsification is equivalent to normal eyes. However, in the nanophthamic eyes with AC depth <2.5 mm, the percentage cell loss was significantly higher warranting the need for extensive intraoperative care. Increasing age was found to be the only significant risk factor influencing the ECD in short eyes.     

Intracorneal scleral patch supported cyanoacrylate application for corneal perforations secondary to rheumatoid arthritis

Purpose:To describe a new technique of intracorneal scleral patch (ICSP) supported cyanoacrylate tissue adhesive (CTA) application in corneal perforations, greater than 3.0 mm secondary to rheumatoid arthritis (RA).Methods:This Prospective, non-randomized, non-comparative, interventional series included 14 eyes (14 patients). All patients had corneal perforations sized 3.5 to 4.5 mm due to RA, which were treated with ICSP supported CTA application. A partial thickness scleral patch 1.0 mm larger than diameter of corneal perforation was prepared. A lamellar corneal pocket 0.5 mm all around the corneal perforation was created. The partial thickness scleral patch was placed in the corneal perforation site and the edge was fitted into the lamellar intracorneal pocket. A minimum quantity of CTA was applied on the scleral patch to seal the perforation.Results:The corneal perforations healed in 14 eyes (100%) in a mean 7.71 ± 1.14 (range, 6–9) weeks. One eye (7.14%) had inadvertent extrusion of ICSP due to premature removal of CTA but, Seidel''s test was negative, and the corneal epithelial defect healed with BCL alone. One eye each (7.14%) developed steroid induced cataract and glaucoma. None of eyes developed infective keratitis, re-opening of corneal perforation (necessitating repeat procedure) or enlargement of corneal perforation requiring penetrating keratoplasty (PKP).Conclusion:ICSP supported CTA application is a successful alternative option to emergency PKP in treating corneal perforations sized 3.5 to 4.5 mm with associated RA.     

The molecular basis of neurotrophic keratopathy: Diagnostic and therapeutic implications. A review

Neurotrophic keratopathy (NK) is a degenerative corneal disease produced by different factors, including infection, trauma, and neurogenesis, that lead to trigeminal nerve damage and impaired corneal sensitivity. Extensive epithelial breakdown, impaired corneal epithelial healing and corneal ulceration, stromal melting, and perforation are main NK features. The proliferation of the corneal epithelium is endogenously regulated by a balance between adrenergic cAMP-dependent and cholinergic cGMP-dependent pathways. A careful balance of epitheliotropic neuromediators and neurotrophic factors expressed by corneal nerves and epithelial cells, respectively, is required to maintain corneal homeostasis. Even in its early stages, NK can cause reduced vision secondary to epithelial disturbance. Diagnosing NK is challenging, requiring the acquisition of a thorough clinical history and a comprehensive neurological and ophthalmic examination. Following suspicion of a clinical NK diagnosis, corneal sensitivity must be assessed qualitatively with the wisp of the cotton-tipped applicator and quantitatively through Cochet-Bonnet esthesiometry (CBE). A myriad of therapies is used for NK, and new, more specific modalities are being developed and investigated. Medical treatment with topical recombinant human nerve growth factor and surgical treatment through corneal neurotization are promising therapies aiming to target NK pathophysiology. Coexistent ocular surface disorders must be managed concomitantly to improve its prognosis. This review describes the up-to-date knowledge of the molecular basis regarding the pathogenesis of NK, and the novel target-specific therapeutic approaches based on this molecular mechanism.     

The role of nitric oxide in ocular surface physiology and pathophysiology

Nitric oxide (NO) has a wide array of biological functions including the regulation of vascular tone, neurotransmission, immunomodulation, stimulation of proinflammatory cytokine expression and antimicrobial action. These functions may depend on the type of isoform that is responsible for the synthesis of NO. NO is found in various ocular tissues playing a pivotal role in physiological mechanisms, namely regulating vascular tone in the uvea, retinal blood circulation, aqueous humor dynamics, neurotransmission and phototransduction in retinal layers. Unregulated production of NO in ocular tissues may result in production of toxic superoxide free radicals that participate in ocular diseases such as endotoxin-induced uveitis, ischemic proliferative retinopathy and neurotoxicity of optic nerve head in glaucoma. However, the role of NO on the ocular surface in mediating physiology and pathophysiological processes is not fully understood. Moreover, methods used to measure levels of NO in the biological samples of the ocular surface are not well established due to its rapid oxidation. The purpose of this review is to highlight the role of NO in the physiology and pathophysiology of ocular surface and propose suitable techniques to measure NO levels in ocular surface tissues and tears. This will improve the understanding of NO's role in ocular surface biology and the development of new NO-based therapies to treat various ocular surface diseases. Further, this review summarizes the biochemistry underpinning NO's antimicrobial action.