Jouve L, Borderie V, Temstet C, Labbé A, Trinh L, Sandali O, Basli E, Laroche L, Bouheraoua N
Service d'ophtalmologie 5, Centre hospitalier national d'ophtalmologie des Quinze-Vingts, 28, rue de Charenton, 75012 Paris, France; Université UPMC Paris VI, UMR S 968, Institut de la vision, 17, rue Moreau, 75012 Paris, France.
Université UPMC Paris VI, UMR S 968, Institut de la vision, 17, rue Moreau, 75012 Paris, France; Service d'ophtalmologie 3, Centre hospitalier national d'ophtalmologie des Quinze-Vingts, 28, rue de Charenton, 75012 Paris, France; Service d'ophtalmologie, hôpital Ambroise-Paré, AP-HP, 9, avenue Charles-De-Gaulle, 92100 Boulogne-Billancourt, France.
J Fr Ophtalmol. 2015 May;38(5):445-62. doi: 10.1016/j.jfo.2014.12.003. Epub 2015 Apr 24.
Corneal collagen crosslinking (CXL) is, at present, the only treatment that can slow or even stop the progression of keratoconus. It uses riboflavin and ultraviolet A (UVA) to create covalent bonds ("crosslinks") between collagen fibrils thus increasing corneal rigidity. Although to date there has been no direct evidence of intrastromal corneal crosslinking, several studies have reported the safety and efficacy of the conventional CXL protocol. This protocol is indicated for progressive keratoconus with a minimal corneal thickness (without the epithelium) of at least 400 μm. It should be performed as early as possible in patients under 18 years with keratoconus or with post-LASIK ectasia. Because of the epithelial debridement, it may rarely induce complications such as infectious keratitis or stromal scars. A variety of new protocols is under investigation and may reduce the rate of these complications. In addition, combination of CXL with other surgical treatments (intracorneal ring segments or photorefractive keratectomy) may improve visual outcomes in patients with keratoconus. Finally, the antimicrobial and anti-edematous properties of CXL have been shown, suggesting new therapeutic indications of this procedure such as infectious keratitis or stromal edema in the future.
角膜胶原交联(CXL)是目前唯一能够减缓甚至阻止圆锥角膜进展的治疗方法。它利用核黄素和紫外线A(UVA)在胶原纤维之间形成共价键(“交联”),从而增加角膜硬度。尽管迄今为止尚无基质内角膜交联的直接证据,但多项研究报告了传统CXL方案的安全性和有效性。该方案适用于角膜最小厚度(无上皮)至少为400μm的进行性圆锥角膜。对于18岁以下的圆锥角膜患者或准分子激光原位角膜磨镶术(LASIK)后角膜扩张患者,应尽早进行该治疗。由于去除了上皮,它可能很少引发感染性角膜炎或基质瘢痕等并发症。目前正在研究多种新方案,可能会降低这些并发症的发生率。此外,CXL与其他手术治疗方法(角膜内环植入或准分子激光角膜切削术)联合使用,可能会改善圆锥角膜患者的视力预后。最后,CXL的抗菌和抗水肿特性已得到证实,这表明该治疗方法未来可能有新的治疗适应症,如感染性角膜炎或基质水肿。