Mah Francis S, Romanowski Eric G, Dhaliwal Deepinder K, Yates Kathleen A, Gordon Y Jerold
Charles T. Campbell Ophthalmic Microbiology Laboratory, Department of Ophthalmology, University of Pittsburgh, Pittsburgh, Pennsylvania 15203, USA.
J Cataract Refract Surg. 2006 Feb;32(2):264-8. doi: 10.1016/j.jcrs.2005.09.024.
To investigate the potential role of commercially available topical fluoroquinolones in diffuse lamellar keratitis (DLK) using New Zealand White rabbit models.
Campbell Ophthalmic Microbiology Laboratory at the University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
In a DLK challenge model, laser in situ keratomileusis flaps were created by a microkeratome in rabbit eyes (n = 10 per group) and the stromal beds were treated with 1 drop of Ciloxan (ciprofloxacin 0.3%), Ocuflox (ofloxacin 0.3%), balanced salt solution (BSS), or Pseudomonas aeruginosa endotoxin before flap closure. After the procedure, eyes were treated with the same drugs 4 times daily. On postoperative day 1, the eyes were examined by slitlamp and graded (modified Linebarger DLK grading scale) in a masked fashion. In a DLK exacerbation model, all eyes received 1 drop of endotoxin on the stromal interface followed by flap closure. After the procedure, the rabbit eyes (10 per group) were treated 4 times daily with Ciloxan, Ocuflox, or BSS and graded for DLK on postoperative day 1 as before.
In the challenge model, Ciloxan, Ocuflox, and endotoxin all produced higher median DLK scores than the BSS control (P = .02). Ciloxan produced significant DLK in more eyes and had higher median scores (70%, 1.0) than Ocuflox (40%, 0.5) or endotoxin (45%, 0.5) (P = .05). In the endotoxin-induced model, Ciloxan produced significantly higher DLK scores than Ocuflox or BSS (P = .05).
Topical fluoroquinolones caused and exacerbated DLK in rabbit models. Ocuflox was associated with less DLK than Ciloxan. The clinical significance of these findings can only be assessed in clinical trials.
使用新西兰白兔模型研究市售局部用氟喹诺酮类药物在弥漫性板层角膜炎（DLK）中的潜在作用。
美国宾夕法尼亚州匹兹堡大学的坎贝尔眼科微生物学实验室。
在DLK激发模型中，用微型角膜刀在兔眼（每组10只）制作准分子原位角膜磨镶术瓣，在瓣关闭前，基质床分别用1滴西洛欣（环丙沙星0.3%）、氧氟沙星（氧氟沙星0.3%）、平衡盐溶液（BSS）或铜绿假单胞菌内毒素处理。术后，每天用相同药物对眼睛治疗4次。术后第1天，用裂隙灯检查眼睛，并采用盲法分级（改良的Linebarger DLK分级量表）。在DLK加重模型中，所有眼睛在基质界面滴入1滴内毒素，随后关闭角膜瓣。术后，兔眼（每组10只）每天用西洛欣、氧氟沙星或BSS治疗4次，并如前所述在术后第1天对DLK进行分级。
在激发模型中，西洛欣、氧氟沙星和内毒素产生的DLK中位数评分均高于BSS对照组（P = 0.02）。西洛欣在更多眼中产生显著的DLK，且中位数评分（70%，1.0）高于氧氟沙星（40%，0.5）或内毒素（45%，0.5）（P = 0.05）。在内毒素诱导模型中，西洛欣产生的DLK评分显著高于氧氟沙星或BSS（P = 0.05）。
局部用氟喹诺酮类药物在兔模型中可引发并加重DLK。与西洛欣相比，氧氟沙星引起的DLK较少。这些发现的临床意义只能在临床试验中评估。
