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Association of Iris Damage With Reduction in Corneal Endothelial Cell Density After Penetrating Keratoplasty

Ibrahim, Osama, MD, PhD; Yagi-Yaguchi, Yukari, MD, PhD; Kakisu, Koji, MD, PhD; Shimazaki, Jun, MD, PhD; Yamaguchi, Takefumi, MD

doi: 10.1097/ICO.0000000000001819
Clinical Science
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Purpose: To evaluate the effect of iris damage on endothelial cell loss in the early phase after penetrating keratoplasty (PKP).

Methods: This prospective consecutive study included 74 patients who underwent PKP without graft rejection during the follow-up period. Endothelial cell density (ECD) was measured using specular microscopy at 1, 3, 6, and 12 months after PKP. Iris damage scores (IDSs) were determined on the basis of slit-lamp microscopy or anterior segment optical coherence tomography imaging. Graft survival rates were compared among the different IDSs. Using multivariate analysis, the factors influencing postoperative ECD were assessed, taking into consideration the presence of glaucoma, history of graft failure, donor age, and graft ECD as independent variables.

Results: Graft ECD decreased from 2674 ± 329 cells/mm2 to 2114 ± 570 at 1 month, 1907 ± 629 at 3 months, 1669 ± 738 at 6 months, and 1404 ± 792 at 12 months (all, P < 0.0001). ECD at 12 months was associated with the IDS (β = −0.444, P < 0.0001), graft ECD (β = 0.309, P = 0.003), and history of graft failure (β = −0.251, P = 0.016). The IDS was significantly correlated with %ECD loss at 1 month (r = 0.427, P = 0.003), at 3 months (r = 0.376, P = 0.002), at 6 months (r = 0.301, P = 0.013), and at 12 months (r = 0.517, P < 0.0001). The graft survival rates in eyes with severe iris damage were significantly lower than those in eyes with either no or mild iris damage (P < 0.0001).

Conclusions: Severe iris damage is associated with rapid reduction in ECD and graft endothelial failure after PKP.

Department of Ophthalmology, Tokyo Dental College, Ichikawa General Hospital, Chiba, Japan.

Correspondence: Takefumi Yamaguchi, MD, Department of Ophthalmology, Ichikawa General Hospital, Tokyo Dental College 5-11-13, Sugano, Ichikawa, Chiba 272-8513, Japan (e-mail: tym.i.eye.i@gmail.com).

Supported by the Grant-in-Aid for Scientific Research 15K10906 from the Ministry of Education, Culture, Sports, Science and Technology (T. Yamaguchi), Takeda Scientific Foundation (T. Yamaguchi), and Clinical Pharmacological Research Foundation (T. Yamaguchi). The funding organization had no role in the design or conduct of this research.

The authors have no conflicts of interest to disclose.

Received July 01, 2018

Accepted October 06, 2018

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