Case ReportCorneal Endothelial Cytotoxicity of the Calotropis procera (Ushaar) PlantAl-Mezaine, Hani S MD*; Al-Amry, Mohammed A MD†; Al-Assiri, Abdullah MD†; Fadel, Talal S MD, FRCS*; Tabbara, Khalid F MD, ABO, FRCOphth‡; Al-Rajhi, Ali A MD, FRCS, FRCOphth†§ Author Information From the *Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia; †the Anterior Segment Division, King Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia; ‡Eye Center and The Eye Foundation For Research, Riyadh, Saudi Arabia; and §Research Department, King Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia. Received for publication July 16, 2007; revision received November 1, 2007; accepted November 4, 2007. The authors state that they have no proprietary interest in the products named in this article. Reprints: Hani S. Al-Mezaine, Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, PO Box 230387, Riyadh 11321, Kingdom of Saudi Arabia (e-mail: [email protected]). Cornea: May 2008 - Volume 27 - Issue 4 - p 504-506 doi: 10.1097/ICO.0b013e3181611c34 Buy Metrics Abstract Purpose: To report 6 eyes of 5 patients with transient corneal edema after exposure to the milky latex of Calotropis procera (ushaar). Methods: Interventional case series. Results: Intracorneal penetration of ushaar latex can lead to permanent endothelial cell loss with morphologic alteration. Corneal edema resolved completely in ∼2 weeks in all cases, despite reduced endothelial cell count and abnormal morphology. Conclusions: Corneal endothelial toxicity of ushaar latex is caused by its ability to penetrate the corneal stroma and induce permanent loss of endothelial cells. Corneal edema resolves if sufficient endothelial cell viability is still present after resolution of ushaar keratitis. © 2008 Lippincott Williams & Wilkins, Inc.