Descemet's Stripping Without Endothelial Keratoplasty

Daniel Garcerant; Nino Hirnschall; Nicholas Toalster; Meidong Zhu; Li Wen; Gregory Moloney

Disclosures

Curr Opin Ophthalmol. 2019;30(4):275-285. 

In This Article

The Role of Additional Rho-associated Kinase Inhibitor

Since their discovery in 1995, the Rho-associated kinase (ROCK) family of enzymes has been the subject of much research as therapeutic targets. The primary effects of Rho proteins are to induce structural change in the internal cell cytoskeleton, inhibiting smooth muscle vasodilation, cellular delamination and migration.[14] An in-vitro study of Ripasudil's effect on the trabecular meshwork and Schlemm's canal endothelial cells also showed cytoskeletal rearrangement (cell rounding and reduced actin bundles). It also decreases ZO-1 cell junctional complex proteins.[52] Although via kinase pathways proliferative effects may be modulated, as corneal surgeons our expectation that inhibition of this activity will safely induce mitotic activity and replenish situations of low endothelial cell counts is likely misplaced.[12,13,15,16,53–55] There is however justified confidence in their ability to promote cell migration in situations where this has stalled, with two cases of failing DSO salvaged by topical ripasudil use in our center.[44] The first double armed prospective study of ROCK inhibitor as an adjuvant to DSO has recently been published by Macsai et al. In a comparison of DSO in patients with ripasudil postoperatively with DSO without ripasudil, the ripasudil group had a significantly faster recovery and a higher central endothelial cell count compared with patients without ripasudil.[47] The trial is small with further analysis now required but is a positive first step.

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