Eyeworld

EW GLAUCOMA 104 February 2018 Research highlight by Liz Hillman EyeWorld Staff Writer cleral veins. Endothelial cells line Schlemm's canal, which is charac- terized by an outer wall and inner wall. 3 The endothelial cells of Schlemm's canal's inner wall have been shown to be a source of resis- tance to aqueous humor drainage. 4 This inner wall of the endothelium has giant vacuoles and pores. Giant vacuoles contribute elasticity that al- lows the lumen of Schlemm's canal to change shape in response to IOP fluctuation, 5 while it's thought the pores help facilitate outflow. 6 Some think fluid flow is controlled by the location of these giant vacuoles and pores. 7 Prior research had shown how the Angpt-Tie2 pathway controls the vascular maturation and stabiliza- tion of Schlemm's canal for congen- ital glaucoma. Mice with Angpt1/ Angpt2 or Tie2 deleted develop with primary congenital glaucoma, and email to EyeWorld. "Our findings highlight Schlemm's canal as a func- tional reservoir of AHO as well as a main structure for glaucomagenesis when severely impaired." Drs. Kim and Koh added that the main aque- ous humor outflow pathway in mice is similar to that of humans. For a bit of review, Schlemm's canal, as described in the Kim et al. study and other published research, has both lymphatic and vascular characteristics. Schlemm's canal, in development, originates from the choroidal vein, but with upregulation of the gene Prox1, a master transcription factor for lymphatic endothelial cells, it takes on lymphatic characteristics, such as expression of related proteins. 2 In the healthy eye, after aqueous humor passes through the trabecular meshwork, it moves through Schlemm's canal and intras- cleral collector channels that funnel it out through aqueous and epis- factors angiopoietin-1 (Angpt1) and angiopoietin-2 (Angpt2) and their receptor Tie2 as "indispensably required" for maintaining the integ- rity and functionality of Schlemm's canal in an adult mouse model. The investigators also showed how these factors could be injected as a thera- peutic agent to restore function to Schlemm's canal. "In our study, we demonstrated that deletion of Angpt1/Angpt2 or Tie2 in adult mice severely impaired integrity of Schlemm's canal and transcytosis of aqueous humor, leading to elevated intraocular pres- sure, retinal neuron damage, and impairment of retinal ganglion cell function, all hallmarks of primary open angle glaucoma in humans," Jaeryung Kim, MD, PhD candidate, Korea Advanced Institute of Science and Technology (KAIST), and Gou Young Koh, MD, PhD, director, Center for Vascular Research, Insti- tute for Basic Science, wrote in an Regulator system identified as important for continued maintenance and integrity of Schlemm's canal I t's well known that increased intraocular pressure due to fluid buildup in the eye causes glaucoma and sight-threaten- ing damage to the optic nerve. But just what causes the structures in the eye to malfunction leading to reduced aqueous humor outflow is less understood. A recent study published in the Journal of Clini- cal Investigation sheds light on a pathway that can lead to aqueous humor outflow (AHO) resistance in Schlemm's canal in primary open angle glaucoma, the most common form of the disease. 1 The study from the Center for Vascular Research at the Institute for Basic Science, Daejeon, South Korea, identified certain vascular growth Study sheds light on underlying pathogenesis of primary open angle glaucoma continued on page 106 bleb failure are bleb leak, aqueous misdirection, retained lens frag- ments, or iris incarceration in the sclerectomy or the tube. "Most commonly, however, we worry about inflammatory mediated fibrosis postoperatively. We can mitigate this with extra steroid use at the end, either subconjunctival or intravitreal, and avoid prostaglan- dins and miotics to help decrease any inflammation postoperatively. These patients may require more aggressive steroids and NSAIDs than you would do in a typical cataract patient. It is important to keep them on a longer steroid taper in order to decrease the amount of inflam- mation and keep their glaucoma surgery functioning and filtering postoperatively." The patient underwent an uncomplicated cataract surgery, requiring a pupil expansion device at the time of surgery. Her uncor- rected visual acuity was 20/40 and 20/25 with correction, and her IOP went from 20 mm Hg immediately postoperatively to 15 mm Hg. She required a slow prednisone taper and was back on three medications, with controlled intraocular pres- sures. Dr. Chaku was satisfied to be able to keep her functioning tube viable after the cataract surgery. EW Editors' note: Dr. Chaku has no finan- cial interests related to her comments. Contact information Chaku: meenakshi.chaku@lumc.edu Planning continued from page 102 Intraoperative gonioscopy images before (left) and after (right) blood reflux into Schlemm's canal. A recent study could lead to a better understanding of how primary open angle glaucoma originates, with research describing a potential pathway that leads to aqueous humor outflow resistance in Schlemm's canal. Source: Leonard Seibold, MD

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