Eyeworld

JAN 2011

EyeWorld is the official news magazine of the American Society of Cataract & Refractive Surgery.

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EW MEETING REPORTER 61 S essions continued Thurs- day, December 2, at the Asia Cornea Society meet- ing in Kyoto, Japan. Among highlighted ses- sions: corneal imaging, meibomian gland dysfunction, keratoconus, contact lens and infections, ptery- gium & tumors, and endothelial ker- atoplasty. "Long term" DSEK data Francis Price, M.D., and his col- leagues at the Price Vision Group, Indianapolis, Ind., first used DSEK in 2003, so that any "long-term" data they have on outcomes is, he said, "relative." Still, the data so far has been encouraging. On average, the data shows that DSEK is at least as safe as PK in terms of endothelial cell loss. Initially, at one year post- op, DSEK resulted in greater en- dothelial cell loss than PK—37% vs. 11%, respectively; however, the situ- ation reversed at five years, with cell loss at 53% for DSEK and 69% for PK. Meanwhile, graft survival has similarly been as good as or better than reports for PK. Moreover, said Dr. Price, much of this data comes from a time when DSEK was still rel- atively primitive—i.e., before the ad- vent of endothelium-protective strategies and devices such as the Busin glide and the Tan endoglide.These new strategies promise even better long-term re- sults. Dr. Price's experience so far has led him to recommend certain strategies for better outcomes: use self-sealing scleral tunnels, and use a pull-through technique. Endothelial keratoplasty: ROCKing the endothelium But perhaps the most exciting devel- opment in endothelial health at the moment is the possibility of treating corneal endothelial dystrophy with drugs, avoiding transplant surgery. Naoki Okumura, M.D., and col- leagues—among them Noriko Koizumi, M.D., and Shigeru Ki- noshita, M.D., Ph.D.—have already reported on several drugs that en- hance corneal endothelial cell prolif- eration. Today, they have their sights on one particularly promising agent: Rho-kinase (ROCK) inhibitor. Rho-kinase, said Dr. Okumura, binds to GTPase RhoA to carry out a wide range of cellular activities. Y-27632 is a selective ROCK inhibitor. In cell culture, the addition of Y-27632 to the medium resulted in larger colonies compared with control. Flow cytometric analysis with cell cycle proliferation marker Ki67 showed a significantly elevated number of Ki67-positive cells, indi- cating enhanced cell cycle prolifera- tion. Dr. Okumura and colleagues have already carried out several in vivo trials, the first of which in- volved Japanese white rabbits and cynomolgus monkeys. In the rabbit model, Dr. Okumura found that eyes treated with topical ROCK inhibitor significantly enhanced corneal wound healing compared with con- trol eyes; the treated group also had thinner corneas. In the monkey model, both treated and control eyes were transparent 1 month after they were damaged by freezing. Dr. Oku- mura and colleagues have since begun trials involving patients with corneal endothelial dystrophy. In their first human trial, they removed about 2–3 mm of damaged endothe- lium by transcorneal freezing. They then applied Y-27632 eye drops six times daily for a week. In this patient, ROCK inhibitor resulted in the recovery of corneal thickness and transparency. The pa- tient's visual acuity (VA) changed from 0.2 to 1.5; follow up six months later revealed that both the transparency and VA were retained. Although they failed to measure baseline cell density, the density after treatment was 1,700 cells/mm2; in addition, the cell den- sity at the center of the cornea was higher than at the periphery. This, said Dr. Okumura, suggests that the ROCK inhibitor did in fact promote cell proliferation. At this point, ROCK inhibitor is certainly proving to be an exciting new tool in the management of corneal endothelial dystrophy. Editors' note: Drs. Price and Okumura have no financial interests related to the content of their lectures. The finer points of MGD Dry eye disease (DED) and meibo- mian gland disease (MGD) are often thought of as co-morbid conditions; in fact, said Michael A. Lemp, M.D., MGD is a principal form of DED. DED can be the result of aque- ous deficiency—that is, either Sjö- gren's syndrome or non- Sjögren's conditions such as lacrimal defi- ciency, lacrimal gland duct obstruc- tion, and reflex block—or evaporative conditions, either in- trinsic or extrinsic. MGD, said Dr. Lemp, is basically an intrinsic evapo- rative form of DED. It is present in 84% of patients with DED, and on its own has a six to 10 times greater prevalence than aqueous deficiency- type DED. How it works is MGD re- sults in abnormalities in the lipid composition and behavior of meibum, said Gary N. Foulks, M.D. It had previously been thought that lipids in meibum alone prevented premature evaporation of the tear film, said Dr. Foulks; now we know that it is in fact the interaction be- tween lipids and proteins in the tear film—particularly lipocalins, the most potent lipid-binding proteins in the tear film—that stabilizes the tear film, reducing evaporation and improving the spread of tear film over the eye. In the clinic, evaluation of MGD has been limited by the inability to evaluate the structure of diseased meibomian glands. To be sure, a method does exist; however, said Reiko Arita, M.D., meibography isn't commonly done due to its in- vasive nature and the technical diffi- culty of performing the procedure. Meibography, she said, had previ- ously been the only way clinicians could observe the meibomian gland structure in silhouette, doing so by illuminating the lid from the side. Now Dr. Arita and her col- leagues have developed non-contact meibography, basically using a slit lamp combined with an infrared transmitting filter. This allows better evaluation of MGD, allowing, for in- stance, the direct differentiation of obstructive MGD from normal eyes. Just over a year ago, before the Tear Film and Ocular Surface Society held its MGD Workshop, the treat- ment of MGD varied all over the world. However, a review of current practice patterns does reveal some commonly accepted practices: lid hygiene with warm compresses and lid massage; the use of lubricants and topical antibiotic ointments; the use of systemic tetracycline; incision and curettage with optional steroid use in the presence of chalazion. Based on the findings of the MGD Workshop, Gerd Geerling, M.D., recommended an approach to treatment based on disease stage: Stage 1—minimally altered ex- pressibility and secretion quality; asymptomatic; no corneal staining. At this stage, treatment involves in- forming the patient, educating her about the condition, about dietary, environmental, and medication ef- fects, and prescribing eyelid hygiene (lid warming, expression). Stage 2—mildly altered express- ibility and secretion quality; mini- mal to mild symptoms; none to limited corneal staining. Eyelid hy- giene may or may not be combined with lubricant, topical azithromycin, and tetracycline derivatives. Stage 3—moderately altered ex- pressibility and secretion quality; moderate symptoms; mild to moder- ate, mainly peripheral corneal stain- ing. Oral tetracyclines are added to the above regimen, and may or may not be combined with nocturnal ointment, cyclosporine or steroid. Stage 4—severely altered ex- pressibility and secretion quality; marked symptoms; marked, central corneal staining. Anti-inflammatory therapy is added to the regimen at this point. Plus disease—coexisting or ac- companying disorders of the ocular surface and/or eyelids. Steroids, con- tact lenses, and surgery, depending on the comorbidity. These guidelines and other in- formation from the MGD workshop, said Dr. Geerling, will be published as a supplement to the January 2011 issue of Investigative Ophthalmology and Visual Science. EW Editors' note: Dr. Foulks has financial interests in various ophthalmology com- panies. None of the other doctors have any financial interests related to the January 2011

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