Week in review: Gene therapy for LCA, Susvimo voluntary recall, smoking accelerates RNFL thinning

A weekly roundup of ophthalmic news from around the web.

It took just 2 weeks to ease years of congenital blindness, say researchers at the University of Pennsylvania, who have just published results of their study of an experimental gene therapy given to 2 adult patients with Leber congenital amaurosis (LCA). This rare disease is caused by mutations in the GUCY2D gene, and the patients were given subretinal injections of an AAV gene therapy containing the healthy version of GUCY2D. Within 14 days, increased rod sensitivity and better visual function (in terms of night vision) were observed. Dr. Samuel Jacobson, lead author of the published paper, said, “These exciting results demonstrate that the basic molecular machinery of phototransduction remains largely intact in some cases of LCA, and thus can be amenable to gene therapy even after decades of blindness.” University of Pennsylvania, iScience

Alert: Voluntary recall of the Susvimo ranibizumab injection system. On October 17, 2022, Genentech announced a voluntary recall of the Susvimo ranibizumab ocular implant and injection tool. A company-issued statement said that “The voluntary recall is based on recent testing of our commercial supply in which Susvimo implants were exposed to repeated puncturing with a needle. The results showed that some implants did not perform to our standards.” Formerly called the Port Delivery System, Susvimo was approved by the FDA in November 2021 for the treatment of neovascular AMD. Genentech stressed the voluntary nature of the recall, saying that patients already given the implant do not need to have it removed and can continue to receive refills. Ophthalmology Times

Heavy smoking accelerates retinal thinning. Greater smoking intensity, rather than a general history of smoking, appears to increase retinal nerve fiber layer (RNFL) thinning in patients with primary open-angle glaucoma (POAG), according to results from a longitudinal study of 314 patients (466 eyes) with POAG. Every additional 10 pack-year of cigarette smoking at baseline led to a 0.06 µm/year faster circumpapillary RNFL thinning rate; moderate-to-fast RNFL thinning was linked to a mean smoking intensity of 24.3 pack-year. Other risk factors for circumpapillary RNFL thinning included hypertension, higher mean IOP at follow-up, longer axial length, and thinner central corneal thickness. Tobacco control measures and monitoring patients with POAG who smoke continue to be important for public health. British Journal of Ophthalmology