Do impotence drugs cause NAION?

Article

The impotence drugs Viagra (sildenafil) and Cialis (tadalafil) may increase the risk of developing non-arteritic anterior ischaemic optic neuropathy (NAION), according to a study published in the February 2006 issue of the British Journal of Ophthalmology.

The impotence drugs Viagra (sildenafil) and Cialis (tadalafil) may increase the risk of developing non-arteritic anterior ischaemic optic neuropathy (NAION), according to a study published in the February 2006 issue of the British Journal of Ophthalmology.

Specialists have long noted an association between the two agents and light sensitivity and colour vision problems; however, this is the first study to investigate the possibility of optic nerve damage.

Gerald McGwin, MD of the University of Alabama, Birmingham, USA, and colleagues, performed a telephone survey to assess the use of both erectile dysfunction treatments among 38 men with NAION and 38 control subjects without a history of NAION.

At present, impotence drugs are contraindicated in patients with pre-existing NAION. Authors of this study have, however, urged physicians to warn their patients of the increased risk of vision-related problems, associated with these medications.

This issue has sparked a great deal of debate in recent months, with lawsuits having been filed against the manufacturers of Viagra, Pfizer, because of the drug's potential link with permanent vision loss.

In response to these recent claims, both Pfizer and Eli Lilly, makers of Viagra and Cialis, respectively, have changed their drug labelling to reflect these, as yet, unsubstantiated concerns.

Aspirin: a protective agent in diabetic retinopathy

Low-dose aspirin protects retinal vessels against experimental diabetic retinopathy, according to a study published in the December 2005 issue of Diabetes.

Researchers at Boston's Schepens Eye Research Institute at Harvard Medical School, USA, embarked on a study to determine whether the beneficial effects of aspirin on retinopathy were attributable to its antithrombotic mechanism of action, by performing a comparative study with the antiplatelet drug clopidogrel in streptozotocin-induced diabetic rats.

The authors noted that aspirin, at doses well below the anti-inflammatory range for humans (<0.6 mmol/l), prevented capillary cell apoptosis and the development of acellular capillaries, but it did not prevent neuroglial abnormalities. Increased expression of the transcription factor CCAAT/enhancer-binding protein-beta, a known target of low-intermediate concentrations of aspirin, was evident in the diabetic rat retina during the study. Clopidogrel, on the other hand, induced no changes in the retina of diabetic rats.

Using the aldose reductase inhibitor sorbinil as the benchmark for drug efficacy, the authors concluded that aspirin, at low-intermediate concentrations, selectively prevented microangiopathy in diabetic retinopathy. They also called for additional research into this area in order to elucidate the minimal effective dose required.

Potential role for gene therapy in ocular disease

An adenoviral-based vector containing the gene for human pigment epithelium-derived factor (AdPEDF.11) may prevent the progression of neovascular AMD, according to a study published in the February 2006 issue of Human Gene Therapy.

The study, led by Peter Campochiaro of the Wilmer Eye Institute, John Hopkins University School of Medicine in Baltimore, Maryland, USA, and colleagues, administered a single intravitreous injection of an E1-, partial E3- and E4-deleted adenoviral vector expressing PEDF to 28 patients with advanced neovascular AMD.

The Phase I multicentre, open-label, dose escalation study was designed to investigate the safety of the gene therapy at eight dose levels.

AdPEDF.11 was found to be well-tolerated at all doses with no dose-limiting toxicities or drug-related serious adverse events, suggesting a role for E1-, partial E3- and E4-deleted adenoviral vectors in ocular therapy. Although the therapy did not cause a reduction in median lesion size from baseline, no increase in lesion size was evident at six and 12 months post-injection in the high-dose gene therapy group.

Overall, the study provided evidence of activity in neovascular AMD and suggests adenoviral vector-mediated ocular gene transfer is a viable treatment approach for ocular disorders.

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