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DIDANOSINE RETINAL TOXICITY.

Sara J Haug¹, Robert W Wong, Shelley Day

¹*West Coast Retina Medical Group, San Francisco, California; †Austin Retina Associates, Austin, Texas; ‡Herzig Eye Institute, Toronto, Ontario, Canada; §Associated Retinal Consultants P.C., Royal Oak, Michigan; ¶Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, University of California-Los Angeles, Los Angeles, California; **Bascom Palmer Eye Institute, University of Miami, Miami, Florida; ††Vanderbilt Eye Institute, Vanderbilt University, Nashville, Tennessee; and ‡‡Greater Los Angeles VA Healthcare Center, Los Angeles, California.

Retina (Philadelphia, Pa.)

|December 23, 2016

Summary

This summary is machine-generated.

Didanosine (ddI) can cause progressive retinal degeneration, even after drug cessation. This study details 19 cases of didanosine toxicity, highlighting ongoing retinal damage in some patients.

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Area of Science:

Ophthalmology
Toxicology
Pharmacology

Background:

Didanosine (ddI) is a nucleoside reverse transcriptase inhibitor used in HIV treatment.
Retinal degeneration is a known, albeit rare, adverse effect of didanosine therapy.
Understanding the spectrum and progression of didanosine-induced retinal toxicity is crucial for patient management.

Observation:

Nine new cases of peripheral chorioretinal degeneration linked to didanosine use were identified.
Literature review identified 10 additional cases, totaling 19 cases analyzed.
Patients presented with well-demarcated, severe midperipheral chorioretinal degeneration.

Findings:

Eight of nine new cases were male, with a median age of 54.
Visual acuity ranged from 20/20 to 20/32.
Three new cases showed progressive retinal atrophy despite discontinuing didanosine.
Literature cases showed similar chorioretinal findings, with 70% being male and an average age of 26.

Implications:

Didanosine toxicity can lead to irreversible retinal damage.
Retinal degeneration may progress even after didanosine cessation.
Newer nucleoside reverse transcriptase inhibitors may also pose a risk for mitochondrial DNA damage and subsequent chorioretinal degeneration.