Masqueraders of RP
• Infections: syphilis, congenital rubella, toxoplasmosis, CMV, and TB
• Drug Toxicities: hydroxychloroquine (Plaquenil), chloroquine, or phenothiazines like thioridazine
• Inflammatory & Autoimmune Diseases: Chronic or intermediate uveitis, pars planitis, white dot syndromes (like acute zonal occult outer retinopathy or AZOOR), systemic rheumatologic conditions
• Paraneoplastic & Autoimmune Retinopathies: Rare immune-mediated responses to systemic cancers, such as cancer-associated retinopathy (CAR) or melanoma-associated retinopathy (MAR), cause rapid photoreceptor degeneration.
• Nutritional Deficiencies: Severe vitamin A deficiency—often secondary to fat malabsorption or bariatric surgery—can cause reversible night blindness and pigmentary alterations.
• Trauma and Vascular Events: Blunt ocular trauma, retained intraocular foreign bodies (siderosis), or ophthalmic artery occlusions can produce pseudo-RP pigmentary shifts
How can we differentiate between them?
• Electroretinogram (ERG): True RP shows generalized, severe, or non-recordable dysfunction, whereas some masqueraders present with localized or atypical patterns
• Symmetry: Inherited RP is characteristically bilateral and symmetrical, whereas asymmetric or strictly unilateral presentation heavily points toward an acquired masquerader (like trauma or localized infection).
• Advanced Diagnostics: Blood serology (for syphilis or nutritional panels) and multimodal imaging like Optical Coherence Tomography (OCT) or fundus autofluorescence help isolate active inflammation, toxicity, or systemic drivers
Image from Rajan Eye Care Hospital
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