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Pseudoexfoliation Glaucoma (PXF / XFG, LOXL1-Associated Open-Angle Glaucoma)

The most common identifiable cause of open-angle glaucoma worldwide; gray-white fibrillar pseudoexfoliation material on the anterior lens capsule and trabecular meshwork causes high intraocular pressure spikes, severe optic nerve damage, and challenging cataract surgery with high zonular dehiscence risk.

Written by: Saygı Hospital Health Guide Editorial Board
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This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

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What is Pseudoexfoliation Glaucoma (PXF / XFG, LOXL1-Associated Open-Angle Glaucoma)?

Pseudoexfoliation syndrome (XFS) is a systemic age-related disorder of elastic-fiber metabolism with deposition of fibrillar grayish-white pseudoexfoliation (PXF) material on multiple anterior-segment structures, most prominently the anterior lens capsule (classic three-zone bullseye pattern), zonules, ciliary body, iris pigment epithelium, trabecular meshwork, corneal endothelium, and conjunctiva. PXF material is also deposited systemically in lung, liver, kidney, heart, and meninges, and may be associated with cardiovascular events, hearing loss, and Alzheimer disease.

Pseudoexfoliation glaucoma (XFG) develops in 25–50 percent of XFS patients over 10–15 years; it is the most common identifiable cause of open-angle glaucoma worldwide (especially in Scandinavia, Mediterranean countries, Saudi Arabia) and is more aggressive than POAG with higher mean and peak intraocular pressure (often > 30 mmHg), greater diurnal IOP fluctuation, faster visual field loss, more advanced disc damage at presentation, worse response to medical therapy, and higher long-term progression rate. Genetic risk: LOXL1 single-nucleotide polymorphisms (G153D, R141L) confer 99 percent of disease susceptibility (population-attributable risk) but penetrance is modulated by environmental factors (UV exposure, coffee, low folate).

Diagnosis: dilated slit-lamp examination (essential — undilated may miss it) reveals classic three-zone bullseye pattern on anterior lens capsule (central disc, intermediate clear zone, peripheral granular zone), iris transillumination defects (peripupillary), pigment dispersion in anterior chamber (Sampaolesi line — pigmented line anterior to Schwalbe line on gonioscopy), pseudoexfoliation flakes at pupillary margin, and weak zonules. IOP measurement frequently reveals high spikes; gonioscopy is open angle with heavy pigmentation; OCT and visual field demonstrate glaucomatous damage.

Symptoms

Often asymptomatic until advanced glaucomatous visual field loss
Gray-white flakes at pupillary margin or on lens capsule (slit-lamp finding)
Iris transillumination defects (peripupillary)
High IOP detected on routine examination (often > 25 mmHg)
Phacodonesis or iridodonesis (zonular weakness)
Poor pupillary dilation
Glaucomatous visual field defects (arcuate, paracentral)
May be unilateral initially but typically becomes bilateral over years

Risk Factors

Age > 60 years (prevalence rises sharply after 70)
LOXL1 polymorphisms (G153D homozygous high risk)
Northern European, Scandinavian, Mediterranean, Middle Eastern ancestry
Female sex (slight predominance)
Chronic UV light exposure
Low folate, low vitamin B12, low coffee consumption (epidemiologic associations)
Family history of pseudoexfoliation
Cardiovascular disease, cerebrovascular disease, sensorineural hearing loss (systemic associations)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Annual comprehensive eye examination after age 60 with dilated lens evaluation
  • Family history of pseudoexfoliation or open-angle glaucoma
  • Newly diagnosed elevated IOP or asymmetric IOP
  • Visual field defects on perimetry
  • Blurred vision, halos, or progressive vision loss
  • Before any planned cataract surgery (specialist evaluation for zonular integrity)
  • Asymmetric pupillary dilation or peripupillary iris atrophy

Treatment Methods

01
Comprehensive baseline: dilated slit-lamp, gonioscopy, IOP (Goldmann applanation, multiple measurements), pachymetry, optic disc photography, OCT RNFL/GCC, automated visual field (24-2 SITA-Standard)
02
First-line medical: prostaglandin analogs (latanoprost, travoprost, bimatoprost, tafluprost) — once daily, very effective
03
Add fixed combinations as needed (latanoprost-timolol, brimonidine-timolol, dorzolamide-timolol) for IOP target
04
Selective laser trabeculoplasty (SLT) — very effective in XFG, often dramatic IOP reduction; consider as first-line in newly diagnosed XFG (LiGHT trial principle)
05
Cataract surgery (if coexistent cataract): meticulous phacoemulsification with capsular tension ring (CTR) for zonular weakness, low-energy phaco, careful hydrodissection, IOL in capsular bag with CTR; expect 5–10 percent zonular dehiscence — be prepared for vitrectomy and scleral-fixated IOL
06
MIGS for mild-moderate XFG: iStent inject, Hydrus microstent, Kahook Dual Blade goniotomy, GATT (often combined with cataract surgery)
07
Trabeculectomy with mitomycin-C for advanced XFG or progressive damage despite maximal medical/laser therapy; consider tube shunt (Ahmed, Baerveldt) if conjunctival scarring
08
Lifelong follow-up every 3–6 months: IOP, OCT progression, visual field; XFG progresses faster than POAG so vigilance is critical

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