Aniridia: Definition, Classification, Causes, Symptoms, Histopathology, Diagnosis and Treatment

It is a congenital, bilateral condition (both eyes) characterized by the complete or partial absence of the iris.

The term aniridia is Greek for “without iris.”

The iris is the colored part of the eye that surrounds the pupil. The iris contains muscles that allow the pupil to get bigger (open or dilate) and smaller (get closer or contract).

The iris regulates the amount of light that enters the eye by adjusting the size of the pupil opening.

The iris also determines the color of your eyes. People with brown eyes have highly pigmented irises, while people with blue or lighter eyes have less pigmented irises.

Causes of Aniridia

Aniridia is a genetic condition caused by a mutation in the PAX6 gene on chromosome 11:

About 2/3 of people with Aniridia, the condition is inherited in an autosomal dominant fashion. To manifest the disease, an individual has to inherit only one abnormal gene from either parent.


In about 1/3 of people with Aniridia, the gene mutation is sporadic, meaning it is not inherited from either parent but develops spontaneously in the person.

Rarely can Aniridia be inherited autosomal recessive, which means that an individual has to inherit two abnormal copies of the gene, one from each parent, to exhibit the disorder?

These people may also have other symptoms, such as ataxia (balance and movement problems) and cognitive disabilities.

The main diagnostic feature is partial or complete congenital hypoplasia of the iris; foveal hypoplasia with reduced visual acuity is almost always present and is associated with early-onset nystagmus.

Other frequently associated ocular abnormalities, generally with later onset, include cataracts, Glaucoma, corneal opacification, and vascularization secondary to limbal stem cell deficiency.

In most cases, Aniridia occurs in isolation without systemic involvement due to dominantly inherited mutations or deletions of the paired box gene 6 (PAX6).

It can also occur in a minority of cases as part of the WAGR contiguous gene syndrome (Wilms tumor-aniridia-genital abnormalities-delay). The adjacent genes for PAX6 and Wilms tumor (WT1) are deleted.

Aniridia and Wilms tumor

About 30% of people with sporadic Aniridia may have WAGR syndrome.

Wilms tumor is a rare kidney cancer that mainly affects children. WAGR is an acronym for a constellation of conditions that commonly occur together in this syndrome:

  • W: tumor de Wilms.
  • A: aniridia.
  • G: genitourinary abnormalities, irregularities in the reproductive and urinary organs.
  • R: retraso mental.

Therefore, your ophthalmologist needs to evaluate your family history to see if you have Aniridia. If you have sporadic Aniridia, regular ultrasounds are required to detect Wilms tumor.


While Aniridia is named for its classic effect on the iris, the disorder involves the overall abnormal development of many structures within the eye, all of which can affect vision.

The effects of Aniridia can vary significantly from person to person. Some people exhibit only mild effects of the disorder, while others have profound eye abnormalities:

Iris development

Some people have minimal underdeveloped iris development that is barely noticeable to the inexperienced eye. In contrast, others have a partial absence of the iris, and others completely absent the iris.

Even in people with a “total” absence of the iris, there is usually a very rudimentary remnant of iris tissue that can be seen on careful eye examination under the microscope.

Sensitivity to light

Because the iris helps to block and absorb some of the light that enters the eye, people with Aniridia can be susceptible to light (photophobia) and report symptoms of glare.


Abnormal development of the angle (the area of ​​the eye responsible for draining watery fluid from the eye), blockage of the tip from the rudimentary stump of the iris, or narrowing the angle can lead to Glaucoma.

Corneal problems

People with Aniridia may have a deficiency in limbal stem cells. These are stem cells that arise in the limbus.

The limbus is an area at the edge of the conjunctiva, the thin translucent tissue on the white surface of the eye, and the cornea, the transparent, dome-shaped tissue that forms the front of your eye you can see the colored iris.

These stem cells are responsible for maintaining the health and integrity of the cornea.

As a result of a deficiency in limbal stem cells, the conjunctiva can grow over the cornea, the cornea cannot quickly heal from injuries or scratches, and the cornea may eventually undergo scarring or vascularization (growth of abnormal blood vessels in the usually clear cornea ).

These changes in the cornea can damage vision.

Lens abnormalities

People with Aniridia are also at increased risk for lens abnormalities, including cataracts and lens dislocation.

retinal problems

Individuals with Aniridia often have foveal hypoplasia, which means underdevelopment of the fovea, which is the part of the retina responsible for good visual acuity.

They may also have optic nerve hypoplasia, which transmits visual information from the eye to the brain.

“Hypoplasia” is a term that refers to a deficiency or underdevelopment of body tissue or structure.


Babies with Aniridia may exhibit abnormal, involuntary, rapid movements from side to side or up and down of the eyes called nystagmus.


Aniridia is seen in approximately 1.8 / per 100,000 live births. The incidence ranges from 1:40,000 to 1: 100,000. No significant racial or gender predilection has been described.


Three phenotypes are recognized:

  • Isolated Aniridia without systemic involvement.
  • Wilms syndrome-aniridia-genital abnormalities-Delay syndrome.
  • Gillespie syndrome.

The autosomal dominant (AD) mode of inheritance accounts for two-thirds of cases and has no systemic implications. Penetration is complete, but expressiveness is variable.

The mutation causes it in the PAX6 gene on chromosome 11p13 or the removal of regulatory regions that control its expression.

The sporadic form accounts for approximately one-third of patients. It occurs due to de novo deletions on chromosome 11p13 involving the PAX6 gene.

Larger deletions affecting the adjacent WT1 gene (Wilms tumor) are the underlying cause of Wilms tumor-aniridia-genital abnormalities-retardation syndrome (Wilms tumor, Aniridia, genitourinary abnormalities, and mental retardation).

Twenty-five to thirty percent of patients with sporadic Aniridia develops Wilms tumor.

According to Gronskov et al., patients with sporadic Aniridia had a relative risk of 67 (CI, 8.1-241) of developing Wilms tumor. If there is contiguous gene deletion of PAX6 and WT1, patients have up to a 50% risk of developing this tumor.

Autosomal recessive Aniridia accounts for approximately 2% of all cases. It is associated with cerebellar ataxia and mental retardation (Gillespie syndrome).

Nelson et al. considered the specific iris abnormality characterized by circumpupillary aplasia leading to a fixed dilated pupil to be pathognomonic for Gillespie syndrome.

It can help distinguish it from other forms of Aniridia, and a presumptive diagnosis of Gillespie syndrome can be made during the first few months of life.

Due to its rarity, this syndrome’s inheritance pattern and molecular bases are not yet clear. However, at least one form can be caused by a heterozygous mutation of PAX6.


Different theories have been proposed to explain Aniridia. The anterior segment formation involves a complex interaction of superficial ectoderm, neuroectoderm, and neural crest.

Some researchers consider Aniridia a subtype of coloboma, while others propose mesodermal and ectodermal theories.

In ectodermal theory, Aniridia is caused by a developmental failure of the edge of the optic vesicle between 12 and 14 weeks of gestation.

Supporting this theory is the association of Aniridia with other ectodermal defects: abnormalities in the retina, absence of the fovea, and lack of the iris musculature.

Based on the mesodermal theory is the association of some aniridia with hypoplastic discs. In these cases, Aniridia is due to inappropriate migration or proliferation of mesenchymal elements during the second month of gestation.

However, this theory does not explain the common association between neuroectodermal abnormalities and Aniridia (i.e., foveal hypoplasia).

Beauchamp et al. also described a third theory for iris maldevelopment, where Aniridia is partly explained by excessive remodeling and cell death.


Although iris hypoplasia is the most characteristic histopathologic feature and can be pretty severe, small patches of iris tissue can always be found.

The anterior border layer of the iris stump is usually moderately cellular and consists of tightly packed melanocytes that create a flat iris surface with few crypts.

The vasculature of the iris is occasionally prominent, and relatively large vessels can be seen, leading to the standard avascular anterior border layer. The ciliary body is also hypoplastic but to a lesser degree.

The anterior chamber angle may be expected, or there may be congenital angle abnormalities. Congenital angle anomalies have been divided into two categories:

Incomplete and anomalous excision. In incomplete cleavage, the annular recess is filled with loose mesenchymal tissue, whose regular position is relative to the ciliary body and the scleral spur.

In a series of gonioscopic examinations in aniridic patients with and without Glaucoma, Grant and Walton found that initially, the stroma of the iris extends into the trabecular meshwork.

They form synechiae-like junctions, followed by a more homogeneous lamina, resulting in eventual angular closure.

Less frequently, they found that the angle remained open until adolescence and then closed by anterior rotation of the entire iris veil.

In advanced Glaucoma, corneal findings include thick fibrovascular pann, calcified and noncalcified degenerations of Bowman’s layer, and deep stromal vascularization.

Cataract formation is present in most aniridic eyes. Nuclear, cortical, posterior subcapsular, and anterior subcapsular cataracts can occur with varying severity.

Molecular and genetic bases of Aniridia

Heterozygous mutations cause isolated Aniridia in paired picture gene 6 (PAX6; 607108) on chromosome 11p13 or by deletion of a regulatory region that controls its expression.

The Pax genes are a family of developmental genes that encode nuclear transcription factors. PAX6 was cloned in 1991, and to date, no other genetic loci have been implicated in Aniridia.

Most PAX6 mutations cause haploinsufficiency probably due to a nonsense-mediated breakdown mechanism.

Structure and function of the PAX6 gene

PAX6 is a highly conserved gene in evolution, encoding a transcriptional regulatory protein. This protein plays a vital role in developing the eye, the neural tube, the olfactory bud, and the pancreatic tissue.

It is expressed early in the normal morphogenesis of the eye. Regulates cell proliferation, differentiation, migration, and adhesion.

Its targets include PAX6 and genes encoding other developmental regulators, cell adhesion molecules, and structural proteins, such as lens crystals and corneal keratins.

The expression of the PAX6 protein continues in the retina, lens, and cornea of ​​the adult. The PAX6 gene spans 22 kb of genomic DNA, contains 14 exons, and encodes 422 amino acids.

The PAX6 gene contains 2 DNA-binding domains, the paired domain, and the paired-type homeodomain, both with DNA-binding capacity, separated by a lysine-rich linker region.

A C-terminal domain of proline, serine, and threonine (PEST) acts as a transcriptional activator.

Five non-pathogenic normal allelic variants of the PAX6 gene are known.

pathological allelic variants

Three hundred PAX6 mutations have been identified; 286 are associated with congenital ocular malformations.

257 of them cause Aniridia, and reminder 29 cause-related ocular phenotypes, such as Peters’ anomaly, foveal hypoplasia, and optic nerve anomalies:

  1. The Aniridia phenotype can be the result of:
  • Nonsense mutations (39%).
  • Splicing mutations (13%).
  • Frame removals and insertions (25%).
  • Inframe insertions and deletions (6%).
  • Nonsense mutations (12%).
  • Run-on mutations (5%).
  • Most lead to loss of protein function.
  1. In non-aniridic eye disorders, 69% are nonsense mutations.

In the aniridic phenotype, 94% of all intragenic point mutations lead to the introduction of a premature stop codon (PTC), or C-terminal extensions (CTE), or amino acid substitutions (missense mutations). ).

Premature stop codon (null) mutations include missense mutations, frameshift insertions and deletions, and most splice mutations.

Missense mutations produce a protein of reduced function, resulting in variant ocular phenotypes or (if the part of the protein is significantly reduced) in Aniridia.

Mutants of heterozygous mutations of PAX6

Glaser and Solomon et al. described three cases of children inheriting two different PAX6 mutations, one from each affected parent.

Two of these babies died shortly after birth with anophthalmia and brain abnormalities. The third child survived with severe microphthalmia and microcephaly.

Chromosomal rearrangements in isolated Aniridia and Wilms tumor-aniridia-genital anomalies-delay syndrome

Chromosomal deletions affecting all or part of the PAX6 region or translocations and inversions that alter the transcription unit or control elements can also cause isolated Aniridia, typically classical Aniridia.

A small proportion of sporadic aniridia cases are caused by the contiguous elimination of PAX6 and nearby WT1. Deletion provides the first of the two ‘hits’ required to inactivate both WT1 alleles.

The absence of a WT1 allele in the germline carries a high risk (~ 45%) of Wilms tumor.

Other genes and phenotypes similar to Aniridia

The FOXC1 and PITX2 mutations cause Axenfeld-Rieger syndrome (MIM 602482 and 180500). PITX3 mutations most often cause anterior segment dysgenesis and cataracts.

Clinical description

Aniridia is a rare, sight-threatening disorder that affects the cornea, iris, intraocular pressure, lens, fovea, and optic nerve.

Other features include corneal changes, Glaucoma, cataracts, lens subluxation, strabismus, optic nerve coloboma, and hypoplasia. Progressive complications that threaten vision include cataracts, Glaucoma, and corneal opacification.

The phenotype can vary between and within families; however, affected individuals generally show little interocular difference.

Most cases are diagnosed at birth with an obvious iris / pupillary abnormality or in infancy with nystagmus (usually apparent at six weeks of age). Photophobia can also be present.

Slit-lamp examination commonly reveals small anterior polar cataracts, sometimes with attached continuous strands of the pupillary membrane.

Despite their many eye problems, most individuals with Aniridia retain functional vision with proper ophthalmologic management.


Aniridia is a misnomer, as a small portion of the iris tissue is almost always found on gonioscopic or ultrasound biomicroscopy. Variations range from practically total absence to only mild hypoplasia of the iris.

In less severe cases, around normal-appearing pupils may be found. Pupil size may be standard, but there may be a loss of iris surface architecture or the presence of iris transillumination.

Other changes to the iris include partial iris defects (coloboma-like) or eccentric/misshapen pupils and ectropion of the iris.


Congenital lens opacities (especially polar ones) are common. Occasionally there is persistent vascularization of the anterior lens capsule (túnica vasculosa lentils) or remnants of the pupillary membrane.

Lens opacities are rarely dense enough to require lens removal in infancy, but visually significant lens opacities eventually develop in 50% -85% of patients, usually within the first two decades. Of the life.

Lens subluxation or dislocation occurs but is rare. Scheider et al. and Houston et al. found that the anterior capsule of aniridic cataracts is very fragile. Typically, the lens subluxated superiorly.

Intraocular pressure

Ocular hypertension and Glaucoma are common. The exact prevalence is unknown. Congenital Glaucoma with or without buphthalmos is rare in babies with Aniridia; it usually develops in childhood or later adulthood.

In the first, the reported incidence is 6% to 75%, according to Nelson et al. Glaucoma develops due to angle abnormalities that obstruct the outflow of aqueous humor through Schlemm’s canal.

Margo et al. studied the histopathology of seven enucleated eyes of children with Aniridia and Glaucoma. They reported abnormal development of the angle.

Grant and Walton analyzed a series of gonioscopic examinations in aniridic patients with Glaucoma versus aniridic patients without Glaucoma and found that:

Initially, the stroma of the iris extends forward into the trabecular meshwork forming synechiae-like junctions, followed by a more homogeneous lamina, eventually resulting in angle closure.

Less frequently, they found that the angle remained open until adolescence and then closed by anterior rotation of the entire iris veil.


Aniridia-associated keratopathy (AAK) is a late and progressive manifestation. It is a significant threat to vision and is believed to have an incidence of 20%.

Aniridia-associated keratopathy is caused primarily by limbal stem cell deficiency and a combination of other factors such as abnormal differentiated epithelium, abnormal cell adhesion, impaired healing response, and conjunctival cell infiltration.

The trigger for corneal deterioration may be surgical intervention with excessive manipulation of the limbus or after applying topical antimetabolites to treat Glaucoma associated with Aniridia.

Inadequate tear production is expected, exacerbating ocular surface disease.

The first signs of Aniridia-associated keratopathy appear in the first decade of life, with thickening and vascularization of the peripheral cornea, gradually advancing towards the central cornea, ending in pancorneal vascularization, opacification, and keratinization.

The central corneal thickness often increases.

Aniridia-associated keratopathy can be caused by a deficiency in matrix metalloproteinase 9 (MMP-9), which PAX6 also regulates.

In animal models of the PAX6 mutation, MMP-9 deficiency results in fibrin accumulation and infiltration of inflammatory cells.

There is also a significant increase in stromal cell apoptosis, which alters the orderly arrangement of the cornea’s collagen fibers, resulting in a subsequent loss of transparency.

Optic nerve

Optic nerve hypoplasia occurs in approximately 10% of cases; Colobomas of the optic nerve are also seen occasionally.


Foveal hypoplasia is usually present. This can occur independently or as part of the binocular involvement.

Patients present with a reduced foveal reflex, macular hypopigmentation, and crossing the usual foveal vascular zone by the retinal vessels. Pendulum horizontal nystagmus is usually present by six weeks of age.

The electroretinography (ERG) test reveals retinal dysfunction ranging from abnormally abnormal to nearly normal. Rods and cones are equally affected. The etiology of this retinal dysfunction remains unclear.

It may be due to aplasia of foveal hypoplasia, secondary to a PAX6 mutation, or phototoxicity resulting from maldevelopment of the iris.

Refractive error, strabismus

Both are common in aniridic patients. According to Nelson et al., Esotropia is the most frequent deviation found. High refractive errors are not uncommon.


Up to 10% of patients may have bilateral ptosis, usually symmetric.

Diagnosis of aniridia

Differential diagnosis

Differential diagnosis includes:

Anterior segment developmental abnormalities: Rieger and Peters abnormalities, iris coloboma, and albinism (oculocutaneous and ocular).

Other causes of childhood nystagmus and reduced vision without iris abnormalities: are retinal dystrophy, congenital cataract, optic nerve hypoplasia, and congenital infection.

Causes of absence or hypoplasia of the iris in adults: traumatic Aniridia, previous eye surgery, and iridocorneal/endothelial syndromes.

Rieger’s anomaly is characterized by iris stromal hypoplasia, uveal ectropion, corectopia, full-thickness iris defects, and childhood-onset Glaucoma in approximately 50% of cases.

It can be distinguished from Aniridia by the presence of a posterior embryotoxic with attached iris strands, relatively good visual acuity, and the absence of nystagmus or foveal abnormality.

Peters’ anomaly presents with central corneal opacity of variable degree and an underlying defect involving the posterior stroma, Descemet’s membrane, and endothelium with or without iridocorneal or lenticular-corneal adhesions.

Peter’s anomaly may be associated with other ocular abnormalities, such as chorioretinal colobomas, iris coloboma, Aniridia, persistent fetal vasculature, microphthalmia, and optic nerve hypoplasia.

Iris coloboma is a developmental defect that produces a focal absence of the iris and a keyhole-shaped pupil; the remaining iris is normal.

Contrary to Aniridia, most isolated iris colobomas are not associated with reduced visual acuity or nystagmus.

Oculocutaneous albinism (OCA) and ocular albinism are usually present in early childhood with:

  • Nystagmus, diffuse (but structurally complete) iris transillumination, hypopigmented fundus, and, in the case of oculocutaneous albinism, cutaneous and capillary hypopigmentation, which distinguish these disorders from Aniridia.

Other causes of nystagmus and poor vision in childhood (e.g., retinal dystrophy, congenital cataracts, optic nerve hypoplasia) lack the iris changes seen in Aniridia.

Traumatic Aniridia, previous eye surgery, and iridocorneal and endothelial syndromes are the causes of partial or complete absence of the iris in adults.

Medical history, age of onset, history of trauma or surgery, and the lack of other ocular features of aniridia aid in a correct diagnosis.

Clinical diagnosis

Aniridia is diagnosed by clinical examination:

Slit-lamp examination is essential to detect abnormalities in the iris and papilla; Corneal opacification and vascularization, cataracts, and Glaucoma can also be seen.

Slit-lamp fundoscopy and indirect ophthalmoscope may show foveal hypoplasia and associated optic disc malformation.

Optical coherence tomography (OCT) can document foveal hypoplasia in atypical cases, although it can be challenging to perform in the presence of nystagmus and young children.

High-frequency ultrasound biomicroscopy (UBM) is helpful in children with corneal opacity or severe corneal edema, as it can demonstrate complete or partial hypoplasia of the iris.

Genetic diagnosis

When evaluating a baby with Aniridia, considering a family history is essential. Still, an ophthalmic examination should be performed for parental PAX6 spectrum abnormalities even in the absence of apparent family history.

If there is an affected parent, the child is unlikely to have a deletion that extends to WT1, although rare cases have been reported.

How is Aniridia treated?

Since Aniridia can affect the eyes in many ways, aniridia treatment is similarly multifaceted:

  • Opaque or tinted contact lenses can give the appearance of an iris for appearance enhancement or cosmetic purposes, as well as to improve vision and minimize glare/photophobia.
  • Absorbent sunglasses can also help with symptoms of photophobia and glare.
  • Some people may also be candidates for the surgical placement of an artificial iris, although this procedure may be associated with complications. Lubrication with artificial tears can help maintain the health of the cornea.
  • The primary corneal disease may require more aggressive surgery, including transplants and stem cell transplantation to replace some of the missing stem cells.
  • People who have cataracts may require surgery to remove their cataracts. People with Aniridia should be closely monitored for Glaucoma, and those who develop it should be treated accordingly with medications, lasers, and surgery.
  • A comprehensive low vision exam, along with optical, non-optical, and electronic standard vision devices and vision rehabilitation services and training, may be helpful for some people with Aniridia.


Patients should have regular eye exams. Correction of refractive errors and treatment of amblyopia is simple and essential measures.

Optical aids for low vision should be provided for people with significant visual impairment and schooling and social support assistance.

Tinted or photochromic lenses can be used to reduce the sensitivity to light associated with the sizeable papillary opening.

Intraocular pressure and Glaucoma

All patients with Aniridia should undergo annual glaucoma screening throughout their lives with measurement of intraocular pressure, examination of the angle for evidence of closure, the optic disc, and visual field tests when possible.

Measurement of central corneal thickness is also essential, as aniridic patients have corneas up to 100 μm thicker than average, which influences intraocular pressure readings.

Treatment of Glaucoma associated with Aniridia is complex and, if present in childhood, it is even more challenging to treat. Medical treatment is usually the initial approach, although it is generally insufficient.

Trabeculectomy with or without antimetabolites is the operation of choice, and success rates range from 0% to 83%. Drainage tube surgery (with or without antimetabolites) or cyclodiode laser treatment may be necessary in refractory cases.

The latter is very effective in reducing intraocular pressure.

However, it is associated with significant complications, including retinal consumption and detachment in 50% of patients, progressive cataracts, and vision loss, rendering it unsuitable for use as first-line therapy.

The success rate for filtration surgery ranges from 66% to 100%. Prophylactic goniotomy is quite effective in preventing Glaucoma in patients with early signs of angle changes.

Success rates range from 89% to 100%. In contrast, therapeutic goniotomy has shown inferior results, with success rates of 0% to 20%.


Treatment of mild aniridic keratopathy includes preservative-free lubricants.

In moderate aniridic keratopathy, serum drops and amniotic membranes may be temporarily helpful in enhancing the survival and expansion of surviving limbal stem cells.

In severe cases, a limbal cell transplant is recommended.

Penetrating keratoplasty (PK) may be considered; however, penetrating keratoplasty alone has a poor prognosis, probably due to primary limbal stem-cell failure.

Homologous laminariolimbokeratoplasty appears to be very effective: its success rate increases with systemic immunosuppressants.


Cataract extraction is indicated in those patients with severe lens opacities. Mild to moderate lens opacity may not require surgery, as it should be remembered that visual improvement after surgery in Aniridia is limited by foveal hypoplasia.

Children rarely require lens surgery. Cataract surgery in aniridic patients has an increased risk of intraoperative complications due to poor zonular stability.

It also influences the type of intraocular lens implanted.

Aniridic black diaphragm intraocular lenses are used to reduce glare or sensitivity to light and are associated with improved visual acuity but may be associated with a slightly higher rate of surgical complications.

Aniridic fibrosis syndrome

Patients with Aniridia and multiple ocular procedures should be monitored for this syndrome, and surgical intervention is recommended at the first sign.

Tumor de Wilms

Children with Wilms tumor-aniridia-genital abnormalities-delayed deletions require renal ultrasound examinations every three months and a follow-up by a pediatric oncologist until the age of 8.


A detailed audiological examination is recommended as children with Aniridia may have an abnormal hearing.

Living with Aniridia

Daily life with Aniridia requires constant adaptation to the environment.

Some of the challenges are common for people with visual impairments: studying, working, using low vision aids, moving, traveling, and playing sports.

Even the most common activities can be challenging for a visually impaired child or adult in a world where most knowledge and information is conveyed through visual data.

The exact causes and consequences of low vision are, in general, not fully understood; people with Aniridia can share this difficulty with all visually impaired people.

Other problems, however, are specific to Aniridia. Nystagmus, if present, makes it difficult to maintain eye contact and can lead others to think that patients with Aniridia are not paying attention.

For children in school, this can lead their teachers to think that the child is distracted or disinterested, resulting in an incorrect assessment of the student’s attention.

People with Aniridia often have difficulty adjusting to rapidly changing light conditions.

They can be sensitive to intense light and reflections from windows, mirrors, and wet, metallic, or white surfaces and often adapt their home, work, and school environments accordingly.

Glare caused by reflections can decrease your ability to see details or cause visual discomfort, dry sneezing, and headaches.

Moving inside out, turning lights on and off, moving on foggy or cloudy days, and crossing in front of car headlights produce painful glare that reduces visual acuity and causes uncertainty in movement.

People with Aniridia often wear sunglasses with high protection lenses outdoors, which may also be needed on cloudy days or indoors.

Some people with Aniridia can wear contact lenses with an artificial iris and a fixed pupil that blocks light.

The use of contact lenses includes advantages such as correction of hyperopia or myopia, greater comfort, and greater discretion, but it requires constant monitoring of the state of the cornea.

On the other hand, some keratopathies can take advantage of therapeutic contact lenses.