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What Is Lattice Corneal Dystrophy?

Lattice corneal dystrophy is a hereditary disorder in which abnormal amyloid material deposits in the corneal stroma, creating branching, lattice like lines. These deposits scatter light and weaken the corneal structure over time. The condition usually starts in early to mid adulthood and slowly progresses. Patients develop recurrent erosions, increasing glare, and gradual blurring of vision. In advanced cases, dense central opacity may require corneal transplantation.

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What Is Lattice Corneal Dystrophy?

Lattice corneal dystrophy is a hereditary disorder in which abnormal amyloid material deposits in the corneal stroma, creating branching, lattice like lines. These deposits scatter light and weaken the corneal structure over time. The condition usually starts in early to mid adulthood and slowly progresses. Patients develop recurrent erosions, increasing glare, and gradual blurring of vision. In advanced cases, dense central opacity may require corneal transplantation.

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Causes and Genetics of Lattice Corneal Dystrophy

Most classic forms of lattice dystrophy are inherited in an autosomal dominant pattern, often linked to mutations in the TGFBI gene. Different mutations produce variants that differ in age of onset, severity, and associated systemic disease. Abnormal protein accumulation in the stroma forms refractile, branching deposits. Family history is frequently positive, though new mutations can occur. Genetic counseling and testing are considered in affected families.

Symptoms and Clinical Features

Early symptoms include recurrent painful erosions from a fragile epithelium, often upon waking. Over time, patients notice glare, halos, and blurred vision, particularly in bright or nighttime conditions. On slit lamp exam, thin, branching refractile lines are seen in the anterior and mid stroma, radiating from the central cornea. As deposits thicken, the cornea becomes more opaque and irregular. Secondary stromal haze and scarring contribute to visual decline.

How Is Lattice Corneal Dystrophy Diagnosed?

Diagnosis is based on characteristic slit lamp findings plus family history. The eye doctor documents the pattern, depth, and density of stromal lines. Corneal topography helps assess irregular astigmatism, and optical coherence tomography can show the depth of deposits. In uncertain cases, genetic testing for TGFBI mutations or corneal biopsy with histology and Congo red staining supports the diagnosis. Other dystrophies and degenerations that mimic lattice patterns are considered.

How Is Lattice Corneal Dystrophy Managed?

Early management centers on treating recurrent erosions with lubricants, hypertonic saline, bandage contact lenses, and sometimes epithelial debridement or anterior stromal puncture. For progressive haze and visual decline, phototherapeutic keratectomy or lamellar or penetrating keratoplasty is considered. Patients are counseled about recurrence of dystrophic deposits in grafts over time. Regular monitoring tracks changes in vision, corneal clarity, and refractive error.

FAQs About Lattice Corneal Dystrophy

Is lattice corneal dystrophy always inherited?

Most cases follow autosomal dominant inheritance, so close relatives have an increased risk. Rare sporadic cases occur from new mutations. Family members with symptoms are often encouraged to have eye exams.

Can glasses or contact lenses correct vision in lattice dystrophy?

In early stages, spectacles or soft lenses can improve vision by correcting refractive error. As irregular astigmatism and opacity progress, rigid gas permeable or scleral lenses might be needed. Very advanced disease often needs surgery.

Do deposits come back after corneal transplantation?

Yes, dystrophic material can re accumulate in grafts over time because the underlying genetic defect persists. Even so, transplantation can provide many years of better clarity and comfort.

When do symptoms usually start in lattice corneal dystrophy?

Many patients begin to notice erosions or visual disturbance in the second to fourth decade of life, though exact timing depends on the specific genetic variant and family pattern.