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Related Experiment Videos

Corneal opacity in LCAT disease.

D G Cogan1, H S Kruth, M B Datilis

  • 1Cornea and Cataract Section, National Eye Institute, Bethesda, Maryland 20892.

Cornea
|November 1, 1992
PubMed
Summary

Lecithin:cholesterol acyltransferase (LCAT) deficiency causes corneal opacification due to lipid deposits. This study provides the first histopathologic evidence of unesterified cholesterol in the corneal stroma of LCAT disease patients.

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Area of Science:

  • Ophthalmology
  • Biochemistry
  • Genetics

Background:

  • Lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare dyslipoproteinemia.
  • It is characterized by abnormal lipid metabolism and characteristic corneal opacities.
  • Previous studies have described corneal changes, but detailed histopathology is limited.

Observation:

  • A full-thickness corneal specimen from a patient with LCAT deficiency was analyzed.
  • Clinical examination revealed progressive corneal opacification and peripheral arcus extending to the sclera.
  • Microscopic examination showed vacuoles in the corneal stroma containing extracellular, membranous deposits.

Findings:

  • Light microscopy identified prevalent vacuoles in the anterior corneal stroma.
  • Electron microscopy revealed extracellular, membranous deposits within these vacuoles.

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  • This study presents the first histopathologic evidence of unesterified cholesterol in the corneal stroma of LCAT deficiency.

    • Implications:

    • These findings enhance the understanding of corneal pathology in LCAT deficiency.
    • Provides crucial histopathologic details of lipid deposition in the cornea.
    • May guide future diagnostic and therapeutic strategies for LCAT deficiency-related eye conditions.