Corneal lipid dystrophy

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Corneal lipid dystrophy in a Cairn Terrier[1]

Corneal lipid dystrophy (corneal dystrophy) is a genetic canine corneal disease characterized by lipid and calcium accumulation within the cornea[2].

This condition may develop consequent to metabolic dysfunction of lipid processing by keratocytes[3], hyperlipidemia or pre-existing corneal pathology[4]. In most cases, lipid keratopathy directly complicates corneal neovascularisation following trauma or keratitis and are associated commonly with a systemic disorder of lipid metabolism. These conditions are classified as secondary lipid keratopathies[5].

Three types of corneal lipid deposition have been linked with hyperlipoproteinaemia. In corneal arcus, this condition is associated with initial extracellular lipid deposition followed by the appearance of intracellular lipid and vascularisation, so that established corneal arcus tends to become more typical of lipid keratopathy. In dogs, corneal arcus is always associated with hyperlipoproteinaemia. Corneal vascularisation is a ubiquitous feature of lipid keratopathy and both necrotic fibroblasts and foam cells are common in progressive lesions[6].

Hyperlipoproteinaemia, especially hypercholesterolaemia is the commonest systemic abnormality.

In crystalline stromal dystrophy (Schnyder's crystalline stromal dystrophy) of the cornea there is no inflammatory element and no vascularisation. The dystrophy is associated with accumulation of lipid within the corneal fibroblasts, but typical foam cells are absent, the crystalline opacity involves the coolest part of the cornea, correlates with local fibroblast death, and is always bilateral. Hyperlipoproteinaemia, may be present, but this is not universally so[7].

Clinical symptoms are primarily corneal clouding, which can be confirmed on slit lamp biomicroscopy. Clinically, the opacities progress in severity from the nebular type through the more dense race-track type to the white-arc type with subepithelial crystalline deposits[8].

Lipid histochemistry indicated the presence of cholesterol, cholesterol ester, and phospholipid in the superficial stroma. The epithelium, basal lamina, Descemet's membrane, and endothelium were unaffected, apart from an irregularity of the basal lamina in some cases[9].

In dogs with confirmed hyperlipidemia, dietary manipulation may help reduce the speed of lesion progression.

Superficial keratectomy to remove lipid deposits in severe cases.


  2. Barsotti G et al (2008) Corneal crystalline stromal dystrophy and lipidic metabolism in the dog. Vet Res Commun 32(1):S227-S229
  3. Ekins MB et al (1983) Oval lipid corneal opacities in beagles: VI. Quantitation of excess stromal cholesterol and phospholipid. Exp Eye Res 36(2):279-286
  4. West C (1980) Corneal disease. In: Peyman GA, Sanders DR, Goldberg MF, eds. Principles and practice of ophthalmology. Philadelphia: Saunders. pp410-412
  5. Friedlaender MH et al (1977) Bilateral central lipid infiltrates of the cornea. Am J Ophthalmol 84:781-787
  6. Crispin S (2002) Ocular lipid deposition and hyperlipoproteinaemia. Prog Retin Eye Res 21(2):169-224
  7. Crispin SM et al (1988) Crystalline corneal dystrophy in the dog. Histochemical and ultrastructural study. Cornea 7(2):149-161
  8. Spangler WL et al (1982) Oval lipid corneal opacities in beagles. Vet Pathol 19(2):150-159
  9. Morrin LA et al (1982) Oval lipid corneal opacities in beagles: ultrastructure of normal beagle cornea. Am J Vet Res 43(3):443-453