The corneal changes in the hyper- and hypoproteinaemias may affect vision and/or provide a diagnostic clue to a systemic disorder. This article describes the structure and function of the major
lipoprotein classes and the means by which dietary
lipid is absorbed and by which exogenous and endogenous
lipid is distributed to and cleared from the tissues. In hyper-beta-lipoproteinaemia,
lipid arcus formation may be related to the duration and height of the raised
cholesterol levels. The peripheral location of the
lipid deposit is presumed to be related to peripheral trapping of
low-density lipoprotein (
LDL) by
glycosaminoglycan binding and tight stromal packing with maintained central clearing by
high-density lipoprotein (HDL), whose smaller molecular diameter should allow freer stromal diffusion. In the hypolipoproteinaemias, e.g.,
Tangier disease, generalised (alpha and
beta) lecithin cholesterol acyltransferase (
LCAT) deficiency, and
alpha-LCAT deficiency (
fish-eye disease), the absence or abnormality of HDL may impair clearance of endogenous and possibly exogenous stromal
lipid. The hyperlipoproteinaemia that sometimes accompanies Schnyder's crystalline
corneal dystrophy is thought to modify the effects of a primary failure of corneal stromal lipid metabolism.