In order to investigate the known associations between hyperlipidaemia and various rheumatic complaints, immune arthritis and hyperlipidaemia have been induced concurrently in rabbits. The results obtained show that: (1) Rabbit apolipoprotein B-containing lipoproteins (LpB), which are normally virtually excluded from joint fluid, gain access to the inflamed joint in the serous effusion and serve as intrinsic indicators of altered local permeability to macromolecules. (2) Much of the LpB entering the joint space is taken up by the phagocytic cells and, following intracellular hydrolysis, leaves a lipid residue. In some chronically affected joints these residues are modified so as to give rise to crystalline cholesterol and its esters. Such crystals may serve as a chronic irritant in the joint. (3) In addition intact LpB is found sequestered in the superficial layers of intra-articular collagenous structures of the challenged joint in a distribution identical with that of similarly sequestered immune complexes and complement, suggesting altered permeability of these intra-articular structures also.
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