The cause of the rise in cholesterol levels in pleural exudates is unknown. Two possible explanations have )een put forward. According to the first, the cholesterol is synthesized by pleural cells themselves for their own needs (extrahepatic synthesis of cholesterol is now known to be much greater than was once thought, depends on the metabolic needs of cells, and is in dynamic equilibrium with cholesterol supply by LDL and cholesterol removal by HDL) and the concentration of cholesterol in the pleural cavity is increased by the degeneration of leukocytes and erythrocytes, which contain large quantities. The second possible explanation is that pleural cholesterol derives from plasma; some 70 percent of plasma cholesterol is bound to low density, high molecular weight lipoproteins (LDL) and the rest to HDL or very-low-density lipoproteins (VLDL), and the increased permeability of pleural capillaries in pleural exudate patients would allow plasma cholesterol to enter the pleural cavity.
We found no correlation between cholesterol concentration and the number of leukocytes/cu nun in pleural fluid, suggesting that the two are unrelated. Pleural cholesterol and plasma cholesterol were uncorrelated in the transudate group, but they were correlated in the three exudate groups, suggesting that in the latter cases the increase in pleural cholesterol is related to a rise in capillary permeability allowing the pleural cavity to be entered by high molecular weight substances that would otherwise by excluded, rhis hypothesis appears to be supported by the correlation between the pleural and plasma LDL/ CHOL ratios found in the three exudate groups but not in the transudate group: if cholesterol were released by degenerate pleural cells, the major contribution to PCHOL would be by free or esterified cholesterol, making the pleural LDL/CHOL ratio miall and probably uncorrelated with the plasma LDL/CHOL ratio. It would nevertheless be desirable to letermine whether PCHOL is correlated with any dnd of pleural cell.