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Bile salts have been shown to act on lipoprotein-X (LP-X) in vitro to induce a false-negative electrophoretic test. The aim of the present study was to investigate the relationship

The in vitro effect of post-heparin and post-heparin plus post-protamine normal serum on serum lipoprotein X (LP-X) is described. Serum LP-X is cleared after incubation with post-heparin normal serum, and serum LP-X remain unmodified when it is incubated with post-heparin plus post-protamine normal serum. The action of phospholipase A from snake venom on serum LP-X is also studied. A very small quantity of phospholipase is necessary to degrade LP-X and to transform lecithin into lysolecithin. It is concluded that phospholipase seems to be the enzyme that most likely induces the LP-X chnges after heparin administration.

Serum lipoprotein-X was investigated in 12 patients with cholestasis in basal conditions and 20 minutes after intravenous heparin. In all cases, lipoprotein-X was positive in the first sample and became negative after heparin. A decrease in triglycerides was observed in all patients after heparin with an increase in free fatty acids and mobilization of prebetalipoproteins, and a transformation of lecithin into lysoleithin in 4 cases after heparin. These facts suggest that heparin plays an important role in the mobilization of serum lipoprotein-X.

The effect of phospholipase A from snake venom and deoxycholic acid on lipoprotein-X (LP-X) recovered from the cathode side of a previous agar gel electrophoresis is described. Adding phospholipase A and deoxycholic acid to the removed cathodal fraction is followed by a marked migration to the anode side on a second electrophoresis procedure. This seems to confirm that phospholipase A and bile salts on LP-X particles modifying their agar gel electrophoretic migration characteristics.

The effect of heparin on the proportion of cholesterol esters, lecithin/ lysolecithin ratio, and lecithin:cholesterol acyltransferase (LCAT) activity was studied in twelve patients with cholestasis. A good correlation was observed between a decreased LCAT activity and the proportion of cholesterol esters, and no consistent variation was noted after heparin. The lecithin/lysolecithin ratio was increased in 7 patients and became normal after heparin in 6 cases. The clearance of lipoprotein-X after heparin seems to be not related to LCAT activity. These results demonstrate that heparin does not modify the LCAT activity, and suggest that heparin induces an increase of phospholipase activity in some patients with cholestasis.

A case of λ -type IgG myeloma with serum hyperviscosity, a strong positive Sia test, and few clinical manifestations is described. As the M-component concentration is not excess