Lipoprotein X in Cholestasis and Questionable Atherogenic Risk

Lipoprotein X is still an enigma for its lack of evidence as a risk association with atherosclerosis. Primary biliary cirrhosis is a chronic, autoimmune cholestatic liver disease characterized by the presence of T cells that destroy the biliary epithelium. In patients with primary biliary cirrhosis, total cholesterol levels may reach values between 500 and 1000 mg/dL, with cutaneous xanthomas similar to those observed in genetic hypercholesterolemias. The rise in cholesterol is largely due to increased serum levels of lipoprotein-X. It has a small amount of albumin, apoprotein AI, apoprotein Cs and apoprotein E and has no apoprotein B. The formation of lipoprotein-X results from regurgitation of bile lipids in plasma, as well as the accumulation of plasma phospholipids and free cholesterol, resulting from the lower activity of lecithin: acyltransferase cholesterol. Multicenter randomized trials are needed to assess the impact of lipid-lowering patients on lipid reduction and cardiovascular risk, as well as the effect on hepatic cholestasis. Treatment with statins is not indicated for lowering cholesterol in patients with primary biliary cirrhosis and dyslipidemia, as there is no evidence that these patients have high cardiovascular risk.

Keywords: Atherosclerosis; Cholesterol; Lecithin cholesterol acyl transferase; Lipoprotein X; Primary Biliary cirrhosis

Abbreviations: LCAT: Lecithin Cholesterol Acyl Transferase; LDL: Low Density Lipoprotein; LDL-c: Low Density Lipoprotein Cholesterol; LP-X: Lipoprotein X; PBC: Primary Biliary Cirrhosis