title: Pathophysiology of elevated ascites fluid cholesterol in malignant ascites. Increased ascites to serum relation of proteins and lipoproteins in patients with peritoneal carcinomatosis as compared to patients with cirrhosis of the liver.
abstract: The existence of marked elevations of ascitic fluid cholesterol has been observed in patients with peritoneal carcinomatosis compared to patients with cirrhosis and has been found useful in differential diagnosis. This finding could be caused by an enhanced movement of plasma lipoproteins into the peritoneal cavity. To test this hypothesis we determined the fasting concentrations of total, high density lipoprotein (HDL)- and low density lipoprotein (LDL)-cholesterol, apolipoprotein-A1 (apo-A1) and apolipoprotein-B (apo-B) in serum and ascites of 17 patients with cirrhosis and 16 patients with peritoneal carcinomatosis. The movement of proteins from plasma to ascites was calculated from the ascites/serum concentration ratios of six different sized proteins with a molecular mass ranging from 54 kDa to 971 kDa. Mean values (mg/dl) for total cholesterol (92.6 vs. 21.0), HDL-cholesterol (15.6 vs. 1.8), LDL-cholesterol (63.4 vs. 16.1), apo-A1 (50.2 vs. 13.6) and apo-B (41.2 vs. 12.9) in ascites were significantly higher in peritoneal carcinomatosis than in cirrhosis. These differences could only partially be explained by the higher serum concentrations of these parameters in peritoneal carcinomatosis, but were mainly due to a lower selectivity for the movement of plasma proteins and lipoproteins into ascites (mean ascites/serum (A/S) ratio: 0.30-0.77) in peritoneal carcinomatosis as compared to cirrhosis (mean ascites/serum ratio: 0.11-0.21). In both groups about 85% of the total cholesterol in serum and ascites consisted of HDL- and LDL-cholesterol. These findings support the hypothesis that elevations in ascitic cholesterol in peritoneal carcinomatosis compared to cirrhosis are mainly caused by the increased movement of plasma HDL and LDL into the peritoneal cavity.
authors.affiliation: Department of Medicine II, Ludwig-Maximilians-University of Munich, Federal Republic of Germany.
authors.forename: D
authors.initials: D
authors.lastname: Jüngst
authors.forename: Y
authors.initials: Y
authors.lastname: Xie
authors.forename: A L
authors.initials: AL
authors.lastname: Gerbes
mesh_terms: D016632:Apolipoprotein A-I / Q000378:metabolism; D001055:Apolipoproteins B / Q000097:blood / Q000378:metabolism; D001201:Ascites / Q000378:metabolism / Q000503:physiopathology*; D001798:Blood Proteins / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D008076:Cholesterol, HDL / Q000097:blood / Q000378:metabolism; D008078:Cholesterol, LDL / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000503:physiopathology*; D011506:Proteins / Q000378:metabolism
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001798:Blood Proteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007136:Immunoglobulins; D008074:Lipoproteins; D011506:Proteins; D002784:Cholesterol