Elevation of CA 125 and CA 19-9 in patients with end-stage liver disease.

BACKGROUND: The serum tumor markers CA 19-9 and CA 125 are the serologic markers used for the monitoring of biliopancreatic and ovarian cancer, respectively. They are reported to be elevated in a variety of nonneoplastic clinical situations, including end-stage liver disease (ESLD). However, their prevalence and degree of elevation in patients with ESLD remained unclear. AIM: To examine the prevalence and degree of elevation of CA 19-9 and CA 125 in patients with ESLD and to determine their association with severity of liver disease. METHODS: Retrospective analysis of 161 patients with ESLD that were evaluated for liver transplantation at our institution between March 2009 and December 2010. The mean age was 55.15 ± 8.75 years and 107 (66.4%) of the patients were men. Serum CA 19-9 and CA 125 levels were determined during evaluation of their candidacy for liver transplantation. RESULTS: Eighty-three (51.5%) patients had elevated CA 125 and 44 (53%) of them had a serum concentration >5 times the upper limit of normal (ULN). Elevated CA 125 was associated with alcoholic liver disease, high Model for End-Stage Liver Disease (MELD) score, and presence of ascites. Similarly, 37 (23%) patients had elevated CA 19-9 and 8 (21.6%) of them had a serum concentration >5 times ULN. Elevation of CA 19-9 was associated with high MELD score. CONCLUSIONS: CA 125 and CA 19-9 concentrations were elevated in 51.5% and 23% of patients with ESLD, respectively. Although the definite etiology remained unclear, their elevation was associated with the pathological conditions associated with advanced liver disease. Further studies are needed to clarify the underlying mechanism(s) responsible for their increased levels.

Hypercoagulability in end-stage liver disease: prevalence and its correlation with severity of liver disease and portal vein thrombosis.

Contrary to well-recognized bleeding diathesis in chronic liver disease, thrombotic events can occur in these patients due to reduction or loss of synthesis of anticoagulant proteins. Forty-seven consecutive patients with end-stage liver disease (ESLD) were investigated for activity of protein C, protein S, antithrombin, and factor V Leiden mutation. Forty-two (89.4%) patients had low levels of at least 1 while 33 (70.2%) patients were deficient for all anticoagulant proteins studied. Forty-six (97.9%) patients were negative for factor V Leiden mutation. The deficiencies were more marked in hepatitis C virus-positive patients and patients with model for end-stage liver disease (MELD) score >15. Six (12.8%) patients had portal vein thrombosis (PVT), and all had diminished protein S activity. In conclusions, deficiency of anticoagulant proteins occur in early phase of chronic liver disease. The severity of deficiency is proportional to the severity of liver disease. Despite the high prevalence of hypercoagulability, the incidence of PVT is low. Further studies with larger cohort of patients are needed to support these conclusions and to study other associated factors.