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Anticardiolipin antibodies in patients with liver disease
A Mangia1, M Margaglione, I Cascavilla
1Division of Gastroenterology, and Atherosclerosis and Thrombosis Unit, Hospital Casa Sollievo della Soffferenza, IRCCS, San Giovanni Rotondo, Italy.
Insights
Anticardiolipin antibodies (aCL) in liver disease patients are often a consequence of liver damage, not a cause of blood clots. Hepatitis C virus (HCV) is not linked to antiphospholipid syndrome in these cases.
Area of Science:
- Hepatology
- Immunology
- Vascular Medicine
Background:
- Anticardiolipin antibodies (aCL) are associated with antiphospholipid syndrome and thrombosis.
- The role of aCL in patients with liver disease, particularly concerning thrombotic events, requires further investigation.
Purpose of the Study:
- To investigate the association between anticardiolipin antibodies (aCL) and thrombotic events in patients with various types of liver disease.
- To determine if aCL contribute to antiphospholipid syndrome in the context of liver pathology.
Main Methods:
- Measurement of aCL in 372 patients with liver disease (HCV, HBV, alcoholic, cryptogenic) and 116 healthy controls.
- Recording of prior thrombotic events and correlation with demographic, clinical, and serological data.
- Conditional logistic regression analysis to identify independent predictors of aCL and thrombosis.
Main Results:
- aCL were significantly more prevalent in patients with liver disease (18.8%) compared to controls (4.4%).
- aCL presence was associated with male gender, advanced cirrhosis, anti-smooth-muscle antibodies (ASMA), and HBV or alcoholic liver disease.
- Thrombosis was linked to advanced age, hepatocellular carcinoma, HBV, and cryptogenic liver disease; only one patient with new portal thrombosis had aCL.
Conclusions:
- In nonautoimmune liver disease, aCL production appears to be an epiphenomenon of liver damage, not a cause of thrombosis.
- The findings do not support the hypothesis that hepatitis C virus (HCV) causes antiphospholipid syndrome in patients with liver disease.
Objective:
Our aim was to test the hypothesis that anticardiolipin antibodies (aCL) may cause an antiphospholipid syndrome and thrombotic events in patients with liver disease.
Methods:
aCL were measured in 116 healthy controls and 372 patients with liver disease of different stage and etiology: 136 cases secondary to hepatitis C virus (HCV) infection, 139 due to hepatitis B virus (HBV) infection, 69 with alcoholic liver damage, and 28 cryptogenic in origin. Prior thrombotic events were recorded. The results were related to age, gender, stage, severity, and etiology of the liver disease, as well as to the occurrence of organ- and nonorgan-specific autoantibodies.
Results:
aCL were positive in 4.4% of controls and in 18.8% of patients (p < 0.0002). Patients with aCL were more frequently men with an advanced cirrhosis and simultaneous occurrence of anti-smooth-muscle antibodies (ASMA) in serum (p < 0.0006); their liver damage was often secondary to HBV (37.3%) or alcohol abuse (18.5%). At conditional logistic regression analysis, only the presence of ASMA (odds ratio [OR] = 3.02, 95% confidence interval [CI] 1.7-5.5, p = 0.0003), HBV (OR = 3.4, 95% CI 1.6-7.2, p = 0.0013), or alcoholic liver disease (OR = 5.3, 95% CI 2.3-12.2, p = 0.0001) were independently associated with aCL. Thrombosis was encountered in 24 patients (6.4%). At conditional logistic regression analysis, thrombosis was significantly associated with advanced age (OR = 1.07, 95% CI 1.0-1.1, p = 0.0094), development of hepatocellular carcinoma (OR = 17.8, 95% CI 1.6-196.0, p = 0.01), HBV etiology (OR = 6.3, 95% CI, 1.6-24.6, p = 0.0076), or cryptogenic liver disease (OR = 54.8, 95% CI 5-599.9, p = 0.001). Of the five patients with newly documented portal thrombosis during the follow-up, only one tested positive for aCL.
Conclusions:
In patients with nonautoimmune liver disease, aCL production is an epiphenomenon of the liver damage and is not associated with thrombotic complications. These data do not support the hypothesis that HCV is a cause of the antiphospholipid syndrome.