Key result
Liver disease links to ~4-fold higher anticardiolipin antibodies without increasing thrombotic complications.
Why the study?
The role of anticardiolipin antibodies in causing antiphospholipid syndrome and thrombotic events in patients with liver disease was uncertain.
Does the presence of anticardiolipin antibodies increase the risk of thrombotic events in patients with liver disease?
Observational (n=488)
Does the presence of anticardiolipin antibodies increase the risk of thrombotic events in patients with liver disease?
Absolute Event Rate: 18.8% vs 4.4%
p-value: p=< 0.0002
In patients with nonautoimmune liver disease, anticardiolipin antibody production is an epiphenomenon of liver damage and is not associated with an increased risk of thrombotic complications.
aCL positivity in nonautoimmune liver disease warrants no thrombotic risk adjustment; leaves open whether it solely marks disease severity.
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.
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Mangia et al. (1999) conducted an observational in Liver disease (n=488). Liver disease vs. Healthy controls was evaluated on Anticardiolipin antibody (aCL) positivity (p=< 0.0002). Liver disease was associated with higher anticardiolipin antibody positivity than healthy controls (18.8% vs 4.4%, P<0.0002), but this was an epiphenomenon not linked to thrombotic complications.
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