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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3364-3368
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Increased lipoprotein (a) levels as an independent risk
factor for venous thromboembolism
Mario von Depka,
Ulrike Nowak-Göttl,
Roswith Eisert,
Christian Dieterich,
Monika Barthels,
Inge Scharrer,
Arnold Ganser, and
Silke Ehrenforth
From the Department of Hematology/Oncology, Hannover
Medical School, Hannover, Germany; Department of
Pediatrics, Westphalian Wilhelms- University, Münster, Germany;
Center of Internal Medicine I, University Hospital Frankfurt,
Frankfurt, Germany; Clinical Chemistry, Hannover Medical
School, Hannover, Germany.
Elevation of serum lipoprotein (a) (Lp[a]) is a known risk factor
predisposing to cardiovascular and cerebrovascular disease. However,
little is known about the role of increased Lp(a) in venous
thromboembolism (VTE). This study evaluated the role of Lp(a) among a
panel of established hereditary thrombogenic defects in patients with
VTE. A total of 685 consecutive patients with at least one episode of
VTE and 266 sex- and age-matched healthy controls were screened with
regard to activated protein C resistance, protein C, protein S,
and antithrombin deficiency, elevated serum levels of Lp(a), and the
factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations.
Elevated Lp(a) levels above 30 mg/dL were found in 20% of all
patients, as compared to 7% among healthy controls (P < .001, odds ratio [OR] 3.2, 95% confidence
interval [CI], 1.9-5.3). The coexistence of FV G1691A and elevated
Lp(a) was significantly more prevalent among patients with VTE than in
the control group (7% versus 0.8%; P < .001, OR 9.8, 95% CI, 2.4-40.7). No other established prothrombotic risk factor was
found to be significantly combined with increased Lp(a). These data
suggest that Lp(a) concentrations greater than 30 mg/dL are a frequent and independent risk factor for VTE. Furthermore, elevated Lp(a) levels
might contribute to the penetrance of thromboembolic disease in
subjects being affected by other prothrombotic defects, such as FV
G1691A mutation.
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