PMID: 11229832

Issn Print: 0957-5235

Publication Date: 2001/01/01


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. . .relationship between dislipidemia and thrombosis yet unproven

G. Lippi; G. Guidi

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Excerpt

There is unequivocal scientific evidence that lipid and lipoprotein disorders play a pivotal role in genesis, progression and complication of arterial thrombosis [1]. However, a causal relationship between dislipidemia and thrombosis in the venous district is yet unproven. Although preliminary reports recognized a potential contribution of lipid and lipoprotein disorders to the development of venous thromboembolism (VTE) [2–4], further investigations could not confirm such an association [5–7]. To provide further insight into this phenomenon, McColl et al. recently investigated the potential effects of isolated or combined lipid disorders on the risk of VTE in 62 young women who had suffered an earlier episode of VTE [8]. Besides plasma triglycerides, no additional relevant associations could be identified. Similar conclusions issued from our previous investigations, analysing the concentration of lipoprotein (a) [Lp(a)] and additional lipid and lipoprotein parameters included in a routine profile for the assessment of the cardiovascular risk [6,7]. In fact, we concluded that neither the conventional lipid and lipoprotein profile nor Lp(a) are predictive of VTE. Among others, results of Lp(a) measurement are of a particular clinical relevance. In fact, although the connection between conventional lipoproteins and the fibrinolytic system remains speculative, there are several lines of evidence confirming the inhibitory effect of Lp(a) on fibrinolysis [9]. However, taken together, present and earlier results demonstrate that the inclusion of Lp(a) measurement among screening tests for thrombophilia adds little or null to the clinical reasoning.
Different to McColl et al., and despite a trend towards raised values in patients with VTE, we could not observe a significant correlation between VTE and plasma triglycerides (172 ± 93 versus 155 ± 67 mg/dl;P = 0.27) [7]. The most plausible explanation for such a discrepancy is the heterogeneity of the two study populations, as McColl et al. investigated young women aged < 50 years, whereas the mean age of our patients was 59 years. Additionally, male and female patients were mixed in our investigation. Hence, a different hormonal homeostasis due to multiple metabolic differences, such as sex, age, administration of oral contraceptives and hormone replacement therapy, might have played a key role in the disparity of results for plasma triglycerides. Additionally, to add clinical relevance to our data, we expressed results in terms of percentage of subjects with undesirable values according to the guidelines of the National Cholesterol Education Program Adult Treatment Panel II [10], and we further compared subjects with or without VTE by chi-square analysis. Neither, in this case, did the statistical analysis reveal significant differences for any of the parameters tested [6,7]. Owing to the difference with our study population, we believe that the investigation of McColl et al. might issue additional valuable clinical information by comparing the percentage of patients and controls displaying undesirable values.

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