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Increased Lipoprotein (a) concentrations in patients with chronic venous leg ulcers: a study on patients with or without postthrombotic syndrome
Author(s) -
Zutt Markus,
Krüger Ulrich,
Rosenberger Albert,
Schön Michael P.,
Neumann Christine,
von Ahsen Nico,
Kretschmer Lutz
Publication year - 2011
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2010.00657.x
Subject(s) - medicine , pathogenesis , lipoprotein(a) , gastroenterology , pathophysiology , venous leg ulcer , chronic venous insufficiency , thrombophilia , proinflammatory cytokine , fibrinolysis , disease , case control study , lipoprotein , surgery , cholesterol , thrombosis , inflammation
Chronic venous leg ulcers are common and cause considerable burden of disease for affected patients with significant costs for health care systems worldwide. The complex pathophysiology of chronic venous leg ulcers is still not entirely understood. In addition, reliable pathogenic and/or prognostic parameters are not known. Published data suggest that patients with chronic venous leg ulcers reveal congenital or acquired thrombophilia. We examined the serum Lipoprotein (a) [Lp(a)] level, a proatherogenic and prothrombotic risk factor, in patients with chronic venous leg ulcers ( n =210, stratified into patients with postthrombotic syndrome or without) and in a healthy control group ( n =341). Forty‐two percent of all patients, compared with 20% of healthy controls, revealed significantly increased Lp(a) serum concentrations above 0.3 g/L. Furthermore, 49% without postthrombotic syndrome but only 35% with postthrombotic syndrome showed increased Lp(a) levels. The increase of Lp(a) level was significantly different between all three groups ( p <0.001). There was no correlation of Lp(a) levels and CRP values in all groups. Based on these data, it is conceivable that Lp(a) plasma level is a novel pathogenic parameter for chronic venous leg ulcers. Elevated concentrations may contribute to the pathogenesis through induction of thrombogenic microcirculatory dysregulations, impaired extravascular fibrinolysis, or other mechanisms like proinflammatory effects.