Open AccessAnalysis of Blood Clotting Factor Activities in Canine Legg‐Calvé‐Perthes' Disease
Author(s) -
Brenig Bertram,
Leeb Tosso,
Jansen Stephan,
Kopp Thorsten
Publication year - 1999
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.1999.tb02212.x
Subject(s) - medicine , thrombosis , disease , ischemia , legg calve perthes disease , femoral head , clotting factor , factor ix , occlusion , protein c , etiology , pathology , gastroenterology , cardiology , surgery
Legg‐Calve‐Perthes' (LCP) disease is a noninflammatory aseptic necrosis of the femoral head and neck in small‐breed dogs. The etiology of the disease is not known, but ischemia resulting from vascular compression or occlusion has been proposed. A latent ischemic phase during development of the femoral epiphysis seems to be responsible for the onset of the typical clinical features of LCP disease. Ischemia might result from insufficient oxygen supply either caused by a reduced number of afferent arterial vessels or an occlusion of the efferent venous vessels by thrombosis. In humans, LCP disease has been linked to hypercoagulability and hypofibrinolysis caused by deficiencies of protein C, protein S, or resistance to activated protein C. To determine whether canine LCP disease is caused by similar deficiencies, we determined protein C, protein S, activated protein C, factor II, factor V, factor VIII:C, and AT III activities in plasma samples of 18 dogs with clinically and histopathologically verified LCP disease. All dogs had normal plasma activities of these factors, indicating that in these dogs LCP disease was not caused by deficiencies of the analyzed blood clotting factors.