Article

Analysis of blood clotting factor activities in canine Legg-Calvé-Perthes' disease.

Institute of Veterinary Medicine, University of Göttingen, Germany.
Journal of Veterinary Internal Medicine (Impact Factor: 2.22). 11/1999; 13(6):570-3. DOI: 10.1111/j.1939-1676.1999.tb02212.x
Source: PubMed

ABSTRACT 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.

0 Followers
 · 
59 Views
  • Seminars in Arthroplasty 09/2007; 18(3):184-191. DOI:10.1053/j.sart.2007.06.005
  • [Show abstract] [Hide abstract]
    ABSTRACT: A juvenile, male, yellow-eyed penguin (Megadyptes antipodes) with abnormal stance and decreased mobility was captured, held in captivity for approximately 6 weeks, and euthanized due to continued clinical signs. Radiographically, there was bilateral degenerative joint disease with coxofemoral periarticular osteophyte formation. Grossly, the bird had bilaterally distended, thickened coxofemoral joints with increased laxity, and small, roughened and angular femoral heads. Histologically, the left femoral articular cartilage and subchondral bone were absent, and the remaining femoral head consisted of trabecular bone overlain by fibrin and granulation tissue. There was no gross or histological evidence of infection. The historic, gross, radiographic, and histopathologic findings were most consistent with bilateral aseptic femoral head degeneration resulting in degenerative joint disease. Although the chronicity of the lesions masked the initiating cause, the probable underlying causes of aseptic bilateral femoral head degeneration in a young animal are osteonecrosis and osteochondrosis of the femoral head. To our knowledge, this is the first reported case of bilateral coxofemoral degenerative joint disease in a penguin.
    Avian Pathology 08/2011; 40(4):371-5. DOI:10.1080/03079457.2011.586020 · 2.04 Impact Factor