Warfarin Institute of America
DEDICATED TO YOUR HEALTH
IS THERE A LINK BETWEEN AVASCULAR NECROSIS OF BONES AND WARFARIN
Rhiannon Trepanier, Pharm D. Candidate
University of Colorado at Denver and Health Science Center
Avascular necrosis or osteonecrosis is described as the death of bone tissue due to inadequate blood supply. Definite causes have been noted such as alcohol abuse, atherosclerosis, decompression sickness, Gaucher’s disease, hip fracture of the femoral neck, hip dislocation, radiotherapy, Sickle cell disease, tumors, and also high-dose corticosteroid use. Other possible causes include blood clotting disorders, Cushing’s syndrome, diabetes mellitus, fatty liver disease, gout, lipid disturbances, pancreatic cancer, pancreatitis, smoking, and systemic lupus erythematosus (SLE).1, 2 While there is no direct evidence linking the concomitant use of both warfarin and prednisone as a cause for avascular necrosis of the shoulder, there is strong evidence linking the use of prednisone. Avascular necrosis associated with the use of corticosteroid therapy has been noted to occur in the shoulder, knee, jaw, and most notably, the hip (femoral head). In approximately 40% of avascular necrosis cases of the hip, both hips are eventually affected. This adverse drug reaction is more prominent with long-term, high dose therapy, but has also been reported with short-term, moderate doses. Avascular necrosis associated with corticosteroid use has also been noted to occur more commonly in patients with SLE or rheumatoid arthritis. It is believed that the bone tissue necrosis and devascularization is caused by hyperlipidemia and fat emboli created during fat mobilization/redistribution due to corticosteroid use. This fat mobilization affects the arteriole beds in bone tissue and eventually leads to cell death.3
Warfarin, on the other hand, has not been sited as a cause of osteonecrosis, but rather has been used as treatment for forms of idiopathic avascular necrosis. Idiopathic causes are those not contributable to a secondary cause such as medications and include forms of heritable thrombophilia such as 1) low levels of tissue plasminogen activator (tPA-Fx); 2) high levels of plasminogen activator inhibitor (PAI-Fx); 3) high levels of atherogenic, hypofibrinolytic lipoprotein, Lp(a); 4) low levels of proteins C or S leading to unopposed prothrombotic factors Va and VIIIa; and 5) resistance to activated protein C. Patients with resistance to activated protein C or high levels of Lp(a) have been treated with warfarin to stabilize the blood clots leading to osteonecrosis thus allowing the joint to heal.4
The relationship between warfarin and death of bones is not one of cause and effect but rather a disease and a treatment.
References:
1. Avascular Necrosis of the Bone: Merck Manual Home Edition. Available at: www.merck.com/mmhe/sec05/ch064/ch064a.html. Accessed on February 6, 2006
2. Levine M. Osteonecrosis, Shoulder. Available at: www.emedicine.com/orthoped/topic590.htm. Accessed on February 6, 2006.
3. Drugdex Drug Evaluations: Prednisone. Micromedex Healthcare Series Online. Available at: www.thomsonhc.com.library.uchsc.edu/hcs/librarian/ND_PR/Main/SBK/1/PFPUI/wp45xAo1azPoGR/ND_PG/PRIH/CS/E0F4D1/ND_T/HCS/ND_P/Main/DUPLICATIONSHIELDSYNC/1D4978/ND_B/HCS/PFActionId/hcs.common.RetrieveDocumentCommon/DocId/0240/ContentSetId/31/SearchTerm/prednisone/SearchOption/ExactMatch. Accessed on February 7, 2006.
4. Glueck CJ, Freiberg R, Tracy T, Stroop D, Wang P. Thrombophilia and Hypofibrinolysis: Pathophysiologies of Osteonecrosis. Clinical Orthopaedics and Related Research, 1997; 334: 43-56.
© 2006 Rhiannon Trepanier - Used By Permission
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