Consequences of intra-articular bleeding in haemophilia: science to clinical practice and beyond.

Published

Journal Article

Blood in the joint causes a number of physiological and pathological events that eventually lead to haemophilic arthropathy. Animal models show that blood in the joint induces inflammation that continues long after blood has been cleared. TNF-alpha, IL-1 beta and IL-6 are inflammatory mediators that increase following haemarthrosis in haemophilic mice. Conventional anti-inflammatory drugs have failed to demonstrate a lasting effect in preventing haemophilic arthropathy. A new TNF-alpha antagonist has shown promising results in haemophilic mice. Similarly, the use of cyclo-oxygenase-2 inhibitors may reduce angiogenesis associated with the healing process following bleeding and the associated tissue damage. Animal models are useful for studying the pathophysiology of haemarthropathy, however, when applying results from animals to humans, the differences in matrix turnover rate, thickness of cartilage and joint biomechanics must be kept in mind. In people with haemophilia, there is a variable response to haemarthrosis as demonstrated by magnetic resonance imaging (MRI). Up to 30% of subjects have normal MRI despite having three or more haemarthroses into the same joint. Once bone damage is present, little can be done to restore anatomic integrity. Several molecules, including members of the bone morphogenic protein subfamily, have been injected into bone defects in non-haemophilic subjects with some evidence of benefit. To achieve the primary goal of reducing blood in the joint and the negative sequelae, it is questionable to use ice to treat haemarthrosis. Indeed low temperature is associated with impairment of coagulation enzyme activity and platelet function.

Full Text

Duke Authors

Cited Authors

  • Forsyth, AL; Rivard, G-É; Valentino, LA; Zourikian, N; Hoffman, M; Monahan, PE; Van Meegeren, MER; Forriol, F

Published Date

  • July 2012

Published In

Volume / Issue

  • 18 Suppl 4 /

Start / End Page

  • 112 - 119

PubMed ID

  • 22726093

Pubmed Central ID

  • 22726093

Electronic International Standard Serial Number (EISSN)

  • 1365-2516

Digital Object Identifier (DOI)

  • 10.1111/j.1365-2516.2012.02835.x

Language

  • eng

Conference Location

  • England