Mast cells in giant cell arteritis 

For instance mast cells have been identified recetlt to also contribute to the pathogenesis of giant cell arteritis (GCA) putatively by regulating the functions of other inflammatory cells and resident vessel wall cells. Mast cells seem to promote neovascularization, which is one of the causal factors for the neointimal thickening in GCA. ^[2]

Mast cells in Abdominal Aortic Aneurysms

Now, in 2011, mast cells (MC) are regarded as important players in the Orchestrated Pathogenesis of Abdominal Aortic Aneurysms (AAA) by researchers form the Karolinska Institute, in Stockholm, Sweden.

They focus on the fact that activated MCs synthesize and release eicosanoids and a large number of cytokines and chemokines.  Experimentally induced AAA in MC-deficient animals and animals treated with MC inhibitors demonstrate that MCs are involved in the pathogenesis of AAA via various mechanisms.

MC-dependent activation of metalloproteinases and the renin-angiotensin system, contribution to smooth muscle cell apoptosis, and release of proteolytic enzymes are some key examples. Human studies indicate that MCs are the main source of cathepsin G in AAAs and contribute to activation of the renin-angiotensin system via chymase and cathepsin G. Activated MCs also contribute to neovascularization, inflammation, and atherosclerosis, all hallmarks of AAA.

The authors pointed out that new drugs with MC stabilizing properties, as well as leukotriene receptor antagonists and histamine receptor blockers could also be tested for their efficacy in preventing development and growth of AAA ^[3]

Palmitoylethanolamide as a classical and powerfull mast cell degranulation inhibitor might also be such a candidate. This would also be interesting as a putative treatment option for giant cell arteritis.

Jan M. Keppel Hesselink, MD, PhD, January 2011 

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