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FYI, cyclosporin can damage the lining of the microscopic blood vessels causing platelets and fibrin to be sequestered to those areas. As red blood cells travel, the fibrin threads that criss-cross the vessels cut the red cells in half. These mechanically damaged red blood cells are called schistocytes. The damage can also result in misshapen red cells. Premature demise of red blood cells can result in the release of immature red blood cells from the marrow. If the hemoglobin is not dropping at an unreasonably fast rate and the LDH is normal, this damage is tolerable. If transfusions are required more frequently than is expected and the LDH is elevated, this could indicate the cyclosporine's side effects are becoming dangerous.
One can Google "cyclosporine (or tacrolimus) associated microangiopathy".
This side effect post BMT was my son's only complication and it could have been deadly as he experienced severe microangiopathy and at it's worst, needed red cell transfusions every few days.
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Nicole, mom to Evan (20); diagnosed SAA November 2007, hATG mid-November 2007, no response after 6 months, unrelated 9/10 BMT June 2008, no GVH, health completely restored thanks to our beloved donor Bryan from Tennessee.
www.caringbridge.org/visit/evanmacneil
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