02010nas a2200313   4500000000100000008004100001260001300042653001200055653002600067653003100093653002100124653001100145653002300156653002500179653001000204653000900214653002500223653001200248653001000260653001600270100001400286700001600300700001400316245009200330300001000422490000700432520124300439022001401682       2011                            d  c2011 Mar10aAnimals10aComplement Activation10aComplement System Proteins10aErythema Nodosum10aHumans10aLeprostatic Agents10aLeprosy, lepromatous10aLiver10aMice10aMycobacterium leprae10aRabbits10aSheep10aThalidomide1 aShannon E1 aSandoval FG1 aMorales M00aIn vitro thalidomide does not interfere with the activation of complement by M. leprae.  a274-80 v103 a<p>Erythema nodosum leprosum (ENL) is an inflammatory reaction that may occur in multibacillary leprosy patients, and thalidomide is the treatment of choice. Its cause and the mechanism by which thalidomide suppresses ENL are not known. In the skin lesions, im- mune complexes and split products of complement are found. The activation of complement could precipitate ENL, and thalidomide could suppress the inflammation by inhibiting the activation of complement. To determine if thalidomide could suppress the activation of complement, we first incubated normal serum with thalidomide and with M. leprae or zymosan. The amount of residual functional complement was then assessed by determining the dilution of serum required to lyses sheep erythrocytes sensitized by rabbit antibodies (CH50 Assay). M. leprae and zymosan activated complement. The residual complement activity in the serum incubated with M. leprae or with zymosan was equivalent to that incubated with M. leprae or zymosan in the presence of thalidomide, hydrolyzed thalidomide and metabolites of thalidomide. Thalidomide did not inhibit the activation of complement by zymosan, a known initiator of complement activation by the alternative pathway, or by M. leprae.</p>  a1545-9616