title: Increased levels of circulating Annexin A5 in Familial Mediterranean fever.
abstract: BACKGROUND
  Familial Mediterranean fever is a genetic autoinflammatory disease most commonly affecting the ethnic groups originating from around the Mediterranean Sea. Apoptosis plays an important role in down-regulation of the inflammatory response by reducing the lifespan of activated immunocompetent cells. Thus, increased apoptosis may be associated with pathogenesis of familial Mediterranean fever.
  
  
  METHODS
  In the present study we determined the serum levels of apoptotic marker, Annexin A5, in familial Mediterranean fever patients, within an attack and attack-free, in comparison to healthy subjects and assessed the influence of colchicine treatment on this parameter. In addition, in all study subjects serum levels of C-reactive protein and interleukine-1β, and the total leukocyte count were also determined.
  
  
  RESULTS
  Our results demonstrated that pathogenesis of familial Mediterranean fever is characterized by the increased levels of circulating Annexin A5, which is higher in patients within the attack and which associate with the increased levels of C-reactive protein and interleukine-1β and total leukocyte count.
  
  
  CONCLUSIONS
  The results obtained indicate elevated rates of apoptosis of subpopulations of leukocytes involved in autoinflammation and recurrent episodes of fever in familial Mediterranean fever. It was also revealed that regular colchicine treatment sufficiently decreases the rate of apoptosis in familial Mediterranean fever patients by affecting the intensity of autoinflammatory reactions.
authors.affiliation: Institute of Molecular Biology, National Academy of Sciences of the Republic of Armenia 7, Hasratyan St,, Yerevan 0014, Armenia. aboyajyan@sci.am.
authors.forename: Anna S
authors.initials: AS
authors.lastname: Boyajyan
authors.forename: Gohar M
authors.initials: GM
authors.lastname: Mkrtchyan
authors.forename: Lilit P
authors.initials: LP
authors.lastname: Hovhannisyan
authors.forename: Tigran J
authors.initials: TJ
authors.lastname: Hovsepyan