Related Experiment Videos

Increased levels of circulating Annexin A5 in Familial Mediterranean fever

Anna S Boyajyan1, Gohar M Mkrtchyan, Lilit P Hovhannisyan

  • 1Institute of Molecular Biology, National Academy of Sciences of the Republic of Armenia 7, Hasratyan St,, Yerevan 0014, Armenia. aboyajyan@sci.am.

Abstract

Insights

Familial Mediterranean fever patients show increased apoptosis, indicated by higher Annexin A5 levels, especially during attacks. Colchicine treatment effectively reduces this apoptosis and autoinflammation.

Area of Science:

  • Immunology
  • Genetics
  • Cell Biology

Background:

  • Familial Mediterranean fever (FMF) is a genetic autoinflammatory disorder prevalent in Mediterranean populations.
  • Apoptosis, or programmed cell death, is crucial for regulating inflammation by limiting immune cell survival.
  • Dysregulated apoptosis may contribute to the pathogenesis of FMF.

Purpose of the Study:

  • To investigate serum Annexin A5 levels as an apoptotic marker in FMF patients.
  • To compare Annexin A5 levels during FMF attacks and in remission versus healthy controls.
  • To evaluate the impact of colchicine treatment on apoptosis in FMF.

Main Methods:

  • Serum Annexin A5 levels were measured in FMF patients (during attacks and attack-free periods) and healthy controls.
  • Serum C-reactive protein, interleukin-1β, and total leukocyte counts were also assessed.
  • The effect of colchicine treatment on Annexin A5 levels was examined.

Main Results:

  • FMF patients exhibited elevated circulating Annexin A5 levels compared to controls.
  • Annexin A5 levels were significantly higher during FMF attacks.
  • Increased Annexin A5 correlated with elevated C-reactive protein, interleukin-1β, and leukocyte counts.

Conclusions:

  • FMF is associated with increased apoptosis in leukocyte subpopulations driving autoinflammation and fever.
  • Regular colchicine treatment effectively reduces apoptosis rates in FMF patients.
  • Colchicine's mechanism may involve modulating the intensity of autoinflammatory responses.

Related Concept Videos