Macrophage migration inhibitory factor -173 polymorphism and risk of coronary alterations in children with Kawasaki

G Simonini1, E Corinaldesi, C Massai

  • 1Department of Paediatrics, Rheumatology Unit, A. Meyer Children's Hospital, Florence, Italy. gabriele.simonini@unifi.it

Insights

The macrophage migration inhibitory factor (MIF) -173*C polymorphism is linked to an increased risk of coronary artery abnormalities (CAA) in children with Kawasaki disease (KD). This genetic factor also correlates with a higher likelihood of non-response to initial intravenous immunoglobulin (IVIG) treatment.

Area of Science:

  • Genetics
  • Immunology
  • Pediatrics

Background:

  • Kawasaki disease (KD) is an acute febrile illness affecting young children, primarily causing inflammation of medium-sized arteries.
  • Coronary artery abnormalities (CAA) are the most serious complication of KD, leading to long-term cardiovascular risks.
  • Genetic predisposition is suspected to play a role in KD susceptibility and severity, but specific genetic markers are still under investigation.

Purpose of the Study:

  • To investigate the association between the macrophage migration inhibitory factor (MIF) -173 G/C gene polymorphism and the susceptibility to, and severity of, Kawasaki disease (KD) in Italian children.
  • To determine if this MIF polymorphism influences the development of coronary artery abnormalities (CAA) or response to intravenous immunoglobulin (IVIG) treatment in KD patients.

Main Methods:

  • Genotyping for the MIF -173 G/C polymorphism was performed using PCR and restriction fragment length polymorphism (RFLP) analysis.
  • The study included 69 Italian children diagnosed with KD and 60 healthy Caucasian children as controls.
  • Clinical data, including the development of CAA and response to IVIG, were collected and analyzed in relation to the MIF genotype.

Main Results:

  • No significant difference in MIF genotype frequencies was observed between KD patients and healthy controls.
  • KD patients carrying the MIF -173*C allele showed a significantly higher frequency of developing coronary artery abnormalities (CAA) compared to those without the allele (77.8% vs. 26.7%).
  • Children with the MIF -173*C allele were also more likely to be non-responders to initial IVIG treatment (75% vs. 28%) and had an increased risk of coronary involvement in regression analysis.

Conclusions:

  • The study suggests a potential relationship between the MIF -173*C polymorphism and an increased risk of developing coronary artery abnormalities (CAA) in Kawasaki disease (KD) patients.
  • Carriage of the MIF -173*C allele may be a predictive factor for poor response to IVIG and increased risk of coronary complications in KD.
  • Further research is warranted to elucidate the role of MIF in KD pathogenesis and its implications for treatment strategies.
Abstract