The role of mannose binding lectin on fever episodes in pediatric oncology patients

Ferenc Fekete, Balázs Fadgyas, Éva Papp, Ágnes Szilágyi, Z. Prohászka, Brigitta Müller, Gábor Kovács

Research output: Contribution to journalArticle

2 Citations (Scopus)


Despite significant changes in pediatric oncological therapy, mortality is still high, mainly due to infections. Complement system as an ancient immune defense against microorganisms plays a significant role in surmounting infections, therefore, deficiency of its components may have particular importance in malignancies. The present paper assesses the effect of promoter (X/Y) and exon 1 (A/0) polymorphisms of the MBL2 gene altering mannose binding lectin (MBL) serum level in pediatric oncological patients with febrile neutropenia. Furthermore, frequency distribution of MBL2 alleles in children with malignancies and age-matched controls was analysed. Fifty-four oncohematological patients and 53 children who had undergone pediatric surgery were enrolled into this retrospective study. No significant differences were found in the frequency of MBL2 alleles between the hemato-oncologic and control group. The average duration of fever episodes was significantly shorter (p = 0.035) in patients carrying genotypes (AY/AY and AY/AX) that encode normal MBL level, compared to individuals with genotypes associated with lower functional MBL level (AX/AX, AY/0, AX/0, or 0/0) (days, median (IQ range) 3.7(0–5.4) vs. 5.0(3.8–6.6), respectively). In conclusion, our data suggest that MBL2 genotypes may influence the course of febrile neutropenia in pediatric patients with malignancies, and may contribute to clarification of the importance of MBL in infections.

Original languageEnglish
Pages (from-to)139-143
Number of pages5
JournalPathology and Oncology Research
Issue number1
Publication statusPublished - Jan 1 2016


  • Febrile neutropenia
  • MBL
  • Oncohematology
  • Polymorphism

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Pathology and Forensic Medicine

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