Association of mannose-binding lectin 2 (MBL2) and suppressor of cytokine signaling-1 (SOCS1) gene variants in children with febrile neutropenia.


Uysalol E. P., Uysalol M., Pehlivan M., Oyaci Y., Pehlivan S., Serin I.

Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy, cilt.28, sa.5, ss.657-662, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 28 Sayı: 5
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1016/j.jiac.2022.01.012
  • Dergi Adı: Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.657-662
  • Anahtar Kelimeler: Febrile neutropenia, Mannose-binding lectin 2 ( MBL2 ), Suppressor of cytokine signaling-1 ( SOCS1 ), Prognosis, POLYMORPHISM, EXPRESSION
  • İstanbul Üniversitesi Adresli: Evet

Özet

© 2022 Japanese Society of Chemotherapy and The Japanese Association for Infectious DiseasesIntroduction: Febrile neutropenia (FEN) was reported in patients with solid malignancies at a rate of 5–10% and in patients with hematological malignancies at a rate of 20–25%. In our study, we aimed to investigate the effects of mannose-binding lectin 2 (MBL2) (rs1800450) and suppressor of cytokine signaling-1 (SOCS1) (rs33989964) gene variants on patients with FEN. Methods: A total of 123 patients who applied to pediatric emergency department between December 2019–12/2020 included in the study. Thirteen patients were excluded from the study due to the inability to obtain DNA. Demographic-clinical features at initial diagnosis and genotype distributions were recorded. The control group consisted of volunteers with the same ethnicity, age and gender, no active infection, and no consanguinity. Results: CA/CA genotype of SOCS1 was found to be significantly higher in the healthy control group (p = 0.028). AB/BB genotype of MBL2 was significantly higher in FEN patients with a MASCC score of high risk, AA genotype was found to be higher in patients with low risk (p = 0.001). While the rate of microbiologically documented infection (MDI) was significantly lower in patients with the AA genotype of MBL2, it was significantly higher in patients with AA/BB genotypes (p = 0.025). MDI rate in patients with the del/del genotype of SOCS1 was found to be significantly lower than in patients with CA/CA + CA/del genotypes (p = 0.026). Conclusions: In this study, it was revealed that low expression-related MBL2 genotypes were riskier for FEN and also, gene variants associated with high SOCS1 transcription were both protective against FEN and increased the rate of culture-negativity.