Journals / Turkish Journal of Pediatrics / 2021 / Cilt: 63 - Sayı: 2

Transient positivity of anti-tissue transglutaminase IgA autoantibody in febrile children: a case-control study

Pages
257–262
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

It is recommended for pediatricians to be vigilant in interpreting anti-tTG IgA results during fever episodes and repeat positive cases after the cease of fever.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Fever is a physiological response activated by integrative interactions between the neuronal and immune systems.
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Key Findings & Data:We here evaluated if fever was associated with increased levels of anti-tissue transglutaminase (tTG) IgA autoreactive antibodies in children.
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Conclusion & Impact:It is recommended for pediatricians to be vigilant in interpreting anti-tTG IgA results during fever episodes and repeat positive cases after the cease of fever.
🔬Design:Research Article
📍Scope:2018 Verileri
⚙️Variables:Domain Parameters

Özet

Background. Fever is a physiological response activated by integrative interactions between the neuronal and immune systems. The association of fever with the development of autoantibodies against various self-antigens is controversial. We here evaluated if fever was associated with increased levels of anti-tissue transglutaminase (tTG) IgA autoreactive antibodies in children. Methods. This was a case-control study performed the Amir-Al-Momenin Hospital of Zabol City from January to December 2018. Febrile children (N=135) and apparently healthy counterparts (N=135) were included. Total IgA and anti-tTG IgA were measured by ELISA. Results. From 270 children evaluated, 144 (53.6%) and 126 (46.4%) were males and females, respectively. The mean age was 4.7 ± 2.6 years. The mean total IgA titer was 208 ± 100 mg/dl, and the mean anti-tTG IgA titer was 15.9 ± 68 mg/dl. There was a significant difference in the mean titer of anti-tTG IgA between apparently healthy controls (1.97 ± 1.12 mg/dl) and febrile children (30.2 ± 94.9 mg/dl, p=0.002). Positivity for anti-tTG IgA was observed in 16 (11.8%) out of 135 febrile children while no subject in the control group had positive results. One out of the 16 positive cases showed persistent elevated levels after fever disappearance. On biopsy examination, this child was confirmed to have celiac disease. Conclusions. We showed that fever can trigger the production of anti-tTG IgA autoantibody in children. It is recommended for pediatricians to be vigilant in interpreting anti-tTG IgA results during fever episodes and repeat positive cases after the cease of fever. It is also recommended to reassess anti-tTG IgA seropositivity in other clinical settings in future studies.

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Cite This Article

SHAHRAMİAN, I., SALAHİFAR, M., AKBARİZADEH, M. R., MOHAMMADİ, M. H., BAZİ, A. (2021). Transient positivity of anti-tissue transglutaminase IgA autoantibody in febrile children: a case-control study. Turkish Journal of Pediatrics, Cilt: 63 - Sayı: 2, 257–262. https://ajindex.com/articles/411954

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References (14)

  1. Ogoina D. Fever, fever patterns and diseases called ‘fever’--a review. J Infect Public Health 2011; 4: 108- 124
  2. Romanovsky AA, Steiner AA, Matsumura K. Cells that trigger fever. Cell Cycle 2006; 5: 2195-2197
  3. Ziemssen T, Kern S. Psychoneuroimmunology- -cross-talk between the immune and nervous systems. J Neurol 2007; 254 (Suppl 2): II8-II11
  4. Netea MG, Kullberg BJ, Van der Meer JW. Circulating cytokines as mediators of fever. Clin Infect Dis 2000; 31 (Suppl 5): S178-S184
  5. Conti B, Tabarean I, Andrei C, Bartfai T. Cytokines and fever. Front Biosci 2004; 9: 1433-1449
  6. Jiang Q, Cross AS, Singh IS, Chen TT, Viscardi RM, Hasday JD. Febrile core temperature is essential for optimal host defense in bacterial peritonitis. Infect Immun 2000; 68: 1265-1270
  7. Cunha BA. Fever myths and misconceptions: the beneficial effects of fever as a critical component of host defenses against infection. Heart Lung 2012; 41: 99-101
  8. Horwitz MS, Ilic A, Fine C, Balasa B, Sarvetnick N. Coxsackieviral-mediated diabetes: induction requires antigen-presenting cells and is accompanied by phagocytosis of beta cells. Clin Immunol 2004; 110: 134-144
  9. Beyerlein A, Wehweck F, Ziegler AG, Pflueger M. Respiratory infections in early life and the development of islet autoimmunity in children at increased type 1 diabetes risk: evidence from the BABYDIET study. JAMA Pediatr 2013; 167: 800-807
  10. Johnson Rowsey P. Thermoregulation: cytokines involved in fever and exercise. Annu Rev Nurs Res 2013; 31: 19-46
  11. Koshy M, Mathew J, Alex R, et al. Antinuclear antibodies in scrub typhus: transient occurrence during acute illness. J Vector Borne Dis 2018; 55: 52- 57
  12. Werz O, Bürkert E, Samuelsson B, Rådmark O, Steinhilber D. Activation of 5-lipoxygenase by cell stress is calcium independent in human polymorphonuclear leukocytes. Blood 2002; 99: 1044-1052
  13. Kettritz R, Choi M, Salanova B, Wellner M, Rolle S, Luft FC. Fever-like temperatures affect neutrophil NF-kappaB signaling, apoptosis, and ANCA-antigen expression. J Am Soc Nephrol 2006; 17: 1345-1353
  14. Lee JJ, Huang WT, Shao DZ, Liao JF, Lin MT. Blocking NF-kappaB activation may be an effective strategy in the fever therapy. Jpn J Physiol 2003; 53: 367-375. 15. von Vietinghoff S, Choi M, Rolle S, Luft FC, Kettritz R. Febrile temperatures control antineutrophil cytoplasmic autoantibody-induced neutrophil activation via inhibition of phosphatidylinositol 3-kinase/Akt. Arthritis Rheum 2007; 56: 3149-3158