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Haptoglobin Polymorphism and Morbidity in Children Born Prematurely

Received: 26 January 2020    Accepted: 24 February 2020    Published: 28 February 2020
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Abstract

Haptoglobin (Hp) is an acute phase protein. There exists three different Hp phenotypes that differ in their pro-inflammatory and anti-inflammatory action. Inflammation and oxidative stress are critically involved in many pathophysiological processes in childhood. We previously reported on the relationship of in-hospital clinical events and the Hp phenotype in a cohort of consecutive premature infants. This study provides follow up of childhood morbidity data and its relationship to the Hp phenotype for the previously reported study premature infant cohort. A phone questionnaire was carried out among the parents and medical history records were evaluated. The age of participants varied from eight to eleven years. The questionnaire included information about diseases with an inflammatory component in pathogenesis, infections and need for hospitalization. Of the original 122 study participants, morbidity data at eight to eleven years was available for 101 participants, and 100 were enrolled in the study. A less anti-inflammatory Hp phenotype (Hp 2-2) was more prevalent in participants who suffered from diseases with an inflammatory component in their pathogenesis (RTI, pneumonia, UTI, OM and tonsillitis) when these entities were analyzed as a group (p=0.043). Subsequent comparison of the cumulative number of episodes of these entities between Hp phenotypes during all follow up period detected a trend in the same direction. Further research involving a larger population is required for better understanding of the Hp phenotype role in infantile and pediatric morbidity.

Published in American Journal of Pediatrics (Volume 6, Issue 1)
DOI 10.11648/j.ajp.20200601.23
Page(s) 73-77
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Childhood Morbidity, Haptoglobin Phenotype, Infection, Inflammation

References
[1] Levy A P, Asleh R, Blum S et al. Haptoglobin: Basic and Clinical Aspects. Antioxidants & Redox Signaling 2010 Feb; 12 (2): 293-304. doi: 10.1089/ars.2009.2793.
[2] Wasserzug O, Blum S, Klement E, Leibkowicz F, Miller-Lotan R, Levy AP. Haptoglobin 1-1 genotype and the risk of life-threatening Streptococcus infection: evolutionary implications. J Infect 2007; 54: 410.
[3] Asleh R, Briasoulis A, Berinstein E M, Wiener J B, Palla M, Kushwaha S S, Levy A P. Meta-analysis of the association of the haptoglobin genotype with cardiovascular outcomes and the pharmacogenomic interactions with vitamin E supplementation. Pharmgenomics Pers Med. 2018 Apr 23; 11: 71-82. doi: 10.2147/PGPM.S159454.
[4] Blum S, Asaf R, Guetta J, et al. Haptoglobin genotype determines myocardial infarct size in diabetic mice. J Am Coll Cardiol 2007; 49: 82-87.
[5] Yilmaz T, Koçan EG, Besler HT, Yilmaz G, Gusel B. The role of oxidants and antioxidants in otitis media with effusion in children. Otolaryngol Head Neck Surg 2004; 131: 797-803.
[6] Teran LM, Johnston SL, Schröder JM, Church MK, Holgate ST Role of nasal interleukin-8 in neutrophil recruitment and activation in children with virus-induced asthma. Am J Respir Crit Care Med 1997; 155: 1362-6.
[7] Marlow R, Finn A, Henderson J. Assessing the association between bronchiolitis in infancy and recurrent wheeze: a whole English birth cohort case-control study. Thorax. 2019; 74 (5): 503-505. doi: 10.1136/thoraxjnl-2018-212203.
[8] Kessel I, Leib M, Levy A, et al. Does haptoglobin phenotype influence postnatal morbidity in preterm neonates? Am J Perinatol 2016; 33: 130-5.
[9] Cheong JL, Doyle LW. An update on pulmonary and neurodevelopmental outcomes of bronchopulmonary dysplasia. Semin Perinatol 2018; 42: 478-484.
[10] Todorović MM, Zvrko EZ. Immunoregulatory cytokines and chronic tonsillitis. Bosn J Basic Med Sci 2013; 13: 230-6.
[11] Cemek M, Caksen H, Bayiroğlu F, Cemek F, Dede S. Oxidative stress and enzymic-non-enzymic antioxidant responses in children with acute pneumonia. Cell Biochem Funct 2006; 24: 269-73.
[12] Cemek M, Dede S, Bayiroğlu F, Caksen H, Cemek F, Yuca K. Oxidant and antioxidant levels in children with acute otitis media and tonsillitis: a comparative study. Int J Pediatr Otorhinolaryngol 2005; 69: 823-7.
[13] Vaidya NA, Bulakh PM. Antioxidant enzymes and antioxidants in children with pneumonia. J Dent Med Scienc 2013; 8: 01-05.
[14] Scharer G, Zaldivar F, Gonzalez G, Vargas-Shiraishi O, Singh J, Arrieta A. Systemic inflammatory responses in children with acute otitis media due to Streptococcus pneumoniae and the impact of treatment with clarithromycin. Clin Diagn Lab Immunol 2003; 10: 721-4.
[15] Giuffrida MJ, Valero N, Mosquera J et al. Increased systemic cytokine/chemokine expression in asthmatic and non-asthmatic patients with bacterial, viral or mixed lung infection. Scand J Immunol 2017; 85: 280-290.
[16] Speeckaert R, Speeckaert MM, Padalko E, Claeys LR, Delanghe JR. The Hp phenotype is associated with the Epstein-Barr virus antibody titer. Clin Chem Lab Med 2009; 47: 826-8.
[17] Bachert C, van Kempen MJ, Höpken K, Holtappels G, Wagenmann M. Elevated levels of myeloperoxidase, pro-inflammatory cytokines and chemokines in naturally acquired upper respiratory tract infections. Eur Arch Otorhinolaryngol 2001; 258: 406–412.
[18] Klemens C, Rasp G, Jund F, et al. Mediators and cytokines in allergic and viral-triggered rhinitis. Allergy Asthma Proc 2007; 28: 434-441.
[19] Emonts M, Veenhoven RH, Wiertsema SP, et al. Genetic polymorphisms in immune response genes TNFA, IL6, IL10, and TLR4 are associated with recurrent acute otitis media. Pediatrics 2007; 120: 814-23.
[20] Rudack C, Jörg S, Sachse F. Biologically active neutrophil chemokine pattern in tonsillitis. Clin Exp Immunol 2004; 135: 511-8.
[21] RenataY, Jassar H, Katz R, Hochberg A, Nir RR, Klein-Kremer A. Urinary concentration of cytokines in children with acute pyelonephritis. Eur J Pediatr 2013; 172: 769-74.
[22] Yang F, Ghio AJ, Herbert DC, Weaker FJ, Walter CA, Coalson JJ. Pulmonary expression of the human haptoglobin gene. Am J Respir Cell Mol Biol 2000; 23: 277–282.
[23] Papp M, Foldi I, Nemes E, et al. Haptoglobin polymorphism: a novel genetic risk factor for celiac disease development and its clinical manifestations. Clin Chem 2008; 54: 697-704.
[24] Speer CP. Pulmonary inflammation and bronchopulmonary dysplasia. J Perinatol 2006; 26: S57–S62.
[25] Bogdan RD, Rusu L, Toma AL, Natase L. Respiratory Outcome of the Former Premature Infants. J Med Life. 2019; 12 (4): 381-394. doi: 10.25122/jml-2019-0123.
Cite This Article
  • APA Style

    Irena Kessel, Michal Molad, Rada Nemirovsky, Keren Lavie-Nevo, Andrew Peter Levy, et al. (2020). Haptoglobin Polymorphism and Morbidity in Children Born Prematurely. American Journal of Pediatrics, 6(1), 73-77. https://doi.org/10.11648/j.ajp.20200601.23

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    ACS Style

    Irena Kessel; Michal Molad; Rada Nemirovsky; Keren Lavie-Nevo; Andrew Peter Levy, et al. Haptoglobin Polymorphism and Morbidity in Children Born Prematurely. Am. J. Pediatr. 2020, 6(1), 73-77. doi: 10.11648/j.ajp.20200601.23

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    AMA Style

    Irena Kessel, Michal Molad, Rada Nemirovsky, Keren Lavie-Nevo, Andrew Peter Levy, et al. Haptoglobin Polymorphism and Morbidity in Children Born Prematurely. Am J Pediatr. 2020;6(1):73-77. doi: 10.11648/j.ajp.20200601.23

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  • @article{10.11648/j.ajp.20200601.23,
      author = {Irena Kessel and Michal Molad and Rada Nemirovsky and Keren Lavie-Nevo and Andrew Peter Levy and Shany Blum and Avi Rotschild},
      title = {Haptoglobin Polymorphism and Morbidity in Children Born Prematurely},
      journal = {American Journal of Pediatrics},
      volume = {6},
      number = {1},
      pages = {73-77},
      doi = {10.11648/j.ajp.20200601.23},
      url = {https://doi.org/10.11648/j.ajp.20200601.23},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajp.20200601.23},
      abstract = {Haptoglobin (Hp) is an acute phase protein. There exists three different Hp phenotypes that differ in their pro-inflammatory and anti-inflammatory action. Inflammation and oxidative stress are critically involved in many pathophysiological processes in childhood. We previously reported on the relationship of in-hospital clinical events and the Hp phenotype in a cohort of consecutive premature infants. This study provides follow up of childhood morbidity data and its relationship to the Hp phenotype for the previously reported study premature infant cohort. A phone questionnaire was carried out among the parents and medical history records were evaluated. The age of participants varied from eight to eleven years. The questionnaire included information about diseases with an inflammatory component in pathogenesis, infections and need for hospitalization. Of the original 122 study participants, morbidity data at eight to eleven years was available for 101 participants, and 100 were enrolled in the study. A less anti-inflammatory Hp phenotype (Hp 2-2) was more prevalent in participants who suffered from diseases with an inflammatory component in their pathogenesis (RTI, pneumonia, UTI, OM and tonsillitis) when these entities were analyzed as a group (p=0.043). Subsequent comparison of the cumulative number of episodes of these entities between Hp phenotypes during all follow up period detected a trend in the same direction. Further research involving a larger population is required for better understanding of the Hp phenotype role in infantile and pediatric morbidity.},
     year = {2020}
    }
    

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  • TY  - JOUR
    T1  - Haptoglobin Polymorphism and Morbidity in Children Born Prematurely
    AU  - Irena Kessel
    AU  - Michal Molad
    AU  - Rada Nemirovsky
    AU  - Keren Lavie-Nevo
    AU  - Andrew Peter Levy
    AU  - Shany Blum
    AU  - Avi Rotschild
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    DO  - 10.11648/j.ajp.20200601.23
    T2  - American Journal of Pediatrics
    JF  - American Journal of Pediatrics
    JO  - American Journal of Pediatrics
    SP  - 73
    EP  - 77
    PB  - Science Publishing Group
    SN  - 2472-0909
    UR  - https://doi.org/10.11648/j.ajp.20200601.23
    AB  - Haptoglobin (Hp) is an acute phase protein. There exists three different Hp phenotypes that differ in their pro-inflammatory and anti-inflammatory action. Inflammation and oxidative stress are critically involved in many pathophysiological processes in childhood. We previously reported on the relationship of in-hospital clinical events and the Hp phenotype in a cohort of consecutive premature infants. This study provides follow up of childhood morbidity data and its relationship to the Hp phenotype for the previously reported study premature infant cohort. A phone questionnaire was carried out among the parents and medical history records were evaluated. The age of participants varied from eight to eleven years. The questionnaire included information about diseases with an inflammatory component in pathogenesis, infections and need for hospitalization. Of the original 122 study participants, morbidity data at eight to eleven years was available for 101 participants, and 100 were enrolled in the study. A less anti-inflammatory Hp phenotype (Hp 2-2) was more prevalent in participants who suffered from diseases with an inflammatory component in their pathogenesis (RTI, pneumonia, UTI, OM and tonsillitis) when these entities were analyzed as a group (p=0.043). Subsequent comparison of the cumulative number of episodes of these entities between Hp phenotypes during all follow up period detected a trend in the same direction. Further research involving a larger population is required for better understanding of the Hp phenotype role in infantile and pediatric morbidity.
    VL  - 6
    IS  - 1
    ER  - 

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Author Information
  • Department of Neonatology, Carmel Medical Center, Haifa, Israel; Rappaport School of Medicine, Technion–Israel Institute of Technology, Haifa, Israel

  • Department of Neonatology, Carmel Medical Center, Haifa, Israel

  • Department of Pediatrics, Carmel Medical Center, Haifa, Israel

  • Department of Neonatology, Carmel Medical Center, Haifa, Israel; Rappaport School of Medicine, Technion–Israel Institute of Technology, Haifa, Israel

  • Department of Cardiovascular Biology, Rappaport School of Medicine, Technion–Israel Institute of Technology, Haifa, Israel

  • Department of Cardiovascular Biology, Rappaport School of Medicine, Technion–Israel Institute of Technology, Haifa, Israel

  • Department of Neonatology, Carmel Medical Center, Haifa, Israel; Rappaport School of Medicine, Technion–Israel Institute of Technology, Haifa, Israel

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