Skip to main content
Erschienen in: Inflammation 5/2014

01.10.2014

High Serum Trypsin Levels and the −409 T/T Genotype of PRSS1 Gene Are Susceptible to Neonatal Sepsis

verfasst von: Qingquan Chen, Heng Xue, Min Chen, Feng Gao, Jianping Xu, Qicai Liu, Xiulin Yang, Lie Zheng, Hong Chen

Erschienen in: Inflammation | Ausgabe 5/2014

Einloggen, um Zugang zu erhalten

Abstract

Neonatal sepsis remains an important and common cause of morbidity and mortality among newborn infants, especially in developing countries. The aim of the present study was to determine whether serum trypsin levels and genotypes of cationic trypsinogen (PRSS1) gene could be served as markers for predicting neonatal sepsis. The serum trypsin levels and genotypes of PRSS1 were examined in both 50 infants with infection during neonatal period and 56 healthy neonates as controls. The infected infants were further subdivided into infants with sepsis group (n = 18) and infected infants without sepsis (n = 32). The genotype of PRSS1 was analyzed by direct sequencing, and the serum trypsin level was measured by immunoassay. It showed that the median value of serum trypsin was significantly higher in infected infants (31.90 ng/mL) than in controls (12.85 ng/mL; P = 0.030). More importantly, sepsis subgroup (50.95 ng/mL) had significantly higher median serum trypsin than infected infants without sepsis subgroup (19.10 ng/mL) and controls (12.85 ng/mL) (P = 0.015 and P = 0.002, respectively). Additionally, the median serum trypsin levels were found significantly higher in infants who had T/T (37.90 ng/mL) genotype of PRSS1 compared with those who had C/T genotype (12.80 ng/mL; P = 0.005). This study suggested that serum trypsin and rs10273639 C/T of PRSS1 were revealed to be novel markers for predicting neonatal sepsis.
Literatur
1.
Zurück zum Zitat Lawn, J.E., S. Cousens, and J. Zupan. 2005. 4 million neonatal deaths: when? where? why? Lancet 365: 891–900.PubMedCrossRef Lawn, J.E., S. Cousens, and J. Zupan. 2005. 4 million neonatal deaths: when? where? why? Lancet 365: 891–900.PubMedCrossRef
2.
Zurück zum Zitat Chan, D.K., and L.Y. Ho. 1997. Usefulness of C-reactive protein in the diagnosis of neonatal sepsis. Singapore Medical Journal 38: 252–255.PubMed Chan, D.K., and L.Y. Ho. 1997. Usefulness of C-reactive protein in the diagnosis of neonatal sepsis. Singapore Medical Journal 38: 252–255.PubMed
3.
Zurück zum Zitat Vasiljevic, B., O. Antonovic, S. Maglajlic-Djukic, and M. Gojnic. 2008. The serum level of C-reactive protein in neonatal sepsis. Srpski Arhiv za Celokupno Lekarstvo 136: 253–257.PubMedCrossRef Vasiljevic, B., O. Antonovic, S. Maglajlic-Djukic, and M. Gojnic. 2008. The serum level of C-reactive protein in neonatal sepsis. Srpski Arhiv za Celokupno Lekarstvo 136: 253–257.PubMedCrossRef
4.
Zurück zum Zitat Ruiz-Alvarez, M.J., S. Garcia-Valdecasas, R. De Pablo, M. Sanchez Garcia, C. Coca, T.W. Groeneveld, et al. 2009. Diagnostic efficacy and prognostic value of serum procalcitonin concentration in patients with suspected sepsis. Journal of Intensive Care Medicine 24: 63–71.PubMedCrossRef Ruiz-Alvarez, M.J., S. Garcia-Valdecasas, R. De Pablo, M. Sanchez Garcia, C. Coca, T.W. Groeneveld, et al. 2009. Diagnostic efficacy and prognostic value of serum procalcitonin concentration in patients with suspected sepsis. Journal of Intensive Care Medicine 24: 63–71.PubMedCrossRef
5.
Zurück zum Zitat Angeletti, S., F. Battistoni, M. Fioravanti, S. Bernardini, and G. Dicuonzo. 2013. Procalcitonin and mid-regional pro-adrenomedullin test combination in sepsis diagnosis. Clinical Chemistry and Laboratory Medicine: CCLM/FESCC 51: 1059–1067.CrossRef Angeletti, S., F. Battistoni, M. Fioravanti, S. Bernardini, and G. Dicuonzo. 2013. Procalcitonin and mid-regional pro-adrenomedullin test combination in sepsis diagnosis. Clinical Chemistry and Laboratory Medicine: CCLM/FESCC 51: 1059–1067.CrossRef
6.
Zurück zum Zitat Gerrits, J.H., P.M. McLaughlin, B.N. Nienhuis, J.W. Smit, and B. Loef. 2013. Polymorphic mononuclear neutrophils CD64 index for diagnosis of sepsis in postoperative surgical patients and critically ill patients. Clinical Chemistry and Laboratory Medicine: CCLM/FESCC 51: 897–905.CrossRef Gerrits, J.H., P.M. McLaughlin, B.N. Nienhuis, J.W. Smit, and B. Loef. 2013. Polymorphic mononuclear neutrophils CD64 index for diagnosis of sepsis in postoperative surgical patients and critically ill patients. Clinical Chemistry and Laboratory Medicine: CCLM/FESCC 51: 897–905.CrossRef
7.
Zurück zum Zitat de Benedetti, F., C. Auriti, L.E. D’Urbano, M.P. Ronchetti, L. Rava, A. Tozzi, et al. 2007. Low serum levels of mannose binding lectin are a risk factor for neonatal sepsis. Pediatric Research 61: 325–328.PubMedCrossRef de Benedetti, F., C. Auriti, L.E. D’Urbano, M.P. Ronchetti, L. Rava, A. Tozzi, et al. 2007. Low serum levels of mannose binding lectin are a risk factor for neonatal sepsis. Pediatric Research 61: 325–328.PubMedCrossRef
8.
Zurück zum Zitat Abu-Maziad, A., K. Schaa, E.F. Bell, J.M. Dagle, M. Cooper, M.L. Marazita, et al. 2010. Role of polymorphic variants as genetic modulators of infection in neonatal sepsis. Pediatric Research 68: 323–329.PubMedCrossRef Abu-Maziad, A., K. Schaa, E.F. Bell, J.M. Dagle, M. Cooper, M.L. Marazita, et al. 2010. Role of polymorphic variants as genetic modulators of infection in neonatal sepsis. Pediatric Research 68: 323–329.PubMedCrossRef
9.
Zurück zum Zitat Ozkan, H., N. Koksal, M. Cetinkaya, S. Kilic, S. Celebi, B. Oral, et al. 2012. Serum mannose-binding lectin (MBL) gene polymorphism and low MBL levels are associated with neonatal sepsis and pneumonia. Journal of Perinatology: Official Journal of the California Perinatal Association 32: 210–217.CrossRef Ozkan, H., N. Koksal, M. Cetinkaya, S. Kilic, S. Celebi, B. Oral, et al. 2012. Serum mannose-binding lectin (MBL) gene polymorphism and low MBL levels are associated with neonatal sepsis and pneumonia. Journal of Perinatology: Official Journal of the California Perinatal Association 32: 210–217.CrossRef
10.
Zurück zum Zitat Wahab Mohamed, W.A., and M.A. Saeed. 2012. Mannose-binding lectin serum levels in neonatal sepsis and septic shock. The Journal of Maternal-Fetal & Neonatal Medicine: the Official Journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstet 25: 411–414.CrossRef Wahab Mohamed, W.A., and M.A. Saeed. 2012. Mannose-binding lectin serum levels in neonatal sepsis and septic shock. The Journal of Maternal-Fetal & Neonatal Medicine: the Official Journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstet 25: 411–414.CrossRef
11.
Zurück zum Zitat Seitz, C., B. Isken, B. Heynisch, M. Rettkowski, T. Frensing, and U. Reichl. 2012. Trypsin promotes efficient influenza vaccine production in MDCK cells by interfering with the antiviral host response. Applied Microbiology and Biotechnology 93: 601–611.PubMedCrossRef Seitz, C., B. Isken, B. Heynisch, M. Rettkowski, T. Frensing, and U. Reichl. 2012. Trypsin promotes efficient influenza vaccine production in MDCK cells by interfering with the antiviral host response. Applied Microbiology and Biotechnology 93: 601–611.PubMedCrossRef
12.
Zurück zum Zitat Kaljot, K.T., R.D. Shaw, D.H. Rubin, and H.B. Greenberg. 1988. Infectious rotavirus enters cells by direct cell membrane penetration, not by endocytosis. Journal of Virology 62: 1136–1144.PubMedPubMedCentral Kaljot, K.T., R.D. Shaw, D.H. Rubin, and H.B. Greenberg. 1988. Infectious rotavirus enters cells by direct cell membrane penetration, not by endocytosis. Journal of Virology 62: 1136–1144.PubMedPubMedCentral
13.
Zurück zum Zitat Tsujimura, S., K. Saito, S. Nakayamada, and Y. Tanaka. 2008. Bolus infusion of human urinary trypsin inhibitor improves intractable interstitial pneumonia in patients with connective tissue diseases. Rheumatology (Oxford) 47: 907–913.CrossRef Tsujimura, S., K. Saito, S. Nakayamada, and Y. Tanaka. 2008. Bolus infusion of human urinary trypsin inhibitor improves intractable interstitial pneumonia in patients with connective tissue diseases. Rheumatology (Oxford) 47: 907–913.CrossRef
14.
Zurück zum Zitat Levy, M.M., A. Artigas, G.S. Phillips, A. Rhodes, R. Beale, T. Osborn, et al. 2012. Outcomes of the surviving sepsis campaign in intensive care units in the USA and Europe: a prospective cohort study. The Lancet Infectious Diseases 12: 919–924.PubMedCrossRef Levy, M.M., A. Artigas, G.S. Phillips, A. Rhodes, R. Beale, T. Osborn, et al. 2012. Outcomes of the surviving sepsis campaign in intensive care units in the USA and Europe: a prospective cohort study. The Lancet Infectious Diseases 12: 919–924.PubMedCrossRef
15.
Zurück zum Zitat Patuzzo, C., C. Castellani, C. Sagramoso, M. Gomez-Lira, D. Bonamini, F. Belpinati, et al. 2003. Cationic trypsinogen and pancreatic secretory trypsin inhibitor gene mutations in neonatal hypertrypsinaemia. European Journal of Human Genetics: EJHG 11: 93–96.PubMedCrossRef Patuzzo, C., C. Castellani, C. Sagramoso, M. Gomez-Lira, D. Bonamini, F. Belpinati, et al. 2003. Cationic trypsinogen and pancreatic secretory trypsin inhibitor gene mutations in neonatal hypertrypsinaemia. European Journal of Human Genetics: EJHG 11: 93–96.PubMedCrossRef
16.
Zurück zum Zitat Itkonen, O., E. Koivunen, M. Hurme, H. Alfthan, T. Schroder, and U.H. Stenman. 1990. Time-resolved immunofluorometric assays for trypsinogen-1 and 2 in serum reveal preferential elevation of trypsinogen-2 in pancreatitis. The Journal of Laboratory and Clinical Medicine 115: 712–718.PubMed Itkonen, O., E. Koivunen, M. Hurme, H. Alfthan, T. Schroder, and U.H. Stenman. 1990. Time-resolved immunofluorometric assays for trypsinogen-1 and 2 in serum reveal preferential elevation of trypsinogen-2 in pancreatitis. The Journal of Laboratory and Clinical Medicine 115: 712–718.PubMed
17.
Zurück zum Zitat Oiva, J., O. Itkonen, R. Koistinen, K. Hotakainen, W.M. Zhang, E. Kemppainen, et al. 2011. Specific immunoassay reveals increased serum trypsinogen 3 in acute pancreatitis. Clinical Chemistry 57: 1506–1513.PubMedCrossRef Oiva, J., O. Itkonen, R. Koistinen, K. Hotakainen, W.M. Zhang, E. Kemppainen, et al. 2011. Specific immunoassay reveals increased serum trypsinogen 3 in acute pancreatitis. Clinical Chemistry 57: 1506–1513.PubMedCrossRef
18.
Zurück zum Zitat Itkonen, O., L. Kylanpaa, W.M. Zhang, and U.H. Stenman. 2012. Reference intervals for and validation of recalibrated immunoassays for trypsinogen-1 and trypsinogen-2. Clinical Chemistry 58: 1494–1496.PubMedCrossRef Itkonen, O., L. Kylanpaa, W.M. Zhang, and U.H. Stenman. 2012. Reference intervals for and validation of recalibrated immunoassays for trypsinogen-1 and trypsinogen-2. Clinical Chemistry 58: 1494–1496.PubMedCrossRef
19.
Zurück zum Zitat Gao, F., Y.M. Li, G.L. Hong, Z.F. Xu, Q.C. Liu, Q.L. He, et al. 2013. PRSS1_p.Leu81Met mutation results in autoimmune pancreatitis. World Journal of Gastroenterology: WJG 19: 3332–3338.PubMedCrossRefPubMedCentral Gao, F., Y.M. Li, G.L. Hong, Z.F. Xu, Q.C. Liu, Q.L. He, et al. 2013. PRSS1_p.Leu81Met mutation results in autoimmune pancreatitis. World Journal of Gastroenterology: WJG 19: 3332–3338.PubMedCrossRefPubMedCentral
20.
Zurück zum Zitat Gamble, D.R., A. Moffatt, and V. Marks. 1979. Serum immunoreactive trypsin concentrations in infectious and non-infectious illnesses and in juvenile diabetes. Journal of Clinical Pathology 32: 897–901.PubMedCrossRefPubMedCentral Gamble, D.R., A. Moffatt, and V. Marks. 1979. Serum immunoreactive trypsin concentrations in infectious and non-infectious illnesses and in juvenile diabetes. Journal of Clinical Pathology 32: 897–901.PubMedCrossRefPubMedCentral
21.
Zurück zum Zitat Liu, Q., X. Lin, J. Liu, A. Liu, and F. Gao. 2012. The −409 C/T genotype of PRSS1 protects against pancreatic cancer in the Han Chinese population. Digestive Diseases and Sciences 57: 573–579.PubMedCrossRef Liu, Q., X. Lin, J. Liu, A. Liu, and F. Gao. 2012. The −409 C/T genotype of PRSS1 protects against pancreatic cancer in the Han Chinese population. Digestive Diseases and Sciences 57: 573–579.PubMedCrossRef
22.
Zurück zum Zitat Whitcomb, D.C., J. LaRusch, A.M. Krasinskas, L. Klei, J.P. Smith, R.E. Brand, et al. 2012. Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis. Nature Genetics 44: 1349–1354.PubMedCrossRefPubMedCentral Whitcomb, D.C., J. LaRusch, A.M. Krasinskas, L. Klei, J.P. Smith, R.E. Brand, et al. 2012. Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis. Nature Genetics 44: 1349–1354.PubMedCrossRefPubMedCentral
Metadaten
Titel
High Serum Trypsin Levels and the −409 T/T Genotype of PRSS1 Gene Are Susceptible to Neonatal Sepsis
verfasst von
Qingquan Chen
Heng Xue
Min Chen
Feng Gao
Jianping Xu
Qicai Liu
Xiulin Yang
Lie Zheng
Hong Chen
Publikationsdatum
01.10.2014
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 5/2014
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-014-9904-3

Weitere Artikel der Ausgabe 5/2014

Inflammation 5/2014 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.