Table 4. Scientific literature subjected to in-depth review.
Author | Year | Country | Patients | Controls | Findings |
---|---|---|---|---|---|
Aydemir et al.21 | 2011 | Turkey | 31 preterm infants with fungal septicemia | 30 preterm infants who had no invasive fungal infection | No association between codon 54 (B allele) polymorphism in exon 1 of the MBL gene and massive fungal sepsis |
Hartel et al.9 | 2011 | Germany | Cohort 1: 344 septic VLBW infants; Cohort 2: 555 septic VLBW infants | Cohort 1: 1600 non-septic VLBW infants; Cohort 2: 371 non-septic VLBW infants | No association between late onset sepsis and the SNP TNF- 308 G/A |
Abu-Maziad et al.22 | 2010 | USA | 79 preterm infants with sepsis | 202 preterm infants without sepsis | TLR2, TLR5, IL-10 and PLA2G2A polymorphisms predispose to sepsis in preterm infants |
Auriti et al.23 | 2010 | Italy | 42 neonates with sepsis | 85 neonates without infection | No association between the MBL2 genotypes and sepsis |
Koroglu et al.24 | 2010 | Turkey | Proven sepsis: 11 preterm newborns; Clinical sepsis: 42 preterm newborns | 57 preterm infants with no sepsis | No association between MBL polymorphism and culture-proven sepsis; however, a risk of clinical sepsis was shown |
Spiegler et al.25 | 2010 | Germany | 706 septic VLBW infants genotyped for ACE-ins/del genotype; 709 septic VLBW infants genotyped for ATR-1166A/C genotype | 503 non-septic VLBW infants genotyped for ACE-ins/del genotype;495 non-septic VLBW infants genotyped for ATR-1166A/C genotype | No impact of any renin-angiotensin system SNPs; no association was found between the ATR-1166A/C genotype or ACE-ins/del genotype and neonatal sepsis |
Abdel-Hady et al.26 | 2009 | Egypt | 54 septic full-term neonates | 70 non-septic matched full-term neonates | The IL-6 -174 and IL-10-1082 genotypes were not significantly different in neonates with bloodstream infections, compared with controls |
Bertalan et al.27 | 2008 | Hungary | 22 septic preterm neonates | 103 non-septic preterm neonates | BclI, N363S and ER22/23EK polymorphisms of the glucocorticoid receptor gene were not associated with risk of sepsis |
Reiman et al.28 | 2008 | Finland | 11 septic preterm VLBW infants | 96 non-septic preterm VLBW infants | Association between the IL-6-174 CC genotype and increased sepsis prevalence in VLBW infants |
Dzwonek et al.29 | 2008 | England/ Poland | 47 septic preterm infants | 111 non-septic preterm infants | Analyses of the effect of MBL genotype in newborns of gestational age < 28 weeks and birth weight < 1000 g did not show a statistically significant association with sepsis |
van der Zwet et al.30 | 2008 | Holland | Low MBL genotype: 8 septic neonates; Medium MBL genotype: 15 septic neonates; High MBL genotype: 41 septic neonates | Low MBL genotype: 30 non-septic neonates; Medium MBL genotype: 60 non-septic neonates High MBL genotype: 44 non-septic neonates | No relationship was found between MBL genotype and the risk of nosocomial sepsis |
Schueller et al.31 | 2006 | Germany | 67 preterm infants (< 32 weeks of gestation) and early-onset sepsis | 102 healthy newborns born after 32 weeks of gestation | No association between polymorphisms of TNF-308 and LTA +252 and early-onset sepsis in newborns with < 32 weeks of gestation. |
Derzbach et al.32 | 2006 | Hungary | 36 septic LBW infants | 89 non-septic LBW infants | No association was found between the polymorphisms E-selectin Ser128Arg, P-selectin Thr715Pro, L-selectin Pro213Ser and the risk of sepsis |
Hartel et al.33 | 2006 | Germany | 198 septic VLBW infants | 1008 non-septic VLBW infants | Higher rate of sepsis for carriers of factor XIII Val34Leu SNP |
Baier et al.34 | 2006 | Canada | 148 septic VLBW infants | 145 non-septic VLBW infants | The IL-6 -174C allele was associated with increased incidence of late bloodstream infection (BSI) in AA but not in Caucasian infants. The IL-10 -1082A allele was associated with increased incidence of late BSI. The CD14 -260 C/T SNP did not alter the overall risk of BSI in ventilated VLBW infants. |
Göpel et al.35 | 2006 | Germany | 97 VLBW infants who evolved with sepsis | 320 non-septic VLBW infants | No association between sepsis and IL-6-174 genetic polymorphism |
John Baier et al.36 | 2005 | Canada | 149 septic VLBW infants | 146 non-septic VLBW infants | The ACE I/D polymorphism did not have a significant effect on incidence of sepsis |
Hedberg et al.37 | 2004 | USA | 82 mechanically ventilated VLBW infants with late bacteremia | 91 mechanically ventilated VLBW infants without late bacteremia | The TNF-308 G/A SNP had no influence on the incidence of either early or late bacteremia or fungemia |
Ahrens et al.38 | 2004 | Germany | 50 septic VLBW infants | 306 non-septic VLBW infants | VLBW infants carrying the NOD2-3020ins C allele (n = 15) and the IL-6-174 G allele (n = 121) had a significantly higher rate of blood culture-proven sepsis. |
Bessler et al.39 | 2004 | Israel | 34 septic preterm LBW infants aged 24-35 weeks of gestation | 61 non-septic preterm LBW infants aged 24-35 weeks of gestation | No impact of IL-1ra genetic polymorphism on early onset sepsis |
Harding et al.40 | 2003 | England | 51 septic preterm infants aged < 32 weeks of gestation. | 106 non-septic preterm infants aged < 32 weeks of gestation. | Increased confirmed bacteriological sepsis with IL-6-174 GG allele |
Treszl et al.41 | 2003 | Hungary | 33 septic VLBW neonates | 35 non-septic VLBW neonates | TNF-308, IL-1β, IL-4 receptor α chain, IL-6 and IL-10 genes are not risk factors for sepsis in LBW infants |
VLBW = very low birth weight; LBL = low birth weight; BSI = bloodstream infection; MBL = mannose-binding lectin; TNF = tumor necrosis factor; IL-6 = interleukin 6; IL1β = interleukin 1β; IL-4 = interleukin 4; TLR2 = toll-like receptor 2; TLR5 = toll-like receptor 5; ACE I/D = angiotensin converting enzyme insertion/ deletion; ATR = angiotensin II type 1 receptor; PLA2G2A = phospholipase A2, group IIA; LTA = lymphotoxin alpha; SNP = single nucleotide polymorphism.