الفهرس 
NEONATAL SEPSISOnly 14 pages are availabe for public view
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Abstract
P
eroxisome proliferator-activated receptor-𝛾 (PPAR-) is a ligand-binding nuclear receptor, and its activation plays a prominent role in regulating the inflammatory response. Therefore, PPAR- has been suggested as a candidate gene for sepsis. In the present study, we investigated the association between the Pro12Ala polymorphism of PPAR- gene and sepsis disease severity in a sample of Egyptian neonates either premature or mature using Polymerase Chain Reaction.
This Study was a case control study which included 30 newly admitted neonates with neonatal sepsis at the intensive care unit (NICU) of Suez public hospital in the period from February 2015 till May 2015. Patients were 30 in number of (11 females and19 males) (mean age 10.30 ± 6.23)and the controls were 50 in number (23 females and 27 males)(mean age 10.20 ± 5.36)
This study included all neonates (preterm and term) of both gender with clinical signs and laboratory data consistent with neonatal sepsis according to the selected inclusion and exclusion criteria.
All of the patients were subjected to the following: detailed maternal and obstetric history taken from the parents of patient, gravidity and parity and obstetric history including mode of delivery, place of delivery, premature rupture of membrane > 18 hours, duration of labor, maternal pyrexia > 38°C or maternal illness. Gestational age was taken and confirmed by New Ballard score, birth weight. Onset of neonatal sepsis and duration of hospital stay was recorded. Then complete neonatal examination was done:
Newborns with evidence of at least one organ dysfunction (table 12) and those with at least 2 of the following 4 criteria defining systemic inflammatory response syndrome (SIRS) were included in the study.
Core temperature >38.5 or < 36.0°C.
Tachycardia, defined as a mean heart rate >2 SD above normal for age, and bradycardia, defined as a mean heart rate <10th percentile for age. Mean respiratory rate >2 SD above normal for age
All of the patients and controls were also subjected to Complete Blood Count, Erythrocyte Sedimentation Rate, C-reactive protein testing, Blood culture when indicated.
Then DNA extraction was done by DNA isolation from peripheral blood samples followed by the PPAR-𝛾 Pro12Ala genotyping. Genotype analysis of the samples was carried out by Tetra-primer ARMS-PCR method.
The aim of the study was trying to make a correlation between The Pro12Ala Polymorphism in - Gene and occurrence of neonatal sepsis and its severity and trying to find out the prevalence of PPAR- Gene polymorphism among the Egyptian samples in study.
There was no significant statistical difference as regards age and gender in both control and patients group, the mean value for CRP was30.00 ± 19.87 elevated, RBCs was 4.40 ± 1.10within normal, Hb was13.59 ± 3.14 within normal, WBCs was 12.17 ± 6.42 elevated, neutrophils% was49.28 ± 16.20 elevated, lymphocytes(%) was37.81 ± 14.52 elevated and monocytes(%) was 13.28 ± 9.50 elevated.
About 56.7% of the patients group was homozygote (GG) for polymorphic locus (coding for Alanine/Alanine) while 30% of the patients group was heterozygote for polymorphic locus (CG) (coding for Proline/Alanine) and about 13.3% of the patients group was homozygote for the polymorphic locus (CC) (coding for Proline/Proline). There was a strong relationship between the pro 12 Ala polymorphism in PPAR-g gene and occurrence of neonatal sepsis.
The incidence of wild type allele in homozygosity (CC) and in heterozygosity (CG) was 28.33% while the incidence of mutant allele in homozygosity (GG) and in heterozygosity (GC) was 71.67%. The tendency of allele G to segregate in homozygosity was more than allele C (56.66% vs. 13.33% The prevalence of genotypes among patients group compared to control group revealed that among patients group, the homozygote for GG was 56.7% followed by the heterozygote for CG genotype 30% then the homozygotes for CC genotype which appeared in a percentage of 13.3% compared to the control group where homozygotes for CC were the most prevalent (90%) and the CG were 10% with absence of GG genotypes.
So there was a strong statistical significant difference between patients with neonatal sepsis and the normal control group as regards prevalence of PPAR-g gene polymorphism in occurrence of neonatal sepsis and its severity. The percentage of C allele among patients group was 28.33% nearly equally distributed between homo- and heterozygosity while the G alleles among patients group was detected in 71.66% of with more tendency to be in homozygosity (56.66%). On the other hand, the percentage of G allele among control group was 5% and appeared in heterozygosity only, while the percentage of C allele among control group was 95% with more prevalence to be in homozygosity (90%), thus there is statistical significant difference between patients group and the control group which may suggest high risk for occurrence of neonatal sepsis and PPAR-g G allele. There was a significant statistical difference between genotypes in correlation with age but not significant for gender
There was significant statistical difference between alleles regarding age and neonatal sepsis (14 patient were early onset neonatal sepsis and 16 patient were late onset neonatal sepsis)While there was insignificant statistical difference between males and females and neonatal sepsis. Early and late neonatal sepsis occured more with G allele(14 early onset neonatal sepsis of whom 10 were homozygote GG and 2 were heterozygote CG and 16 late onset neonatal sepsis of whom 7 were homozygote GG and 7 were heterozygote CG. The difference between patients group was statistically insignificant for mean value of CRP, RBCS, HB, WBCs, neutrophils, lymphocytes and monocytes