Ficolin-1 gene (FCN1) -144 C/A polymorphism is associated with adverse outcome of severe pneumonia in the under-five Egyptian children: A multicenter study.

BACKGROUND: Pneumonia is the foremost cause of child death worldwide. M-ficolin is encoded by the FCN1 gene and represents a novel link between innate and adaptive immunity. OBJECTIVES: To investigate the FCN1 -144 C/A (rs10117466) polymorphism as a potential marker for pneumonia severity and adverse outcome namely complications or mortality in the under-five Egyptian children. METHODS: This was a prospective multicenter study that included 620 children hospitalized with World Health Organization-defined severe pneumonia and 620 matched healthy control children. Polymorphism rs10117466 of the FCN1 gene promoter was analyzed by PCR-SSP, while serum M-ficolin levels were assessed by ELISA. RESULTS: The FCN1 A/A genotype and A allele at the -144 position were more frequently observed in patients compared to the control children (43.4% vs 27.6%; odds ratio [OR]: 1.62; [95% confidence interval {CI}: 1.18-2.2]; for the A/A genotype) and (60.8% vs 52.5%; OR: 1.4; [95% CI: 1.19-1.65]; for the A allele); P < .01. The FCN1 -144 A/A homozygous patients had significantly higher serum M-ficolin concentrations (mean: 1844 ± 396 ng/mL) compared with those carrying the C/C or C/A genotype (mean: 857 ± 278 and 1073 ± 323 ng/mL, respectively; P = .002). FCN1 -144 A/A genotype was an independent risk factor for adverse outcomes in children with severe pneumonia (adjusted OR = 4.85, [95% CI: 2.96-10.25]; P = .01). CONCLUSION: The FCN1 A/A genotype at the -144 position was associated with high M-ficolin serum levels and possibly contributes to enhanced inflammatory response resulting in the adverse outcome of pneumonia in the under-five Egyptian children.

Serum SP-D levels as a biomarker of lung injury in children suffering of bronchopneumonia.

The efficacy of SP-D concentration as a useful biomarker of the severity of lung injury in children with bronchopneumonia with or without chronic airway disease was studied. A total of 48 patients (2 to 4 years old) diagnosed bronchopneumonia were admitted to Department of Pediatrics, Al-Dar hospital, Al-Madinah, Saudi Arabia over the year 2009. They were divided into two groups: G1 included patients without any underlying disease and G2 included asthmatic patients. They were assigned to one of three categories. Stage A patients without oxygen dosage, Stage B patients required oxygen dosage, and Stage C patients required ICU admission. We evaluated baseline characteristics, clinical features, and serum SP-D concentration in G1, G2, and G3a (healthy control cross-matched infants). The mean serum SP-D concentrations in G1 and G2 were higher than those in G3 (118.7 +/- 46.2 & 39.7 +/- 18.7 ng/ml, respectively), but also higher in G2 than in G1 (149.9 +/- 52.8 & 109.8 + 36.7 ng/ml, respectively). The mean serum SP-D concentrations were higher in Stage C than in Stages A or B patients, and mean serum SP-D concentrations were higher in Stage B than in Stage A.

Placental alkaline phosphatase activity and its relation to foetal growth and nutrition in appropriate and small for gestational age newborns at term.

The placental alkaline phosphatase (PAP) activity progressively rises as pregnancy advances, possibly, because of its increasing synthesis by placental tissue. The present study examined the relationship between placental alkaline phosphatase activity and the biochemical indices of foetal nutrition (cord blood glucose, albumin) and growth (neonatal birth weight). Placental and umbilical cord blood samples were collected from 56 term deliveries 30 of them were appropriate for gestational age (AGA) and 26 were small for gestational age(SGA) and prepared for placental alkaline phosphatase assay, glucose and albumin estimations using standard procedures. The birth weights of the neonates at term were taken and recorded. Correlation analyses of the data obtained show significant positive relationships between PAP and cord blood glucose, albumin and birth weight in AGA newborn (r2 = 0.86, 0.71, 0.68 p<0.05) and (r2 = 0.69, 0.81, 0.73 p<0.05) in SGA newborn but no significant relationship with gestational age, also there was significant statistical difference between both groups in level of PAP, glucose and albumin.

Influence of serum cortisol levels on glycemic control in children with type 1 diabetes.

The association between plasma glucose (PG), HbA1c and serum cortisol levels in children with type 1 diabetes was investigated to determine the influence of serum cortisol on their glycemic control. A total of 45 children, aged 10-15 years, with type 1 diabetes for at least 3 years of diabetes were studied. Most of them did not have pancreatic beta-cell function. The cortisol levels among all patients were stratified according to fasting plasma glucose levels (50-99, 100-199, 200-299, & > or = 300 mg/dL), and the HbAlc levels (<7.0, 7.0-7.9, 8.0-8.9, & > or = 9%). The mean fasting PG, HbA1c and serum cortisol levels were 174 +/- 97 mg/dL, 7.7 +/- 1.3% and 23.04 +/- 16.6 ug/dl, respectively. The cortisol levels were highly correlated with PG levels (r =0.553, P < 0.0001) and mildly correlated with HbA1c levels (r=0.301, P=0.0192). Patients with high PG levels gave significantly higher cortisol levels as compared to those with lower PG levels (18.4 +/- 7.3, 26.8 +/- 18.3, 31.4 +/- 17.0 & 36.3 +/- 17.2ug/dl, P=0.0009). There were no significant differences in serum cortisol levels among patients stratified according to HbA1c levels (P=0.1566), however, patients with HbA1c levels > or = 9% had significantly higher cortisol levels than those with HbA1c levels<7% (32.6 +/- 14.4 vs. 21.8 +/- 11.3ug/dl, P=0.0291).