Association of Single-Nucleotide Polymorphisms of C-Reactive Protein Gene with Susceptibility to Infantile Sepsis in Southern China.

BACKGROUND C-reactive protein (CRP) is an important biomarker of sepsis. Several single-nucleotide polymorphisms (SNPs) in the CRP gene can determine plasma CRP levels and are risk factors in many diseases, such as cancer, arteritis, and diabetes. However, it is unknown whether polymorphisms in CRP are associated with susceptibility to and outcome of infantile sepsis. We explored the effect of these SNPs on CRP response in infantile sepsis, and compared genetic data on patients with sepsis. MATERIAL AND METHODS A total of 49 infants with sepsis and 20 healthy infants were enrolled during hospitalization, and 3 SNPs in the CRP gene region (rs1205, rs2808530, and rs3091244) were genotyped and then analyzed for associations with CRP levels and sepsis. RESULTS The CRP means concentration results showed that mean CRP concentration was different in the 4 groups (healthy, sepsis, severe sepsis, and septic shock) and was positively correlated with the severity of infantile sepsis. There was also a difference in CRP SNP rs1205 between infants with septic shock and healthy infants, and between infants with septic shock and infants with sepsis. No differences were observed in SNP rs2808630 and SNP rs3091244. CONCLUSIONS Our study suggests that rs1205 genetic variability in the CRP gene determines the CRP levels in sepsis of different severities, while SNP rs3091244 and SNP rs2808630 are not associated with sepsis. However, the results of the present study on SNP rs1205, rs3091244, and rs2808630 in the CRP gene should be interpreted with caution due to limited sample size and sample heterogeneity. Large-scale, well-designed studies are needed to validate our findings.

Erythema Multiforme Major Associated With Community-Acquired Pneumonia: Lessons From a Case Report.

Background: Erythema multiforme (EM) is an acute immune-mediated inflammatory mucinous skin disorder. The etiology of pediatric EM involves infections, medications, autoimmune diseases, and genetic factors. Case Report: An 8-year-old girl with Mycoplasma pneumoniae (MP) associated community-acquired pneumonia developed erythema target-like symptoms 1 week after azithromycin administration. The erythema quickly spread throughout the body involving the oral and ocular mucous membranes, the trunk, and the extremities, and eventually developed into erythema multiform major (EMM). Through drug withdrawal and specific treatment including systemic corticosteroids and supportive care, her clinical symptoms were improved. After 31 days, most of the mucocutaneous symptoms were relieved, except pigmentation. Human leukocyte antigen (HLA) gene sequencing was performed and 20 HLA genotypes were identified. The patient follow-up lasted for 18 months. Rashes appeared on her trunk when receiving azithromycin orally after discharge and then disappeared after azithromycin withdrawal. Conclusions: Pediatric EM is a rare disease and recognition of its etiology is important for EM management. In this case, azithromycin and HLA-DQB1 * 03:01 genotype may contribute to EMM. Lesson: For drug-induced EM, rapid identification and withdrawal of the causative drugs is critical. Re-exposure to the same drug or exposure to drugs with similar chemical structures should also be avoided. Patient education and rational use of medicines are essential for pediatric patients.

[CD11b expression in neutrophils and lymphocytes of children with systemic inflammatory response syndrome].

OBJECTIVE: To investigate the significance of CD11b expression in neutrophils and lymphocytes in children with systemic inflammatory response syndrome (SIRS). METHODS: CD11b expression in neutrophils and lymphocytes was measured using flow cytometry in 36 children with SIRS (SIRS group) and 28 children with infectious disease but without SIRS (control group). The sensitivity and specificity of neutrophil CD11b for diagnosis of SIRS were evaluated. RESULTS: During the acute phase, an increased CD11b expression in neutrophils (96.7+/-8.1%) was observed in the SIRS group compared with the control group (85.1+/-5.1%) (p<0.05). Using neutrophil CD11b expression >92.2% as a cut-off value for diagnosis of SIRS, the sensitivity and the specificity were 97.2 % and 92.9% respectively. Lymphocytic CD11b expression in the SIRS group (13.4+/-8.6%) was lower than that in the control group (19.2+/-6.4%) in the acute phase (p<0.05). In the SIRS group, lymphocytic CD11b expression was remarkably suppressed in the severe sepsis subgroup (7.27+/-3.04%), showing significantly decreased expression compared with the non-infectious subgroup (19.3+/-2.9%) and the sepsis subgroup (15.9+/-12.5%) (p<0.01). In the convalescence stage lymphocytic CD11b expression in the SIRS group was similar to that in the control group. CONCLUSIONS: CD11b expression in neutrophils may serve as a reliable indicator for diagnosis of SIRS. The down-regulation of lymphocytic CD11b expression might be a signal of the condition aggravation in children with SIRS.

Kawasaki Disease Complicated With Macrophage Activation Syndrome: Case Reports and Literature Review.

Macrophage activation syndrome (MAS) is a rare and severe complication of Kawasaki disease (KD). The clinical feature, early diagnosis and treatment options, and prognosis need to be further determined in patients with KD complicated with MAS. In this report, we retrospectively analyzed three KD patients complicated with MAS who were treated in pediatric intensive care units (PICU) and reviewed the relevant literatures. We find that being male, being age over 2 years old, incomplete KD, intravenous immunoglobulin (IVIG) non-responder, or persistent fever greater than 10 days are all highly associated with occurrence of MAS. Additional work-ups should be performed promptly in patient with above predisposing factors to rule out complication of MAS. Patients with KD complicated with MAS are at a higher risk of having coronary artery involvement or aneurysm formation, which can be reversed with timely treatment. Early identification and prompt treatment are key points for improving the prognosis of KD patients complicated with MAS.

[Relationship between soluble intercellular adhesion molecule-1 and severe pneumonia].

OBJECTIVE: It has been reported that soluble intercellular adhesion molecule-1 (sICAM-1) participates in many immune and inflammatory reactions. Its expression and role in severe pneumonia has not fully been understood. This study aimed to investigate the changes of sICAM-1 expression in severe pneumonia and the relationship between sICAM-1 and severe pneumonia in children. METHODS: Serum sICAM-1 levels were determined by the double antibody sand using ELISA in 50 children with severe pneumonia and 56 children with mild pneumonia. Fifty-two healthy children served as control group. RESULTS: Serum sICAM-1 levels in children with severe pneumonia (402.36 +/- 31.24 mu g/L) were remarkably higher than those in the mild pneumonia group (278.86 +/- 36.24 mu g/L) at the acute stage and higher than in the control group (180.74 +/- 21.46 mu g/L) (P < 0.01). Serum sICAM-1 levels in children with severe pneumonia decreased significantly at the recovery stage (198.56 +/- 12.63 mu g/L) (P < 0.01), which were not statistically different from those in the mild pneumonia group at the recovery stage and the control group. There were no significant differences in serum sICAM-1 levels among the severe pneumonia subgroups caused by different pathogens (bacteria, virus or Mycoplasma) at the acute stage. Serum sICAM-1 levels at the acute stage in children with severe pneumonia who were treated successfully were not significantly different from those in patients whose symptoms were partly improved. CONCLUSIONS: sICAM-1 might be involved in the inflammation course of severe pneumonia. It can severe as a marker of the diagnosis and the severity evaluation of severe pneumonia.