Prognostic analysis of children with Henoch-Schonlein purpura treated by Helicobacter pylori eradication therapy / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effect of Helicobacter pylori (Hp) eradication therapy on prognosis in children with Henoch-Schonlein purpura (HSP).</p><p><b>METHODS</b>A total of 153 children with HSP were divided into Hp infection treatment group (n=22), Hp infection control group (n=21), and Hp infection-negative group (n=110). The Hp infection treatment group received one-week triple therapy for Hp eradication in addition to conventional treatment, while the Hp infection control group and Hp infection-negative group received conventional treatment. All patients were followed up for prognostic evaluation.</p><p><b>RESULTS</b>The response rates of the Hp infection treatment, control, and negative groups were 86% (19/22), 90% (19/21) and 85% (94/110), respectively (P>0.05). The recurrence rates of HSP in the Hp infection treatment, control, and negative groups were 14% (3/22), 24% (5/21) and 31% (34/110), respectively (P>0.05). The incidence of Henoch-Schonlein purpura nephritis (HSPN) in the Hp infection-negative group (36%, 40/110) and control group (33%, 7/21) was significantly higher than that in the Hp infection treatment group (5%, 1/22) (P<0.05 for both), but no significant difference in the incidence of HSPN was found between the control and negative groups (P>0.05).</p><p><b>CONCLUSIONS</b>One-week triple therapy for Hp eradication may be useful to reduce the incidence of HSPN in children with HSP infected with Hp.</p>

Clinical features of children with acute focal bacterial nephritis / 中华实用儿科临床杂志

Objective To investigate the clinical features of acute focal bacterial nephritis (AFBN) in children,and to evaluate the strategy of diagnosis and therapy on children with AFBN,avoiding any blind spots of clinical treatment.Methods The clinical features of 12 cases of AFBN children admitted in Shenzhen Children's Hospital from Jan.2006 to Dec.2012 were analyzed.The clinical features and treatment strategy of AFBN were summarized.ResultsSeven in 12 cases(58.3％) were younger than 1 year old,fever was the initial and cardinal symptom,most cases were lack of typical or local urinary symptoms and signs.Peripheral blood leukoeytes,C-reactive protein and procalcitonin were highly increased in all cases,comparing with simple urinary tract infection.Five cases combined with pyeloureterectasis.One case combined with vesicoureteral reflux (VUR).Blood culture:staphylococcus aureus (1 case),staphylococcus epidermidis (1 case),E.Coli (2 cases).Urine culture:E.Coli (4 cases),E.Coli and enterococcus faecalis (1case),staphylococcus aureus (1 case),white candida yeast (1 case),mixed flora (2 cases).Urinary ultrasound:renal swelling was showed in involved kidney.Echo of renal parenchyma were enhanced or nonuniform,multiple hypoechoic area were easily visible in involved renal parenchyma,with boundary ambiguity.CT or MRI scan:typical findings were reducing perfusion with multiple wedge-shaped or quasi-circular lesions.Broad-spectrum antibacterial treatment was effective and necessary.The medication of antimicrobial was under the guidance of drug susceptibility test.The average course of treatment was 14-55 days.Eleven cases were cured by conservative treatment.Conclusions The morbility of AFBN in young infants are high.The combination of urinary tract deformity,pyeloureterectasis or VUR should be highly vigilant in AFBN children.Imageological inspection of urinary tract is the necessary method on AFBN diagnosis.The major pathogen is E.Coli,which shows a high resistance to antibiotics.Conservative antibacterial treatment is effective in AFBN.

Role of regulatory T cells in pathogenesis of Henoch-Schonlein purpura in children / 中华儿科杂志

<p><b>OBJECTIVE</b>Henoch-Schonlein purpura (HSP) is one of the most common small vessel forms of autoimmune vasculitis in children. Immunologic derangement including humoral and cellular immunity disequilibrium and proinflammatory factors dysfunction are involved in the acute stage of HSP. Recently data revealed that regulatory T cells (Tr) play a pivotal role in preventing development of autoimmune and allergic diseases. This study aimed to explore the role of Tr cells in pathogenesis of HSP and the factors affecting development of Tr cells.</p><p><b>METHODS</b>Twenty patients with HSP and 20 age-matched healthy children were enrolled into this study. Flow cytometric (FCM) analysis was performed to detect the percentage of regulatory T cells subpopulation (including CD(4+)CD(25+) Tr, Tr1 and Th3) and helper T cells subpopulation (Th1 and Th2). Reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR were used to analyze Foxp3 expression in peripheral blood mononuclear cell (PBMC).</p><p><b>RESULTS</b>Compared with healthy control subjects, the proportions of Th2 cell in patients with HSP were significantly higher (P < 0.05), and the ratio of Th1/Th2 was remarkably decreased (P < 0.05). The proportions of three subpopulation of regulatory T cells including CD(4+)CD(25+) Tr, Tr1, Th3 in patients with HSP were all significantly lower than those of controls (P < 0.05). The mRNA expression of Foxp3 in patients with HSP showed similar tendency (P < 0.001).</p><p><b>CONCLUSIONS</b>The decrease of three subpopulations of regulatory T cells might be involved in pathogenesis of HSP and associated with the decreased expression of Foxp3 gene.</p>

Correlation between mannose-binding lectin gene codon 54 polymorphism and susceptibility of Kawasaki disease / 中华儿科杂志

<p><b>OBJECTIVE</b>Human mannose-binding lectin (MBL) is a C-type serum lectin synthesized by the liver as an acute-phase protein. MBL can bind to glycoproteins terminated with mannose and N-acetylglucosamine present in the cell walls on a variety of microorganisms. Therefore, MBL appears to play an important role in the immune system. Low levels of MBL in human have been associated with a susceptibility to recurrent infections. MBL deficiency and low serum MBL levels are strongly associated with the presence of three point mutations at codon 52, 54 and 57 of exon 1 in the human MBL gene, and in Chinese population, the codon-54 mutation occurs at a frequency of 0.11 - 0.17. The data suggested that MBL insufficiency might also predispose to the development of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The possibility that Kawasaki disease (KD) is an infectious disease has been discussed and investigated for decades, in light of the implication that infections are involved in the pathogenesis of KD. It has been suggested that MBL insufficiency might predispose to the occurrence of KD. This study was aimed to investigate the genetic association of MBL codon-54 polymorphism in patients with KD, and to investigate possible associations with clinical manifestations of the disease.</p><p><b>METHODS</b>There were 95 patients with KD and 160 healthy subjects in the study. The genotype of MBL gene 54 codon was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Clinical characteristics and biochemical examination were also performed.</p><p><b>RESULTS</b>The genotype frequency of heterozygote (GGC/GAC) was significantly higher in KD group than that in healthy subjects (45.2% vs 25.0%, P < 0.01), and the allele frequency of GAC mutation was also higher in KD patients than that in control group (0.258 vs 0.138, P < 0.01). The variant allele (GAC) was markedly associated with KD (OR = 2.18, 95% CI = 1.38 approximately 3.44, P < 0.05). But there was no significant difference in the allele frequency of GAC between patients with and without coronary artery lesion (CAL) in KD cases (0.281 vs 0.246, P > 0.05). In addition, in cases of KD, more patients carrying the variant allele (GAC) had episodes of upper respiratory or gastrointestinal infections prior to the onset of KD than wild homozygotes (P < 0.01).</p><p><b>CONCLUSION</b>The codon 54 polymorphism of MBL gene was associated with KD. It is possible that MBL gene codon 54 mutation might be related to the pathogenesis of KD.</p>

The correlation between Kawasaki disease and polymorphisms of Tumor necrosis factor alpha and interleukin-10 gene promoter / 中华儿科杂志

<p><b>OBJECTIVE</b>Kawasaki disease (KD) is an acute febrile vasculitic syndrome of unknown etiology that preferentially affects coronary artery. It has been suggested that proinflammatory cytokines like tumor necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) are key players during acute KD. Recently, the polymorphisms relative to major transcriptional start site of TNF-alpha and IL-10 gene were shown to influence the level of TNF-alpha and IL-10 production in vitro. This study was aimed to investigate the genetic association of TNF-alpha and IL-10 promoter polymorphisms in juvenile patients of Han nationality with KD, and to investigate the possible associations with clinical manifestations of the disease.</p><p><b>METHODS</b>Four polymorphism sites of TNF-alpha and IL-10 gene promoter regions from 96 children with KD were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). One hundred and sixty age-matched normal children of the Han nationality were used as control. All patients accepted Doppler echocardiography examination in order to differentiate coronary artery lesions.</p><p><b>RESULTS</b>There was significant difference in allele frequencies of -308 (A/G) site of the TNF-alpha gene between children of the Han nationality and those of Japanese and Caucasian in America. There were significant differences in the allele frequencies of -1082 (G/A), -819 (C/T) and -592 (A/C) of IL-10 gene between children of the Han nationality and their British Counterparts (P < 0.01). There was no significant difference in allele frequencies of -308 (A/G) site of TNF-alpha gene between children with KD and normal controls. There was no significant difference in the haplotypes and the allele frequencies of the above three sites of IL-10 between the two groups. However, when clinical features were examined, the genotype frequency of TNF-alpha-308A was significantly higher in IVIG-resistant KD patients than that of TNF-alpha-308G genotype (67% vs 5%, chi(c)(2) = 90.48, P < 0.01). The genotype of TNF-alpha-308A was closely associated with IVIG-resistant KD (P < 0.01, relative risk 42.25, 95% confidence interval 15.81-112.88). The haplotype frequency of IL-10 -1082A/-819T/-592A was also higher in patients with coronary artery lesion (CAL) caused by KD than those of Non-ATA haplotype (52% vs 20%, chi(2) = 18.36, P < 0.01). The haplotypes of IL-10 -1082A/-819T/-592A was significantly associated with CAL caused by KD (P < 0.01, relative risk 4.26, 95% confidence interval 2.20-8.25).</p><p><b>CONCLUSION</b>The genotype of TNF-alpha-308A is one of the important factors that probably influence the therapeutic effect of KD. The haplotypes (-1082/-819/-592) of IL-10 gene promoter might be related to the pathogenesis of coronary artery complication of KD and -1082A/-819T/-592A haplotypes might be regarded as a genetic marker of risk factor for coronary artery lesion in KD.</p>