ABSTRACT
OBJECTIVE@#To investigate the predictive value of complete blood count (CBC) and inflammation marker on the recurrence risk in children with Henoch-Schönlein purpura (HSP).@*METHODS@#One hundred and thirty-three children with HSP admitted to Cangzhou Central Hospital from February 2017 to March 2019 were enrolled. The clinical data of the children were collected, at the time of admission CBC and C-reactive protein (CRP) were detected. After discharge, the children were followed up for 1 year, the clinical data of children with and without recurrence were compared, and multivariate logistic regression was used to analyze the risk factors affecting HSP recurrence. Receiver operating characteristic (ROC) curve should be drawn and the predictive value of CBC and CRP on HSP recurrence should be analyzed.@*RESULTS@#In the follow-up of 133 children, 8 cases were lost and 39 cases recurred, with a recurrence rate of 31.20% (39/125). The age, skin rash duration, proportion of renal damage at the initial onset, percentage of neutrophils, percentage of lymphocytes, platelet count (PLT), mean platelet volume (MPV) and neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), MPV/PLT ratio (MPR), and CRP level of patients with recurrence were statistically different from those without recurrence (P <0.05). Multivariate logistic regression analysis showed that long skin rash duration, renal damage at the initial onset, increased PLR, high PLT, increased MPV and elevated CRP level were independent risk factors for recurrence in children with HSP (P <0.05). The ROC curve analysis showed that the area under the curve (AUC) of the combination of the four blood and inflammation marker (PLT, MPV, PLR and CPR) in the early prediction of HSP recurrence was 0.898, which was higher than the initial renal damage (AUC=0.687) and persistent skin rash time (AUC=0.708), with a sensitivity of 84.62% and a specificity of 83.72%.@*CONCLUSION@#Observation of CBC and CPR can predict the risk of HSP recurrence early and guide early clinical intervention.
Subject(s)
Humans , Child , IgA Vasculitis , Blood Cell Count , Inflammation , C-Reactive Protein , Lymphocytes , Neutrophils , Exanthema , Retrospective StudiesABSTRACT
OBJECTIVE@#To screen and verify the differentially expressed genes related with aging of bone marrow mesenchymal stem cells (BM-MSCs) in acute myeloid leukemia (AML) patients by bioinformatics, so as to provide new molecular markers for the research and clinical treatment of AML.@*METHODS@#The gene expression profiling chip related with BM-MSCs in AML patients in our hospital and the gene chip GSE84881 selected from NCBI database GEO were used for data analysis and exploration. The DAVID analysis software was used to perform gene ontology (GO) enrichment analysis and KEGG pathway enrichment analysis. Furthermore, the differentially expressed genes related with aging of BM-MSCs in AML patients were identified. Bone marrow samples were collected and MSCs were amplified in vitro, and RT-PCR was used to verify the differentially expressed genes, which should be further identified with senescence-associated β-galactosidase staining and MTT cell proliferation assays.@*RESULTS@#A total of 247 differentially expressed genes were screened out by bioinformatics methods, including genes of 132 up-regulated expression and 115 down-regulated expression. Six differentially expressed genes related with aging of BM-MSCs in AML patients were screened out, including the genes of up-regulated expression, COL3A1 (P<0.05), CRYAB (P<0.01), DCN (P<0.05), and the genes of down-regulated expression, including CCL2 (P<0.05), CTSC (P<0.01) and IL6 (P<0.05). These 6 differentially expressed genes were consistent with data from chip assays, and which was significantly correlated with aging of BM-MSCs in AML patients. Meanwhile, the positive rate of senescence-associated β-galactosidase staining in BM-MSCs of AML patients was significantly different from that of healthy donors (P<0.01). MTT cell proliferation assay showed that BM-MSCs in AML patients had proliferative ability lower than the healthy donors' BM-MSCs.@*CONCLUSION@#The data here suggest novel clues for the clinical research and treatment of BM-MSCs aging in AML patients.