The Significance Of Serum Amyloid A In The Risk Model Of Severe Mycoplasma Pneumoniae Pneumonia In Children

Objective By analyzing the clinical characteristics,laboratory test results and other related factors of hospitalized children with Mycoplasma pneumoniae pneumonia(MPP),screening the risk factors that affect the progression of the disease,and initially establishing a risk assessment model for hospitalized children with Mycoplasma pneumoniae pneumonia.The receiver operating curve(ROC)was used to verify the model externally,and analyze the significance of SAA in the development of MPP.The aim of this study was to assess the influence of SAA on innate immunity in the progression of MPPMethods A retrospective research method was used to collect case data of children with MPP from January 1,2016 to December 31,2019,who were hospitalized in the Pediatric Department of Changhai Medical University,the First Affiliated to the Naval Military Medical University.A total of 514 cases were recorded.The children were treated according to the standard treatment of Mycoplasma pneumoniae pneumonia,and recorded the detailed clinical data of children with MPP.According to the severity of their disease progression,427 cases were divided into Mycoplasma pneumoniae pneumonia group(MPP group),including 200 males and 227 females,and 87 cases were divided into severe Mycoplasma pneumoniae pneumonia group(SMPP group),including 42 males and 45 females.Compare their clinical characteristics at admission: age,gender,fever days prior to admission,blood oxygen saturation at admission,whether there is wheezing,rash,convulsions,purpura,anemia,gastrointestinal symptoms;laboratory indicators: including C-reactive protein(CRP),serum amyloid A(SAA),procalcitonin(PCT),white blood cell count(WBC),percentage of neutrophils(NEUT%),percentage of lymphocytes(LYMPH%),percentage of monocytes(MONO%),neutrophil count(NEUT),lymphocyte count(LYMPH),monocyte count(MONO),platelet count(PLT),hemoglobin(Hb),lactate dehydrogenase(LDH),alanine transaminase(ALT),aspartate transaminase(AST),creatine kinase isoenzyme(CK-MB),Mycoplasma pneumoniae-Ig M titer(MP-IGM);chest X-ray findings and other related factors.The modeling group were randomly selected from the MPP group and the SMPP group.Among them,there were 327 cases in the MPP group and 67 cases in the SMPP group.The verification group were consisted of the remaining 100 cases in the MPP group and 20 cases in the SMPP group,a total of 120 cases.The clinical data of children in the SMPP group and the children in the MPP group were analyzed by Wilcoxon rank sum test and chi-square test in the modeling group,and then binary unconditional Logistic regression analysis was used to obtain the disease progression of MPP hospitalized children to SMPP For independent risk factors,use the verification group to verify the diagnostic value of risk factors,and use R software to draw nomograms for clinical diagnosis and treatment based on independent risk factors.Results 1.From January 1,2016 to December 31,2019,a total of 663 children with MPP met the inclusion criteria,149 children met the exclusion criteria,and 514 children were finally included in the study,of which the MPP group accounted for 83.07%(427/514),and the SMPP group accounted for 16.93%(87/514).All the children in the MPP group were cured and discharged.In the SMPP group,8 children were transferred,79 children were discharged after improvement,and there were no deaths.2.There were 514 and 87 children in the MPP group and the SMPP group who met the criteria for admission and discharge,respectively.The age(years)in the MPP group and the SMPP group [6(4-8)vs 6(4-8),P=0.724],gender composition(male)(46.84% vs 48.28%,P=0.807),the difference was not statistically significant.3.There were 327 and 67 children in the MPP group and SMPP group in the modeling group,respectively.Comparing the clinical characteristics of the two groups,the SMPP group had lower blood oxygen saturation than the MPP group at admission [94%(94%-97%)] vs 98%(98%-99%),P<0.001],there is a statistical difference.Remaining age(years)[6(4-8)vs 5(4-8),P=0.895],pre-hospital fever(days)[4(2-6)vs 4(2-7),P=0.220 ],gender(male)(48.01% vs 47.76%,P=0.970),wheezing(23.55% vs 23.88%,P=0.953),rash(3.36% vs 5.97%,P=0.506),convulsions(0.61 % vs 2.99%,P=0.136),purpura(0.31% vs 2.99%,P=0.312),anemia(0.61% vs 1.49%,P=0.429),gastrointestinal symptoms(6.42% vs 8.96%,P=0.630)),with no statistical difference.4.Compared with the laboratory examinations of the children in the MPP group and the SMPP group in the modeling group,the serum amyloid A(SAA,mg/L)in the SMPP group was higher [198(127-338)vs 87.8(23.0-212.0),P <0.001],higher procalcitonin(PCT,ng/ml)[0.157(0.08-0.45)vs 0.092(0.053-0.181),P<0.001],higher C-reactive protein(CRP,mg/L)[ 17.1(9.24-30.4)vs 11.5(4.87-21.8),P=0.006],higher proportion of neutrophils(NEUT%)[59.2%(49.7%-70.9%)vs 52.4%(39.4%-61.8%),P<0.001],higher neutrophil count(NEUT,×109/L)[4.36(2.62-6.70)vs 3.60(2.28-5.06),P=0.016],higher lactate dehydrogenase(LDH,U/ L)[330(268-379)vs 264(225-314),P<0.001],and lower lymphocyte ratio(LYMPH%)[29.7%(22.7%-39.5%)vs 36.2%(27.4%-)48.7%),P<0.001],lower proportion of monocytes(MONO%)[7.4%(5.2%-9.1%)vs 8.4%(6.9%-10.2%),P=0.001],lower lymphocyte count(LYMPH),×109/L)[2.15(1.39-3.08)vs 2.61(1.92-3.37),P=0.007],the difference was statistically significant.There was no statistical difference in the MP-Ig M titer [320(160-1280)vs 320(160-1280),P=0.219],white blood cell count(WBC,×109/L)[7.84(5.66-10.8)vs 7.07(5.63-9.34),P=0.275],monocyte count(MONO,×109/L)[0.59(0.36-0.73)vs 0.61(0.45-0.81),P=0.153],platelet count(PLT,×109/L)[296(218-362)vs 293(232-355),P=0.899],hemoglobin(Hb,g/L)[126(118-130)vs 126(121-133),P=0.500],alanine aminotransferase(ALT,U/L)[16(12-20)vs 14(12-20),P=0.260],aspartate aminotransferase(AST,U/L)[27(21-37)vs 26(21-34),P=0.137],creatine kinase isoenzyme(CK-MB,U/L)[14(10-19)vs 14(10-18),P=0.149] between the MPP group and SMPP group(P>0.05).5.Comparison of chest X-ray findings between the two groups,the SMPP group was mainly characterized by large-area exudation and infiltration of the lungs.In the SMPP group,41.8% had pulmonary inflammatory infiltration area less than 1/3 of the total lung area,and 22.4% had pulmonary inflammatory infiltration area between 1/3 and 2/3 of the total lung area.It was higher than 32.7% and 0.9% in the MPP group respectively,and the difference was statistically significant(P < 0.001).6.According to the variables with statistical differences in the univariate analysis,a binary logistic regression analysis was performed to establish a model.The model showed: serum amyloid A(SAA,mg/L)[OR=1.004,95%CI: 1.001-1.007,P=0.009],neutrophil count(NEUT,×109/L)[OR=1.333,95%CI: 1.028-1.729,P=0.030],lactate dehydrogenase(LDH,U/L)[ OR=1.010,95%CI: 1.004-1.016,P=0.001],chest X-ray [OR=8.208,95%CI:3.056-22.048,P<0.001],and admission oxygen saturation(%)[OR= 0.273,95%CI: 0.195-0.381,P<0.001],which was an influencing factor for the occurrence of SMPP.7.According to the binary Logistic regression analysis results of SAA,NEUT,LDH,chest X-ray and admission blood oxygen saturation,a nomogram was established.The nomogram model was externally validated with an AUC of 0.955(95%CI: 0.895-1.000,P<0.001).Conclusions 1.SAA,NEUT,LDH,chest X-ray,and hospitalized blood oxygen saturation are high risk factors for SMPP.A nomogram constructed based on the risk factors can be used to score all admitted children with MPP to achieve the early warning of SMPP.2.Compared with PCT and CRP,SAA is an independent risk factor for MPP,and the increasing trend of SAA can be used as one of the early,rapid and simple detection indicators of SMPP.3.The AUC for MPP patients was 0.955 in the model,with high discrimination ability.The factors included in this study are all routine laboratory examination items,which are easy to be popularized and suitable for the actual needs of grass-roots medical service support in the army.4.The increase of the acute phase protein SAA in SMPP stimulates the number of neutrophils with innate immunity,which is related to the increase of reactive oxygen species(ROS)release,oxidative respiratory burst and proinflammatory effect of neutrophils.5.The pathophysiological mechanism of the inhibitory effect of SAA on monocytes of innate immune and T lymphocytes of acquired immune in SMPP is still unknown,which requires further study in the future.