RESUMO
Background: Conventional single indicators have low sensitivity and specificity for predicting weaning from mechanical ventilation in pediatric patients, necessitating the establishment of a combined prediction model for predicting weaning outcomes. Objectives: To explore the combined predictive value of PaO2/FiO2 Ratio (P/F ratio), diaphragm excursion-rapid shallow breathing index (DE-RSBI), diaphragm thickening fraction-rapid shallow breathing index (DTF-RSBI), and Pediatric Critical Illness Score (PCIS) in weaning from mechanical ventilation in pediatric patients. Methods: Sixty critically ill pneumonia pediatric patients requiring mechanical ventilation treatment from July 2022 to June 2023 at the Second Affiliated Hospital of Jiaxing University were selected. They all underwent a spontaneous breathing trial (SBT) and were divided into the weaning success group (42 cases) and weaning failure group (18 cases) based on the weaning outcome. Parameters including total duration of illness, mechanical ventilation duration, heart rate (HR), P/F ratio, diaphragm excursion (DE), DE-RSBI, diaphragm thickening fraction (DTF), DTF-RSBI, and PCIS were included in univariate and multivariate logistic regression analyses to determine independent factors affecting pediatric weaning success. Receiver operating characteristic (ROC) curves were plotted to evaluate the predictive value of P/F ratio, DE-RSBI, DTF-RSBI, PCIS alone or in combination for weaning success. Results: Comparing P/F ratio, DE, DE-RSBI, DTF, DTF-RSBI and PCIS, there were statistically significant differences (P < 0.05). Through collinearity analysis and binary logistic regression analysis,P/F ratio [OR = 0.777, 95% CI (0.641,0.941)], DE-RSBI [OR = 1.694, 95% CI (1.172, 2.447)], DTF-RSBI [OR = 1.057, 95% CI (1.002, 1.114)], and PCIS [OR = 0.661, 95% CI (0.445, 0.982)] were identified as independent factors affecting successful weaning(P < 0.05).The regression equation was: LogitP = 73.299-0.253 P/F ratio + 0.525DE-RSBI + 0.055DTF-RSBI-0.43PCIS.The sensitivity of the combined indicator Logit(P) in predicting successful weaning from mechanical ventilation in pediatric patients was 88.9%, with a specificity of 95.2% (optimal cutoff value of 0.511), and the area under the ROC curve (AUC) was 0.960 [95% CI (0.915, 1.000)]. The AUC of the combined prediction model for predicting pediatric weaning was greater than that of P/F ratio, DE-RSBI, DTF-RSBI and PCIS alone (Z values = 9.129, 2.061, 2.075, 8.326, P < 0.05). Conclusions: In mechanically ventilated pediatric patients, the combined prediction model has better predictive value for weaning success compared to using P/F ratio, DE-RSBI, DTF-RSBI, or PCIS alone.
RESUMO
BACKGROUND: Intravenous immunoglobulin (IVIG) is the primary treatment for Kawasaki disease (KD). However, 10-20% of KD patients show no response to IVIG treatment, making the early prediction of IVIG resistance a key focus of KD research. Our aim is to explore the application of the C-reactive protein to albumin ratio (CAR) for predicting IVIG resistance in children with KD through meta-analysis. METHODS: Cochrane Library, PubMed, MEDLINE, EMbase, CNKI, WanFang, the Chinese Biomedical Database, and CQVIP were searched up to November 2023 for cohort studies on predicting IVIG-resistant KD using the CAR. Articles were selected based on pre-established inclusion and exclusion criteria after extracting literature data and assessing them using the QUADAS-2.0 tool for evaluating the accuracy of diagnostic tests. Stata 15.0 software was used for meta-analysis. RESULTS: Four Chinese and English literature reports were included in this meta-analysis. The results revealed the presence of a threshold effect and high heterogeneity among the included studies. The combined sensitivity for CAR predicting IVIG-resistant KD was calculated as 0.65 (95% CI 0.58-0.72), specificity as 0.71 (95% CI 0.57-0.81), and the area under the curve (AUC) as 0.70 (95% CI 0.66-0.74) using the random-effects model. The combined positive likelihood ratio was 2.22 (95% CI 1.35-3.65), the combined negative likelihood ratio was 0.49 (95% CI 0.35-0.69), and the diagnostic odds ratio was 5 (95% CI 2-10). CONCLUSION: CAR is an auxiliary predictive indicator with moderate diagnostic value that provides guidance in the early treatment of the disease, demonstrating a certain predictive value that warrants further investigation. However, CAR cannot yet be considered as a definitive diagnostic or exclusionary marker for IVIG-resistant KD. Therefore, multi-center, large sample, and high-quality long-term follow-up trials are warranted to confirm the current findings.
Assuntos
Proteína C-Reativa , Síndrome de Linfonodos Mucocutâneos , Criança , Humanos , Albuminas , Estudos de Coortes , Imunoglobulinas Intravenosas/farmacologia , Imunoglobulinas Intravenosas/uso terapêutico , Síndrome de Linfonodos Mucocutâneos/diagnóstico , Síndrome de Linfonodos Mucocutâneos/tratamento farmacológico , PrognósticoRESUMO
INTRODUCTION: Developmental dysplasia of the hip (DDH) is a prevalent condition in children. Currently, the exact etiology of DDH remains uncertain. The objective of this study was to conduct a meta-analysis to investigate the risk factors associated with DDH in infants. The findings would provide a theoretical foundation for targeted early screening and diagnosis. HYPOTHESIS: Several indicators, such as gender, intrauterine position, family history of DDH, gestational age, delivery mode, amniotic fluid levels, swaddling, parity, fetus number, combined musculoskeletal deformities, birth weight, and physical examination results, may serve as risk factors for DDH. MATERIALS AND METHODS: Cohort studies investigating the risk factors of DDH in infants through logistic regression analysis were searched in the Wanfang, VIP citation, China National Knowledge Infrastructure (CNKI), China Biology Medicine disc, Excerpta Medica Database (Embase), PubMed, and Cochrane Library databases up to May 2023. After extracting the data from eligible literature and assessing them using the Newcastle-Ottawa Scale (NOS), articles were selected based on pre-established inclusion and exclusion criteria. RESULTS: A total of eleven literature reports covering 979,757 infants were included in this meta-analysis. The publication bias did not significantly influence the results. The incidence rate of DDH was 47.99 among infants with risk factors compared to 3.21 in the general population. Risk factors for DDH included being female (OR=6.97, 95% CI: 5.18-9.39, p<0.001), breech delivery (OR=4.14, 95% CI: 3.09-5.54, p<0.001), positive family history (OR=4.07, 95% CI: 2.20-7.52, p<0.001), cesarean section (OR=1.11, 95% CI: 1.01-1.21, p=0.032), oligohydramnios (OR=3.93, 95% CI: 1.29-12.01, p=0.016), swaddling (OR=6.74, 95% CI: 1.25-36.31, p=0.026), firstborn status (OR=1.84, 95% CI: 1.49-2.53, p<0.001), combined musculoskeletal malformations (OR=2.27, 95% CI: 1.58-3.27, p<0.001), and physical signs of DDH (OR=8.71, 95% CI: 2.44-31.07, p=0.001). Premature delivery (OR=0.91, 95% CI: 0.88-0.95, p<0.001) was a protective factor for DDH. The relationship between multiple pregnancies (OR=0.58, 95% CI: 0.33-1.02, p=0.060) and low birth weight (OR=0.62, 95% CI: 0.14-2.76, p=0.529) in relation to DDH remained uncertain. DISCUSSION: This meta-analysis shows that female, breech delivery, positive family history, cesarean section, firstborn status, oligohydramnios, swaddling and combined musculoskeletal malformations are associated with DDH. Premature delivery appeared to be a protective factor against DDH. Nevertheless, the other factors need more research to reach more conclusive results. LEVEL OF EVIDENCE: III; meta-analysis.
Assuntos
Displasia do Desenvolvimento do Quadril , Humanos , Fatores de Risco , Displasia do Desenvolvimento do Quadril/epidemiologia , Lactente , Recém-Nascido , Feminino , Estudos de Coortes , Incidência , Idade GestacionalAssuntos
Cardiomiopatia Dilatada , Humanos , Cardiomiopatia Dilatada/genética , Masculino , Feminino , Mutação , AdultoRESUMO
Background: Platelet-to-lymphocyte ratio (PLR) is reported to be related to the outcome of intensive care unit (ICU) patients. However, little is known about their associations with prognosis in newborn patients in neonatal ICU (NICU). The aim of the present study was to investigate the prognostic significance of the PLR for newborn patients in the NICU. Methods: Data on newborn patients in the NICU were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III (MIMIC III) database. The initial PLR value of blood examinations within 24 h was analyzed. Spearman's correlation was used to analyze the association of PLR with the length of hospital and ICU stays. The chi-square test was used to analyze the association of PLR with mortality rate. Multivariable logistic regression was used to determine whether the PLR was an independent prognostic factor of mortality. The area under the receiver operating characteristic (ROC) curve was used to assess the predictive ability of models combining PLR with other variables. Results: In total, 5240 patients were enrolled. PLR was negatively associated with length of hospital stay and ICU stay (hospital stay: ρ = −0.416, p < 0.0001; ICU stay: ρ = −0.442, p < 0.0001). PLR was significantly correlated with hospital mortality (p < 0.0001). Lower PLR was associated with higher hospital mortality (OR = 0.85, 95% CI = 0.75−0.95, p = 0.005) and 90-day mortality (OR = 0.85, 95% CI = 0.76−0.96, p = 0.010). The prognostic predictive ability of models combining PLR with other variables for hospital mortality was good (AUC for Model 1 = 0.804, 95% CI = 0.73−0.88, p < 0.0001; AUC for Model 2 = 0.964, 95% CI = 0.95−0.98, p < 0.0001). Conclusion: PLR is a novel independent risk factor for newborn patients in the NICU.
Assuntos
Unidades de Terapia Intensiva Neonatal , Linfócitos , Recém-Nascido , Humanos , Contagem de Plaquetas , Estudos Retrospectivos , Curva ROC , PrognósticoRESUMO
Pathological states in the early life environment of mammalian offspring, including maternal obesity and intrauterine overnutrition, can induce obesity and metabolic disorder later in life. Leptin resistance caused by upregulation of Socs3 in the hypothalamus of offspring was believed to be the main mechanism of this effect. In this study, obese mother (OM) and lean mother (LM) models were generated by feeding C57BL/6N female mice a high-fat diet or standard lean diet, respectively. Additionally, an obese mother with intervention (OMI) model was generated by injecting the high-fat diet group with Socs3-shRNA lentivirus during early pregnancy. The offspring of the groups was correspondingly named OM-F1 , LM-F1 , and OMI-F1 , representing progeny mouse models of different early life environments. The offspring were fed a high-fat diet to test their propensity for obesity. The body weight, food intake and fat accumulation were higher, while glucose intolerance and insulin resistance were worse in the OM-F1 group than LM-F1 group. By contrast, the obesity phenotype, hyperphagia and metabolic disorder were alleviated in the OMI-F1 group compared with the OM-F1 group. The mechanism was identified that downregulation of hypothalamic SOCS3 resulted in an increased level of p-STAT3 and p-JAK2, which ameliorated the leptin resistance and restored the lean expression of appetite regulatory genes (Pomc and Agrp) in hypothalamus of OMI-F1 group. Taken together, these results indicate that reducing maternal Socs3 expression during pregnancy can attenuate obesity caused by the early life environment in mice, which may inspire therapies that enable obese mothers to bear metabolically healthy children.
Assuntos
Obesidade Materna/genética , Hipernutrição/genética , Proteína 3 Supressora da Sinalização de Citocinas/genética , Tecido Adiposo , Animais , Animais Recém-Nascidos , Apetite/genética , Peso Corporal/genética , Modelos Animais de Doenças , Regulação para Baixo , Ingestão de Alimentos , Feminino , Técnicas de Silenciamento de Genes , Fígado/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Hipernutrição/complicações , GravidezRESUMO
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by an excessive accumulation of triacylglycerol in the liver. Autophagy is a lysosome-dependent degradation product recovery process, which widely occurs in eukaryotic cells, responsible for the vital maintenance of cellular energy balance. Previously published studies have demonstrated that autophagy is closely related to NAFLD occurrence and maternal obesity increases the susceptibility of offspring to non-alcoholic fatty liver disease, however, the underlying mechanism of this remains unclear. In the present study, NAFLD mouse models (offspring of an obese mother mouse via high-fat feeding) were generated, and the physiological indices of the liver were observed using total cholesterol, triglyceride, high-density lipoprotein and low-density lipoprotein serum assay kits. The morphological changes of the liver were also observed via HE, Masson and oil red O staining. Reverse transcription-quantitative-PCR and western blotting were performed to detect changes of autophagy-related genes in liver or fibrosis marker proteins (α-smooth muscle actin or TGF-ß1). Changes in serum inflammatory cytokine IL-6 levels were determined via ELISA. The results of the present study demonstrated that the offspring of an obese mother were more likely to develop NALFD than the offspring of a chow-fed mother, due to their increased association with liver fibrosis. When feeding continued to 17 weeks, the worst cases of NAFLD were observed and the level of autophagy decreased significantly compared with the offspring of a normal weight mouse. In addition, after 17 weeks of feeding, compared with the offspring of a chow-fed mother, the offspring of an obese mouse mother had reduced adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation levels and increased mammalian target of rapamycin (mTOR) phosphorylation levels. These results suggested that a reduced level of AMPK/mTOR mediated autophagy may be of vital importance for the increased susceptibility of offspring to NAFLD caused by maternal obesity. In conclusion, the current study provided a new direction for the treatment of NAFLD in offspring caused by maternal obesity.