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Background: Adenoviral infections are most likely to invade the respiratory tract, and the clinical manifestations of the infections are varied; in severe cases, they may cause systemic multi-system damages and so on. At present, early clinical differential diagnosis is difficult under the existing testing methods, so it is important to analyze its clinical characteristics and risk factors for early identification of critical status and early and rational treatment. Methods: The clinical data of 202 children with adenovirus pneumonia admitted to Tianjin Children's Hospital from January 2019 to December 2021 were retrospectively analyzed. According to the evaluation criteria for severe pneumonia, they were divided into a severe group (77 cases) and a non-severe group (125 cases). The clinical characteristics, complications, and laboratory data of the 2 groups were collected for statistical analysis, and then significant factors were analyzed by receiver operating characteristic curve (ROC) and binary logistic regression. Results: Among the 202 children with adenovirus pneumonia, there were 108 males and 94 females. The children ranged in age from 2 months to 13 years. The duration of fever, incidence of wheezing, neutrophil ratio (NEUT%), and serum ferritin (SF) levels were significantly higher in the severe group than in the non-severe group (χ2/Z/P=-9.173/<0.001, 5.469/0.019, 5.831/<0.001, -3.845/<0.001). The incidences of liver injury, electrolyte disturbance, and coagulation dysfunction in the severe group were significantly higher than those in the non-severe group (χ2/Z/P=0.001/0.001, 28.208/0.001, 32.079/0.001). Logistic regression combined with ROC curve analysis suggested that fever duration >4.50 days, with wheezing, NEUT% ≥47.60, and SF ≥139.60 ng/mL were risk factors for developing severe adenovirus pneumonia in children [odds ratio (OR) (95% CI): 1.394 (1.230-1.581), 3.673 (1.246-10.828), 1.034 (1.001-1.067), 1.004 (1.001-1.008)]. Conclusions: Studies have shown that the fever associated with severe adenovirus pneumonia has a long duration, and that severe clinical manifestations and multiple complications, fever duration >4.50 days, wheezing, NEUT% ≥47.60, and SF ≥139.60 ng/mL are risk factors for severe adenovirus pneumonia.
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Purpose: The data on pediatrics with Multidrug-Resistant (MDR) Klebsiella pneumoniae infections are scarce. This study aims to investigate the molecular epidemiology of MDR Klebsiella pneumoniae, detect the mechanism of drug resistance, and determine the clinical risk factors for carbapenem-resistant Klebsiella pneumonia (CRKP) bloodstream infections (BSIs) in a children's hospital. Methods: A total of 62 strains were collected from Tianjin Children's Hospital. Carba NP and polymerase chain reactions (PCR) were performed to detect MDR mechanisms. Multilocus sequence typing (MLST) was used for analyzing strain homology. Clinical data were collected and logistic regression was used for BSI risk factors. Results: ST11 was the principal ST among the CRKP isolates clinically, accounting for 56.45% (35/62); there were also 57.14% (20/35) ST11 CRKP strains co-carrying bla NDM-5 and bla KPC-2, which were resistant to most of the tested antibiotics, being susceptible only to cotrimoxazole and tigecycline. The clinical data showed that 72.73% (40/55) of children with CRKP infection had serious underlying diseases; 20.00% (11/55) patients developed BSIs with the potential to cause multiple organ failure, shock and death. The logistic regression showed that the risk of BSIs caused by CRKP strain infections in children with hematological malignancies after chemotherapy was 7 times that of other children (95%Cl: 1.298-45.415, P=0.025). Conclusion: ST11 was the prevalent clone in our hospital. The emergence of ST11 CRKP co-carrying bla NDM-5 and bla KPC-2 should be a cause for alarm as they were resistant to most of the tested antibiotics. CRKP strain infections are mainly occurring in young immunocompromised patients and the chemotherapy for hematological malignancies is an independent risk factor for BSIs.
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BACKGROUND/AIMS: Blood-retinal barrier (BRB) breakdown and vascular leakage is the leading cause of blindness of diabetic retinopathy (DR). Hyperglycemia-induced oxidative stress and inflammation are primary pathogenic factors of this severe DR complication. An effective interventional modality against the pathogenic factors during early DR is needed to curb BRB breakdown and vascular leakage. This study sought to examine the protective effects of α-Melanocyte-stimulating hormone (α-MSH) on early diabetic retina against vascular hyperpermeability, electrophysiological dysfunction, and morphological deterioration in a rat model of diabetes and probe the mechanisms underlying the α-MSH's anti-hyperpermeability in both rodent retinas and simian retinal vascular endothelial cells (RF6A). METHODS: Sprague Dawley rats were injected through tail vein with streptozotocin to induce diabetes. The rats were intravitreally injected with α-MSH or saline at Week 1 and 3 after hyperglycemia. In another 2 weeks, Evans blue assay, transmission electron microscopy, electroretinogram (ERG), and hematoxylin and eosin (H&E) staining were performed to examine the protective effects of α-MSH in diabetic retinas. The expression of pro-inflammatory factors and tight junction at mRNA and protein levels in retinas was analyzed. Finally, the α-MSH's anti-hyperpermeability was confirmed in a high glucose (HG)-treated RF6A cell monolayer transwell culture by transendothelial electrical resistance (TEER) measurement and a fluorescein isothiocyanate-Dextran assay. Universal or specific melanocortin receptor (MCR) blockers were also employed to elucidate the MCR subtype mediating α-MSH's protection. RESULTS: Evans blue assay showed that BRB breakdown and vascular leakage was detected, and rescued by α-MSH both qualitatively and quantitatively in early diabetic retinas; electron microscopy revealed substantially improved retinal and choroidal vessel ultrastructures in α-MSH-treated diabetic retinas; scotopic ERG suggested partial rescue of functional defects by α-MSH in diabetic retinas; and H&E staining revealed significantly increased thickness of all layers in α-MSH-treated diabetic retinas. Mechanistically, α-MSH corrected aberrant transcript and protein expression of pro-inflammatory factor and tight junction genes in the diseased retinas; moreover, it prevented abnormal changes in TEER and permeability in HG-stimulated RF6A cells, and this anti-hyperpermeability was abolished by a universal MCR blocker or an antagonist specific to MC4R. CONCLUSIONS: This study showed previously undescribed protective effects of α-MSH on inhibiting BRB breakdown and vascular leakage, improving electrophysiological functions and morphology in early diabetic retinas, which may be due to its down-regulating pro-inflammatory factors and augmenting tight junctions. α-MSH acts predominantly on MC4R to antagonize hyperpermeability in retinal microvessel endothelial cells.