Background Data that indicate vitamin A status in critically ill children with sepsis are sparse. The association between serum vitamin A levels and the clinical outcomes of sepsis has not been well assessed. The aim of this study was to assess the prevalence of vitamin A deficiency in critically ill children with sepsis and its association with clinical outcomes. Methods Critically ill children with sepsis admitted to the pediatric intensive care unit were engaged in this prospective study. Sex- and age-matched approximate-health children from the Department of Pediatric Surgery were enrolled as the control group. Blood samples were collected from all patients in the first 24 h of admission for the measurement of serum vitamin A status. We compared vitamin A status between the sepsis group and the control group. In addition, we compared the clinical characteristics of the two subgroups of septic patients with vitamin A deficiency and those without vitamin A deficiency. Univariate and multivariable methods were used to evaluate the association between vitamin A deficiency and septic shock. Results One hundred sixty septic children and 49 approximate-health children were enrolled in this study. Vitamin A deficiency was found in 94 (58.8%) subjects in the study group and 6 (12.2%) subjects in the control group ( P < 0.001). In septic patients, 28-day mortality and hospital mortality in patients with vitamin A deficiency were not significantly higher than that in patients without vitamin A deficiency ( P > 0.05). However, vitamin A levels were inversely associated with higher PRISM scores in septic children with VAD ( r = − 0.260, P = 0.012). Vitamin A deficiency was associated with septic shock with an unadjusted odds ratio (OR) of 3.297 (95% confidence interval (CI), 1.169 to 9.300; P = 0.024). In a logistic model, vitamin A deficiency (OR, 4.630; 95% CI, 1.027–20.866; P = 0.046), procalcitonin (OR, 1.029; 95% CI, 1.009–1.048; P = 0.003), and the Pediatric Risk of Mortality scores (OR, 1.132; 95% CI, 1.009–1.228; P = 0.003) were independently associated with septic shock. Conclusion The prevalence of vitamin A deficiency was high in children with sepsis. Vitamin A deficiency may be a marker of mortality in critically ill children with sepsis. Trial registration Clinicaltrials.gov , NCT03598127 Electronic supplementary material The online version of this article (10.1186/s13054-019-2548-9) contains supplementary material, which is available to authorized users.
Background Infantile hemangioma (IH) is the most common benign tumor in children. Long noncoding RNAs (lncRNAs) play a critical role in tumorigenesis. However, the expression levels and biological functions of lncRNAs in IH have not been well-studied. This study aimed to analyze the expression profile of lncRNAs and mRNAs in proliferating and involuting IHs. Methods The expression profiles of lncRNAs and mRNAs in proliferating and involuting IHs were identified by microarray analysis. Subsequently, detailed bioinformatics analyses were performed. Finally, quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) analyses were conducted to validate the microarray results. Results In total, 146 differentially expressed (DE) lncRNAs and 374 DE mRNAs were identified. The DE mRNAs were enriched mostly in angiogenesis-related biological processes (BPs) and pathways by bioinformatics analysis. In addition, metabolism-related BPs (e.g., “glycogen biosynthetic process” and “metabolic process”) and pathways (e.g., “oxidative phosphorylation”) were identified. A lncRNA-mRNA co-expression network was constructed from 42 DE lncRNAs and 217 DE mRNAs. Twelve lncRNAs were predicted to have cis-regulated target genes. The microarray analysis results were validated by qRT-PCR using 5 randomly selected lncRNAs and 13 mRNAs. The IHC results revealed that both LOXL2 and FPK-1 exhibited higher protein expression levels in proliferating IH than in involuting IH. Moreover, inhibition of PFK-1 could suppress hemangioma-derived endothelial cell proliferation and migration, induce cell arrest, and reduce glucose uptake and lactate and ATP production. Conclusions The findings suggest that the identified DE lncRNAs and mRNAs may be associated with the pathogenesis of IH. The data presented herein can improve our understanding of IH development and provide direction for further studies investigating the mechanism underlying IH.
Aim: The aim of this study was to assess the efficacy of propranolol treatment in multifocal and diffuse infantile hepatic haemangioma (IHH). Methods: A retrospective study of symptomatic or potentially symptomatic IHH was performed in our hospital between 2011 and 2016. Results: Thirteen patients were identified: 2 patients had diffuse lesions, and 11 patients had multifocal lesions, including 2 patients who had combined lesions that shared features of both multifocal and diffuse lesion patterns. Eleven (84.6%) patients had cutaneous infantile haemangioma. Hepatomegaly was the predominant clinical presentation. Hypothyroidism was identified in three patients, including one patient who had documented congestive heart failure (CHF). The median age at diagnosis and the median duration of treatment were 2.0 months (range 1.2-26.0) and 24.0 months (range 4.0-30.0). The median duration of follow-up was 30.0 months (range 3.0-48.0). For patients with hypothyroidism, the thyroid hormone level was normal after 4 weeks of propranolol and levothyroxine treatment. All but one patient responded well to propranolol treatment. The patient who failed to respond to treatment died of CHF and abdominal compartment syndrome induced by hepatomegaly. No significant side effects of propranolol were observed during follow-up. Conclusions: Most multifocal and diffuse IHH respond well to propranolol. However, progressive cases may be fatal despite aggressive treatments. Our data suggest that propranolol may be considered the first-line treatment for multifocal and diffuse IHH due to its efficacy.
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