Three Cases of Rhabdomyolysis Induced by Viral Infections in Children and Literature Review.

The clinical data of 3 patients with rhabdomyolysis (RM) caused by different viral infections were retrospectively reviewed. The diagnoses were established according to the clinical symptoms, physical signs, myocardial enzymes, and muscle biopsy. Case 1 was a 11-year-old boy with influenza A virus infection, whose major symptoms were fever, cough and myalgia. After the treatment of active anti-virus, hydration, and alkalinization, the patient completely recovered. Case 2 was a 10-year-old girl with Epstein-Barr (EB) virus infection who had significant musculoskeletal pain and muscle weakness symptoms with significantly elevated serum creatine kinase. After active hydration and anti-infective treatment, the patient's condition returned to normal. Case 3 was a 15-year-old boy with human cytomegalovirus infection, whose symptoms were mainly repeated fever, accompanied by myalgia and facial edema. Antibacterial therapy was ineffective, and the disease progressed with respiratory muscle weakness and multiple organ injuries. After antiviral treatment, respiratory support and hemofiltration, the symptoms relieved and patient recovered without sequela. With literature review, we believe that although influenza virus, Epstein-Barr virus and cytomegalovirus rarely cause RM in children, it should be attached attention to. With early diagnosis and treatment, the prognosis is favorable.

Mosaicism trisomy 10 in a 14-month-old child with additional neurological abnormalities: case report and literature review.

BACKGROUND: Trisomy 10 is very rarely diagnosed, especially in living persons. Most reports of trisomy 10 pertain to prenatal diagnosis of trisomy 10 in the fetus. In addition, trisomy 10 has been reported as part of partial chromosomal abnormalities in some leukemic cells and tumor specimens. Only 6 cases of mosaicism trisomy 10 have been reported so far. None of these reports pertain to living children with neurological abnormalities. CASE PRESENTATION: We report the case of a 14-month-old girl who was brought for treatment of unusual facies, growth retardation, and patent ductus arteriosus. Karyotype analysis revealed a 47, XX, + 10/46, XX pattern. MRI showed characteristics of Dandy-Walker syndrome and ventricular enlargement in the brain. CONCLUSIONS: This case is distinguished by its extreme rarity and its potential for use as a reference case of this condition in clinical settings.

Maternal vitamin D deficiency impairs Treg and Breg responses in offspring mice and deteriorates allergic airway inflammation.

BACKGROUND: Vitamin D (VitD) can regulate immune responses and maternal VitD-deficiency can affect immune responses in the offspring. This study aimed at investigating the effects of maternal VitD-deficiency during pregnancy on Treg and Breg responses in offspring mice with house dust mite (HDM)-induced allergic airway inflammation. METHODS: Female BALB/c mice were randomized and fed with normal chow or VitD-deficient diet until their offspring weaned. The offspring mice were fed with normal chow and injected with vehicle or HDM to induce allergic airway inflammation. The levels of serum 25(OH)D, cytokines and infiltrate numbers as well as percentages of Tregs and Bregs in the bronchoalveolar lavage fluid (BALF) were analyzed. The relative levels of VitD receptor (VDR), VitD-binding protein (VDBP), Cytochromes P450 (CYP) 27b1, and CYP24A1 mRNA transcripts in the lungs of different groups of mice were measured. RESULTS: Maternal VitD-deficiency significantly reduced serum 25(OH)D levels in offspring mice. VitD-deficiency significantly increased the relative levels of VDR, VDBP and CYP27B1 mRNA transcripts, but decreased CYP24A1 expression in the lungs of mice. In comparison with the control mice, significantly elevated levels of pro-inflammatory cytokines, increased numbers of lymphocytes and eosinophils, but decreased levels of anti-inflammatory cytokines were detected in the BALF of VitD-deficient mice. VitD-deficiency significantly increased the frequency of Th1, Th2, Th9, Th17 cells, but decreased regulatory T (Tregs) and B cells (Bregs) in the BALF of mice with allergic airway inflammation. CONCLUSION: Maternal VitD-deficiency lowed serum 25(OH)D levels and enhanced HDM-induced allergic airway inflammation in the offspring by impairing Breg and Treg responses.

Early Postnatal Exposure to Cigarette Smoke Leads to Later Airway Inflammation in Asthmatic Mice.

BACKGROUND AND OBJECTIVE: Asthma is one of the most common airway inflammatory diseases. In most cases, asthma development is related to ubiquitous harmful environmental exposure factors in early-life. Previous studies have indicated that smoking can promote asthma development and increase the difficulty of asthma control. The aim of this study was to determine the effects of early-life CS exposure on ovalbumin (OVA)-sensitized asthmatic mice. METHODS: Pathological and immunological functions were analyzed in an adult asthma mice model in which mice were sensitized with OVA combined with early-life CS exposure. RESULTS: Mice exposed to CS for only 5 weeks demonstrated significantly reduced pulmonary compliance, increased airway inflammation, and augmented cellular and humoral immune responses. In addition, CS inhalation was sufficient to facilitate OVA sensitization and challenge asthmatic development. Meanwhile, CS exposure amplified regulatory T cell-mediated immunity inhibition, but still did not offset the increased effector T cell-mediated inflammatory response. CONCLUSION: Early-life CS exposure is significantly associated with later pulmonary injury and aggravation of T-cell immunologic derangement in asthmatic mice.

Early-Life Exposure to Clostridium leptum Causes Pulmonary Immunosuppression.

INTRODUCTION: Low Clostridium leptum levels are a risk factor for the development of asthma. C. leptum deficiency exacerbates asthma; however, the impact of early-life C. leptum exposure on cesarean-delivered mice remains unclear. This study is to determine the effects of early-life C. leptum exposure on asthma development in infant mice. METHODS: We exposed infant mice to C. leptum (fed-CL) and then induced asthma using the allergen ovalbumin (OVA). RESULTS: Fed-CL increased regulatory T (Treg) cells in cesarean-delivered mice compared with vaginally delivered mice. Compared with OVA-exposed mice, mice exposed to C. leptum + OVA did not develop the typical asthma phenotype, which includes airway hyper-responsiveness, cell infiltration, and T helper cell subset (Th1, Th2, Th9, Th17) inflammation. Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses. CONCLUSION: These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life.

Effect of respiratory syncytial virus infection on regulated on activation, normal T-cells expressed and secreted production in a murine model of asthma.

PURPOSE: Synthesis of regulated on activation, normal T-cells expressed and secreted (RANTES) in the airway has previously been shown to be elevated after respiratory syncytial virus (RSV) infection. However, since few studies have examined whether RSV-infected asthma patients express a higher level of RANTES than do normal individuals, we used a murine model of asthma to address this question. METHODS: We prepared Dermatophagoides farinae-sensitized mice as an asthma model, and then infected them with RSV and analyzed the changes in airway responsiveness and the cell populations and cytokine levels of bronchoalveolar lavage fluid. RESULTS: RANTES synthesis increased in response to RSV infection in both control mice and in asthma model (D. farinae) mice. However, there was no significant difference in the amount of RANTES produced following RSV infection between control and D. farinae mice. RSV infection affected neither interferon-γsynthesis nor airway responsiveness in either control or D. farinae mice. CONCLUSION: RSV infection did not induce more RANTES in a murine model of asthma than in control mice.