V-A ECMO for neonatal coxsackievirus B fulminant myocarditis: a case report and literature review.

Background: Neonatal (enteroviral) myocarditis (NM/NEM) is rare but unpredictable and devastating, with high mortality and morbidity. We report a case of neonatal coxsackievirus B (CVB) fulminant myocarditis successfully treated with veno-arterial extracorporeal membrane oxygenation (V-A ECMO). Case presentation: A previously healthy 7-day-old boy presented with fever for 4 days. Progressive cardiac dysfunction (weak heart sounds, hepatomegaly, pulmonary edema, ascites, and oliguria), decreased left ventricular ejection fraction (LVEF) and fractional shortening (FS), transient ventricular fibrillation, dramatically elevated creatine kinase-MB (405.8 U/L), cardiac troponin I (25.85 ng/ml), and N-terminal pro-brain natriuretic peptide (NT-proBNP > 35,000 ng/L), and positive blood CVB ribonucleic acid indicated neonatal CVB fulminating myocarditis. It was refractory to mechanical ventilation, fluid resuscitation, inotropes, corticosteroids, intravenous immunoglobulin, and diuretics during the first 4 days of hospitalization (DOH 1-4). The deterioration was suppressed by V-A ECMO in the next 5 days (DOH 5-9), despite the occurrence of bilateral grade III intraventricular hemorrhage on DOH 7. Within the first 4 days after ECMO decannulation (DOH 10-13), he continued to improve with withdrawal of mechanical ventilation, LVEF > 60%, and FS > 30%. In the subsequent 4 days (DOH 14-17), his LVEF and FS decreased to 52% and 25%, and further dropped to 37%-38% and 17% over the next 2 days (DOH 18-19), respectively. There was no other deterioration except for cardiomegaly and paroxysmal tachypnea. Through strengthening fluid restriction and diuresis, and improving cardiopulmonary function, he restabilized. Finally, notwithstanding NT-proBNP elevation (>35,000 ng/L), cardiomegaly, and low LVEF (40%-44%) and FS (18%-21%) levels, he was discharged on DOH 26 with oral medications discontinued within 3 weeks postdischarge. In nearly three years of follow-up, he was uneventful, with interventricular septum hyperechogenic foci and mild mitral/tricuspid regurgitation. Conclusions: Dynamic cardiac function monitoring via real-time echocardiography is useful for the diagnosis and treatment of NM/NEM. As a lifesaving therapy, ECMO may improve the survival rate of patients with NM/NEM. However, the "honeymoon period" after ECMO may cause the illusion of recovery. Regardless of whether the survivors of NM/NEM have undergone ECMO, close long-term follow-up is paramount to the prompt identification and intervention of abnormalities.

Effect of FoxO1 on Cardiomyocyte Apoptosis and Inflammation in Viral Myocarditis via Modultion of the TLR4/NF-κB Signaling Pathway.

To investigate the possible effect of FoxO on coxsackievirus B3 (CVB3) -induced cardiomyocyte inflammation and apoptosis via modulation of the TLR4/NF-κB signaling pathway.Viral myocarditis (VMC) models were establied via CVB3 infection both in vivo and in vitro. Western blotting was adopted to detect FoxO1 and TLR4 expressions in myocardial tissues and cells. Cardiomyocytes of suckling mouse were divided into the control, CVB3, CVB3 + pcDNA, CVB3 + pcDNA-FoxO1, CVB3 + TLR4 siRNA, and CVB3 + pcDNA-FoxO1 + TLR4 siRNA groups. Flow cytometry was employed to evaluate cell apoptosis. The expressions of inflammatory factors including TNF-α, IL-1ß, and IL-6 were detected via quantitative reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay. Then, TLR4/NF-κB pathway-related proteins were determined via Western blotting.VMC mice had increased FoxO1 and TLR4 expressions in myocardial tissues. Cardiomyocytes with CVB3 infection also had upregulated protein expressions of p-FoxO1/FoxO1 and TLR4. Compared with those in the control group, the cardiomyocytes in the CVB3 group were increased in LDH and CK-MB levels, cell apoptosis rate and inflammatory factors (TNF-α, IL-1ß and IL-6), as well as protein expressions of TLR4 and p-p65/p65. Compared with those in the CVB3 group, the cardiomyocytes in the CVB3 + pcDNA-FoxO1 group were further upregulated whereas those in the CVB3 +TLR4 siRNA group were downregulated in the aforementioned indicators. Furthermore, TLR4 siRNA can reverse the effect of pcDNA-FoxO1 on the aggravation of cardiomyocyte injury induced by CVB3 infection.FoxO1 can upregulate the TLR4/NF-κB signaling pathway to promote cardiomyocyte apoptosis and inflammatory injury in CVB3-induced VMC.

Risk Factors for Recurrence of Gestational Diabetes Mellitus and Its Correlation with Maternal and Infant Prognosis.

Objective: To explore and analyze the risk factors of recurrence of gestational diabetes mellitus (GDM) and its correlation with maternal and infant prognosis. Methods: The clinical data of 128 GDM patients admitted to our hospital from May 2018 to May 2020 were retrospectively analyzed, and they were divided into a recurrence group (n = 65) and a nonrecurrence group (n = 63) according to the presence or absence of recurrence after one year of follow-up. The general data and clinical data of the two groups of patients were compared by single factor, and the factors with statistical significance were analyzed by logistic regression, and the maternal and infant outcomes and prognosis of the two groups of patients were compared. Results: Compared with the nonrecurrence group, the recurrence group had a higher proportion of patients aged ≥35 years, with first fasting blood glucose ≥7.0 mmol/L, and with BMI value index ≥25 kg/m2 during repregnancy, and the differences were statistically significant (p < 0.05). Multivariate logistic regression analysis showed that elder maternal age, high blood glucose level in the previous pregnancy, and high BMI index during this pregnancy were all high-risk factors for GDM recurrence (p < 0.05). Compared with the nonrecurrence group, the recurrence group had a lower rate of vaginal delivery, lower rate of premature rupture of membranes, lower rate of premature birth, lower rate of macrosomia, lower rate of neonatal asphyxia, lower rate of postpartum hemorrhage, and lower Apgar score within 1 minute of delivery (p < 0.05). Conclusion: Older maternal age, high blood glucose level in the previous pregnancy, and high BMI index during the present pregnancy are high-risk factors for GDM recurrence that can further lead to adverse outcomes for mothers and infants. Clinicians should place sufficient emphasis on targeted early measures responding to high-risk factors to minimize the risk of GDM recurrence and optimize maternal and infant outcomes.

Retroperitoneal malignant schwannoma in a child.

Retroperitoneal malignant schwannomas are extremely rare. Only a few cases have been reported, only one of which occurred in a child. We herein report a case of retroperitoneal malignant schwannoma in a 2-year-old boy who presented with a painless mass in the right lumbar region. The mass had gradually enlarged during a 1-year period, and it was about the size of the patient's fist at the time of consultation. Whole-abdomen computed tomography revealed a space-occupying lesion in the retroperitoneum infiltrating from the L1 to L4 spinal canal. A preoperative diagnosis of a retroperitoneal tumor was made, and complete tumorectomy was performed. Postoperative pathological examination showed a malignant schwannoma. The tumor recurred 1 month after the first operation, and a second complete excision was carried out; the postoperative pathologic examination findings were similar to the previous findings. The patient recovered well and continued to undergo close follow-up.

MicroRNA-381 protects myocardial cell function in children and mice with viral myocarditis via targeting cyclooxygenase-2 expression.

The present study aimed to determine the expression of cyclooxygenase (COX)-2 and microRNA (miRNA/miR)-381 in the blood of children with viral myocarditis (VM), and investigate the association between COX-2 and miR-381 in the occurrence and development of the disease using a mouse model. A total of 26 children with VM (15 boys and 11 girls) were included in the present study. Peripheral blood was collected from all children. The mouse model of VM was constructed by coxsackievirus B3 (CVB3) infection. Peripheral blood and myocardial tissues were collected from all mice for analysis. Reverse transcription-quantitative polymerase chain reaction was used to determine the expression of COX-2 mRNA and miR-381 in serum and myocardial tissues. ELISA was used to measure the content of COX-2 protein in serum from humans and mice, and western blotting was employed to determine the expression of COX-2 protein in myocardial tissues from mice. Contents of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) were evaluated using an automatic biochemical analyzer. A dual luciferase assay was conducted to identify interactions between COX-2 mRNA and miR-381. Children with VM had increased COX-2 levels and decreased miR-381 expression in peripheral blood, compared with those who had recovered from VM. CVB3 infection resulted in damage in the myocardium of mice, and elevated CK-MB and LDH contents. VM model mice exhibited increased COX-2 levels and decreased miR-381 expression in peripheral blood and myocardial tissues compared with normal mice. miR-381 binds to the 3'-untranslated seed regions of both human and mouse COX-2 mRNA to regulate their expression. The present study demonstrated that children with VM have decreased miR-381 expression and elevated COX-2 expression in peripheral blood. miR-381 may inhibit myocardial cell damage caused by CVB3 infection and protect myocardial cell function by targeting COX-2 expression.