Adenosine deaminase as a marker for the severity of infectious mononucleosis secondary to EBV in children.

BACKGROUND: Infectious mononucleosis, a common disease in children and young adults, is often accompanied by elevated transaminase levels and rarely, liver failure. This study aimed to determine whether adenosine deaminase is a marker of severity in children with infectious mononucleosis, especially those with elevated alanine transaminase levels. METHODS: This case-control study was conducted at the Children's Hospital of Soochow University. A total of 104 children with infectious mononucleosis and 50 controls with other acute infections and fever, tonsillitis, or lymphadenitis, were enrolled in the study. Among the 104 children with infectious mononucleosis, 54 had normal alanine transaminase levels and 50 had elevated alanine transaminase levels. The children's clinical and laboratory data were analyzed to assess the diagnostic value of adenosine deaminase in the three groups. RESULTS: The adenosine deaminase level in the infectious mononucleosis group was significantly higher than that in the control group (P < 0.001). The adenosine deaminase levels were highly correlated with lymphocyte count, CD3+CD8+ T cells (%), CD4+/CD8+ ratio, and CD3-CD19+ (%) (r > 0.7, P < 0.01). The sensitivity and specificity of adenosine deaminase in predicting children with infectious mononucleosis were 97.1% and 94.0%, respectively. Furthermore, multivariate regression analysis revealed that adenosine deaminase level was a risk factor for elevated alanine transaminase in children with infectious mononucleosis. CONCLUSIONS: Adenosine deaminase may be a marker of the severity of infectious mononucleosis in children, and a predictor of elevated alanine transaminase in children with infectious mononucleosis.

Myocardial strain measured via two-dimensional speckle-tracking echocardiography in a family diagnosed with arrhythmogenic left ventricular cardiomyopathy.

BACKGROUND: Arrhythmogenic cardiomyopathy is a myocardial disorder characterized by ventricular arrhythmias, right and/or left ventricular involvement, and fibrofatty infiltrations in the myocardium. We report a family diagnosed with arrhythmogenic left ventricular cardiomyopathy (ALVC) and depict their echocardiographic characteristics. METHODS AND RESULTS: Fifteen family members were divided into three groups based on whether they carried the TMEM43 mutation and had been diagnosed with ALVC. Eight of them had TMEM43 mutations, and four were diagnosed with ALVC according to the Padua criteria. Only the proband experienced sudden cardiac death and had a dilated left ventricle. Left ventricular ejection fraction was reduced in two patients; however, left ventricular global longitudinal strain was depressed in three patients. Low QRS voltages in limb leads were evident in three patients, and five patients had frequent ventricular premature contractions. Late gadolinium enhancement was evident in three patients. Left ventricular layer-specific strain showed that the transmural strain gradient ratio was increased in patients diagnosed with ALVC, and it was elevated in the genotype-positive and phenotype-negative groups compared with healthy individuals. CONCLUSION: Global left ventricular longitudinal strain better evaluated left ventricular function than left ventricular ejection fraction. The transmural strain gradient ratio was elevated in patients diagnosed with ALVC, suggesting that it was useful for the evaluation of ALVC.