Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload.

AIM: To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload. METHODS: The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rheumatic heart disease; G3: congenital left to right shunt; and G4: dilated cardiomyopathy). Twelve healthy children served as a control group. New York Heart Association (NYHA) class, LV dimensions and functions using Vivid 7 dimensions were evaluated. Serum ANP was measured using the ELISA technique, before and 3 months after treatment with angiotensin converting enzyme inhibitor. RESULTS: ANP was raised in all patients as compared to controls (G one: 28.33 ± 5.78, G2: 26.5 ± 4.11, G3: 28.5 ± 6.6, G4: 29.25 ± 4.5 pg/mL, control group: 5.54 ± 1.4 pg/mL, P < 0.001 for all) and varied significantly between different NYHA classes regardless of the underlying cardiac lesion. It was significantly higher in group 1 than 2 (P < 0.05). It decreased significantly after treatment (G1: 15.3 ± 5.3, G2: 10.7 ± 2.5, G3: 11.5 ± 3.8, G4: 15.7 ± 10.7 pg/mL, P < 0.001). The rate of change of ANP correlated with that of LV end diastolic diameter (r = 0.3, P < 0.05) irrespective of the underlying cause. CONCLUSION: ANP increases in cases of LV volume overload irrespective of the aetiology of heart failure. It can differentiate between children in quiescent state from those in clinical failure even in the absence of echocardiographically detectable systolic dysfunction. Furthermore, it can monitor LV remodelling with treatment.

Therapeutic role of mobilized bone marrow cells in children with nonischemic dilated cardiomyopathy.

Dilated cardiomyopathy is an important cause of congestive cardiac failure in infants and children. Mobilizing hematopoietic progenitor cells is a promising intervention to this deadly disease. Aim. Evaluate granulocyte colony stimulating factor (GCSF) as therapeutic modality in children with idiopathic dilated cardiomyopathy (IDCM). Subjects and Methods. This case-control prospective study was conducted on 20 children with IDCM following up at Cardiology Clinic Children's Hospital, Ain Shams University (group 1) who were compared to another 10 age-, sex-, duration-of-illness-, and systolic-function-matched children with IDCM as control (group 2). They were subjected to history taking, clinical examination, echocardiography, and peripheral blood CD34+ cell assessment before and one week after GCSF intake for 5 consecutive days (by group 1 but not group 2). Results. A significant improvement in echocardiographic data and CD34+-T-cell increase was found in group 1 one week after GCSF intake and for the next 6 months CD34+ T cells percentage of change showed no significant correlation with the that of the left ventricular dimensions and systolic function. Conclusion. Administration of GCSF to children with IDCM resulted in clinical and echocardiographic improvement not correlated to mobilized CD34+ T cells, implying involvement of additional mechanisms over simple stem cell mobilization.

Oxidative stress in Egyptian children with autism: relation to autoimmunity.

UNLABELLED: We are the first to study the relationship between oxidative stress (by measuring plasma F2-isoprostane, as a marker of lipid peroxidation, and glutathione peroxidase, as an antioxidant enzyme) and autoimmunity (as indicated by serum antineuronal antibodies) in a group of 44 Egyptian autistic children and 44 healthy matched-children. Our results showed that oxidative stress was found in 88.64% of autistic children. Oxidative stress, resulting from elevated plasma F2-isoprostane and/or reduced glutathione peroxidase, had significant risk for antineuronal positivity, which was found in 54.5% of autistic children, (odds ratio: 12.38 and 6.43, respectively, confidence interval: 1.37-112.10 and 1.21-34.19, respectively). CONCLUSIONS: the strong association between oxidative stress and autoimmunity in autistic children may indicate the possible role of oxidative stress, through induction of autoimmunity, in some autistic patients. Therefore, studies considering the role of antioxidants and immunotherapy in amelioration of autistic manifestations are recommended.

Plasma adrenomedullin level in Egyptian children and adolescents with type 1 diabetes mellitus: relationship to microvascular complications.

BACKGROUND: Adrenomedullin (AM) is known to be elevated in different clinical situations including diabetes mellitus (DM), but its potential role in the pathogenesis of vascular complications in diabetic children and adolescents is to be clarified. Hence, the study aimed at assessment of plasma adrenomedullin levels in children and adolescents with type 1 DM and correlation of these levels with metabolic control and diabetic microvascular complications (MVC). METHODS: The study was performed in the Diabetes Specialized Clinic, Children's Hospital of Ain Shams University in Cairo, Egypt. It included 55 diabetic children and adolescents (mean age 13.93 +/- 3.15 years) who were subdivided into 40 with no MVC and 15 with MVC. Thirty healthy subjects, age-and sex-matched, were included as control group (mean age 12.83 +/- 2.82 years). Patients and controls were assessed for glycosylated hemoglobin (HbA1c) and plasma adrenomedullin assay using ELISA technique. RESULTS: Mean plasma AM levels were significantly increased in patients with and without MVC compared to control group, (110.6 pg/mL, 60.25 pg/mL and 39.2 pg/mL respectively) (P < 0.01) with higher levels in those with MVC (P < 0.05). Plasma AM levels were positively correlated with both duration of diabetes (rho = 0.703, P < 0.001) and glycemic control (HbA1c) (rho = 0.453, P < 0.001). CONCLUSION: Higher plasma AM levels in diabetics particularly in those with MVC & its correlation with diabetes duration and metabolic control may reflect the role of AM in diabetic vasculopathy in the pediatric age group.

Serum interleukin-18 expression in children with bronchial asthma.

BACKGROUND: : Interleukin 18 (IL-18) is reported to have regulatory functions on Th1 and Th2 cytokine production and proinflammatory effects through promoting recruitment of memory Th1 cells to inflammatory sites. We sought to investigate the expression of the serum IL-18 in childhood bronchial asthma in relation to disease activity and severity. METHODS: : Serum IL-18 was measured by enzymatic immunoassay in 25 asthmatic children during exacerbation and after complete quiescence of symptoms and signs. The results were compared to those of 35 nonallergic age- and sex-matched children. RESULTS: : Serum IL-18 levels during asthma exacerbation [median = 125 pg/mL; mean (SD) = 128.6 (43.3) pg/mL] were significantly lower than the follow-up levels during stability [median = 250 pg/mL; mean (SD) = 291.6 (66.7) pg/mL] and both levels correlated positively with each other. The corresponding values of the control group were higher than those of the asthmatic patients whether during exacerbation or stability [median = 380 pg/mL; mean (SD) = 476.1 (259.6) pg/mL]. The serum IL-18 concentrations did not vary significantly according to asthma severity, family history of atopy, or passive smoking. The influence of inhaled corticosteroids on IL-18 expression was not impressive and neither was the relation between serum IL-18 and the peripheral blood eosinophil count or serum total IgE expression. CONCLUSIONS: : Serum IL-18 was found underexpressed in a group of asthmatic children especially during exacerbation. Further studies are needed to outline its exact role in the pathogenesis of asthma.

Soluble CD30 serum levels in atopic dermatitis and bronchial asthma and its relationship with disease severity in pediatric age.

CD30 is a transmembrane molecule that may be expressed on a proportion of activated T-lymphocytes and has been reported to be a marker of Th2 phenotype. A soluble form of CD30 (sCD30) is released by CD30+ cells in vivo. Our objective was to evaluate serum sCD30 levels in children with atopic dermatitis (AD) or bronchial asthma and to investigate its relation to disease severity. This study included of 60 infants and children, of whom 18 had AD, 22 had bronchial asthma and 20 were healthy matched subjects. Severity of AD was assessed according to the objective Scoring Atopic Dermatitis (obj-SCORAD) index. Laboratory investigations included complete blood count, serum total immunoglobulin E (IgE) and serum sCD30 by ELISA. Serum levels of sCD30 in AD (77.7+/-27.9 U/ml) and asthmatic patients (49.2+/-21.5 U/ml) were significantly increased compared with the control group (18.2+/-7.0 U/ml) (t=8.8, p<0.0001; t=6.4, p<0.0001, respectively). In patients with AD, sCD30 levels were shown to correlate with obj-SCORAD (r=0.96, p<0.0001). Patients with moderate persistent asthma had significantly elevated sCD30 levels than those with mild persistent asthma (t=3.4, p<0.01). In addition, sCD30 was inversely correlated to peak expiratory flow rate (r=-0.78, p<0.0001). Levels of sCD30 did not correlate with age, disease duration or serum total IgE (p>0.05). In conclusion, serum sCD30 levels correlate with the severity of AD and bronchial asthma. It appears to be an additional objective marker that may be useful for follow up and may help to improve research and management of these diseases.