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.

The angiogenic cytokine vascular endothelial growth factor (VEGF) may have a role in the pathogenesis of collagen diseases. We aimed to assess its serum levels in children and adolescents with systemic lupus erythematosus (SLE) and to elucidate its correlation with clinical features, laboratory parameters, and the overall disease activity. This study comprised 25 children and adolescents with SLE and 30 healthy controls. Disease activity was evaluated by SLE disease activity index (SLEDAI) score. Laboratory investigations included complete blood count, erythrocyte sedimentation rate (ESR), urine analysis, 24-h total urinary protein, assay of serum creatinine, ANA, anti-DNA, complement component C3, lupus anticoagulant, and VEGF. Serum levels of VEGF were significantly increased in SLE patients (579.5 +/- 184.7 pg/ml) when compared with controls (113.2 +/- 30.8 pg/ml) (p < 0.0001). VEGF serum levels were significantly increased in patients having renal involvement and neurologic symptoms than those who did not have them (p < 0.0001, p < 0.005, respectively). Serum levels of VEGF were higher in patients with antiphospholipid syndrome, vasculitis, and skin symptoms than those without, but the difference did not reach statistical significance. Meanwhile, they were similar in patients with and without arthritis (p > 0.05). VEGF serum levels were not correlated to age; inversely correlated to platelet count, serum C3 level; and positively correlated to ESR. SLEDAI score was positively correlated to VEGF serum level (r = 0.86, p < 0.0001). VEGF may be relevant to SLE pathogenesis. Its concentration seems to be a marker of SLE activity, which could help in disease monitoring and planning of treatment.

beta-thalassaemia is a major health problem in Egypt. It has been estimated that of the 1.5 million live births. 1000 children with beta-thalassaemia major are born annually. Although the available treatment has increased the life expectancy of patients, it is still unsatisfactory and represents a significant drain on the country's resources. National screening and prenatal diagnosis programmes can be provided in Egypt once the spectrum of beta-thalassaemia mutations has been identified within the Egyptian population. We have examined 16 DNA samples with 21 beta-thalassaemia mutations that remained unidentified in a study of 54 patients reported by Rady and colleagues in 1996. Using the polymerase chain reaction and single strand conformation analysis we identified the following changes: frameshift (FS) codon (CD) 8/9 (+G), 4 FS CD 29 (-G) and 2 novel mutations in exon I (15 CD 22 A-C and 1 FS CD 28 -C). In addition, a silent, probably polymorphic mutation, CD 17 G-A was present in all chromosomes.

Thrombomodulin is a thrombin receptor on the vascular endothelial cell surface which is likely released upon endothelial cell damage. Serum soluble thrombomodulin (sTM) was assessed and investigated as a parameter of disease activity in children and adolescents with systemic lupus erythematosus (SLE) and juvenile idiopathic arthritis (JIA). Patients included in this study were regularly attending the Allergy and Immunology Clinic, Children's Hospital, Ain Shams University. They were 38 (76%) females and 12 (24%) males, their ages ranged between 5 and 18 years with a mean of 14.3 +/- 4.84 years and median of 13 years. They were divided into two groups: SLE group which included 20 patients and JIA group which included 30 patients; and the control group which included 30 healthy age and sex-matched individuals for comparison. Disease activity in SLE patients was evaluated by systemic lupus erythematosus disease activity index (SLEDAI) score, while in JIA patients disease activity was determined by number of joints with active arthritis, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Serum levels of sTM were determined by enzyme-linked immunosorbent (ELISA) assay. Serum levels of sTM were significantly higher in SLE and JIA patients in comparison with the control group; there was no significant difference between SLE and JIA patients. In SLE patients, a highly significant correlation was found between sTM and SLEDAI score (r = 0.99, p < 0.001). In JIA patients, a highly significant correlation was found between sTM and number of joints with active arthritis as well as ESR (r = 0.85, p < 0.001; r = 0.93, p < 0.001, respectively). Levels of sTM were significantly higher in CRP-positive than CRP-negative JIA patients. Serum sTM is a useful serologic marker of disease activity in SLE and JIA. It may prove to be a potential indicator for early and more aggressive treatment. Furthermore, sTM may prove to be an important marker for vasculitis in general.

Our findings suggest that Bcl-2 prolongs survival and decreases apoptosis of airway eosinophils in asthma especially during exacerbation. Eosinophil apoptosis and Bcl-2 represent a target for new and effective therapeutic strategies of asthma.