Cytokine pattern and endothelium damage markers in Henoch-Schönlein purpura.
In a longitudinal cohort study our aim was to evaluate the cytokine pattern of children affected by Henoch-Schonlein purpura (HSP) and to correlate this pattern to vascular endothelium damage and to nephropathy. The following parameters were monitored at the onset of the disease (T0) and after 6 months of follow-up (T1): clinical scores, serum levels of tumor necrosis factor alpha (TNF-alpha), interleukin 2 (IL-2), soluble IL-2 receptor (IL-2sRalpha), fibrinogen, von Willebrand factor antigen (vWf:Ag) and soluble thrombomodulin (TMD) levels. A total of 24 children (9 M, 15 F), affected by HSP, aged between 3-14 years (median 6 years), were enrolled into the study. IL-2 serum levels were significantly increased at the onset of the disease compared to control group and T1. The same pattern was observed for IL-2sRalpha and TNF-alpha. Fibrinogen and vWf:Ag concentrations were significantly higher at the onset of disease than t1 and in control group. TMD levels resulted constantly within the normal range. Concerning the analyzed parameters, no significant difference resulted to be in subjects with and without renal involvement (hematuria and/or proteinuria). Finally, raised serum TNF-alpha concentration, related to vascular endothelium damage as shown by increased vWf:Ag levels, occurred invariably in children affected by HSP both with and without renal involvement.
Del Vecchio
Giovanni Carlo
GC
Department of Biomedicine of Development Age, University of Bari, Bari, Italy.
Carlo
Del Vecchio Giovanni
del VG
Penza
Rosa
R
Rosa
Penza
P
Altomare
Maria
M
Maria
Altomare
A
Piacente
Laura
L
Laura
Piacente
P
Aceto
Gabriella
G
Gabriella
Aceto
A
Lassandro
Giuseppe
G
Giuseppe
Lassandro
L
De Mattia
Domenico
D
Domenico
De Mattia
de M
Giordano
Paoala
P
Paola
Giordano
G
D000293:Adolescent; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000097:blood*; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006417:Hematuria / Q000276:immunology / Q000473:pathology; D006801:Humans; D011695:IgA Vasculitis / Q000150:complications / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D007376:Interleukin-2 / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D011507:Proteinuria / Q000276:immunology / Q000473:pathology; D018180:Thrombomodulin / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; D016207:Cytokines; C508594:IL2 protein, human; D007376:Interleukin-2; D053645:Interleukin-2 Receptor alpha Subunit; D018180:Thrombomodulin; D014409:Tumor Necrosis Factor-alpha; D014841:von Willebrand Factor; D005340:Fibrinogen