1Shadia Ali Abd El Latif, 2Fatma M Selim and 3Nawal M Abd El Kawy
Departments of 1Pediatrics, 2Microbiology and 3Clinical pathology, Faculty of Medicine For Girls, Al Azhar University, Cairo, Egypt.
Defects in lymphocyte apoptosis and the breakdown in the delicate balance between cell survival and cell death have been implicated in the pathogenesis of rheumatic diseases. In an attempt to understand the pathogenesis of acute rheumatic fever (ARF), soluble Fas (sFas) - an inhibitor of Fas mediated apoptosis- was measured by ELISA in serum of 28 ARF pediatric patients. They were on the first episode of the disease and their ages ranged from 5-15 years. 15 age and sex matched healthy children served as a control group. On admission and before initiation of anti-inflammatory drug therapy, ARF patients showed a very significantly higher mean serum level of sFas (56.7 ± 19u/ml) as compared with that (12.3 ± 7 u/ml) of normal control (P < 0.0001). sFas level was not affected by neither patient’s age nor sex and its mean serum level among ARF carditis patients (n=7) showed a non-significant difference as compared with that of patients without carditis (n=21). Serum levels of sFas showed no correlation to the parameters of the disease activity (ESR & CRP). After a complete course of anti-inflammatory drug therapy, the mean serum level of sFas was dramatically decreased to 19 ± 9u/ml and showed a very significant difference when compared with that on admission (P<0.0001). In spite of this decline, the mean serum level of sFas was still significantly higher than that of normal control (P< 0.01). It is concluded that, sFas may, at least in part, be involved in the pathogenesis of ARF. Increased level of sFas may have a genetic background which need a further investigation.