RESUMEN
The pathogenesis of rheumatic fever involves an interaction between the group A streptococcus and the immune system. Although an old disease the exact immunopathogenesis still unclear, so our aim is to determine whether interleukin-2 [IL-2] and anticardiolipin antibodies [aCL ab] have a role in immunopathogenesis of rheumatic fever or not. The work was carried out on 60 patients, 30 patients with acute rheumatic fever ARF [group I], 10 of them with rheumatic arthritis and 20 of them with rheumatic carditis and 30 patients with well documented chronic rheumatic heart disease CRHD [group II]. Twenty apparently healthy children were taken as control [group III]. All patients [group I and II] and control group [group III] were subjected to careful history taking, thorough clinical examination, laboratory investigations: Complete blood picture [CBC], Erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], Antistreptolysin-O titre [ASOT], Serum IL-2 and aCL Ab. Furthermore, patients with ARE and CRUD were sitbjected to: Plain X-ray chest and heart, ECG and Echocardiography. Our results showed that: IL-2 was significantly increased in cases of ARF [both in arthritis and carditis] than in patients with CRHD and normal control. No significant difference in IL-2 was found between cases of arthritis and carditis. Although IL-2 increases in rheumatic carditis, it has no relation to severity of carditis or to degree of ESR elevation. There was significant postive correlation between IL-2 and ASOT and CRP. Anti CL Ab was increased significantly in cases of rheumatic carditis [but not in cases of arthritis] than in patients with CRHD and normal control. A direct relationship was found between aCL Ab and the severity of carditis and ESR. There was significant positive correlation between aCL Ab and ESR, TLC and ASOT. So we suggest, the use of IL-2 [although non specific] to confirm the diagnosis of ARF as well as aCL Ab for the diagnosis of rheumatic carditis and a marker of its severity