الفهرس 
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Abstract
Systemic lupus erythematous (SLE) is a heterogeneous systemic autoimmune disease, characterized by immune-mediated inflammation in multiple organs. (Bernatsky et al. 2006). The course of the disease is characterized by exacerbations and remissions, and the severity of the clinical picture is greatly affected by the number and nature of the various organ manifestations (Gustafsson et al. 2012). The mortality in patients with SLE is still considerable, and it may be due to lupus activity, when vital organs are involved; the complications of treatment, in particular infections; or to long term complications, such as cardiovascular disorder. Typically, patients with SLE produce numerous autoantibodies. Some of the SLE-related autoantibodies, e.g. anti-dsDNA, correlate with disease activity, while others appear to be markers of specific disease subsets (e.g. anti-Ro/SSA); moreover, the presence of antiphospholipid antibodies (aPLs) is definitely pathogenic. aPL positivity itself predisposes to accelerated atherosclerosis and to an increased thromboembolic risk The antiphospholipid antibodies form a heterogeneous group of autoantibodies, including lupus anticoagulant (LA), anti-cardiolipin (aCL) and anti-beta2-glycoprotein I (ab2GPI). The latter two antibodies can be present in IgG, IgM and IgA isoforms, and are directed against anionic membrane phospholipids and associated proteins, and the IgG isotypes in particular are of clinical significance (Kaiser et al. 2009).
The reported prevalence of aPL in SLE varies between 15 and 35% (Mok et al. 2005). In the antiphospholipid syndrome (APS), the production of aPLs is accompanied by arterial or venous thrombotic events, or an adverse pregnancy outcome (Laskin et al. 2005). Apart from thrombosis and pregnancy complications, which are the principal clinical features of APS, aPLs in SLE have been shown to be associated with valvular heart disease, livedo reticularis, thrombocytopenia, hemolytic anemia, renal impairment, and neuropsychiatric disease (Zuily et al. 2011). The aim of this study is to detect the relation between thrombocytopenia in systemic lupus erythramatosis patients and presence antiphospholipid antibodies.
Our study population included 100 patients diagnosed SLE who had thrombocytopenia, mean age of them was 33.38 ± 9.36 years with range from 18 to 60 years. Majority of patients in this study were females (90%). Mean of disease duration was 3.47 ± 2.72 years with range 3 to 15 years. As regards family history, we found that only 2 patients had positive family history and 17/100 (17%) patients had positive gestation history.
In this study, most common clinical manifestations of SLE was cutaneous as oral/nasal ulcer which observed in 95 (95%) patients, but new ulcers observed in only 8 patients, this followed by photosensitivity which observed in 83% of patients, then malar rash which found in 68% of patients, however new malar rash observed in only 8/100 patients, hair falling reported by 57% of patients. On the other hand alopecia found in 39% of patients and new alopecia in only 3 patients. DLE was found in only 5/100 patients. Fever observed in 53% of patients and it was more than 38 in 16% of them. Regarding neurological manifestations, psychosis / Seizure found in 19% of patients, cerebrvascular accident in 17%, lupus headache observed in 6% of patients, and visual disturbance in only 1 patient. As regards serositis, precarditis /pleurisy found in 15% of patients. Vasculitis found in only 8 patients. Musculoskeletal manifestations observed as follows: arthralagia reported by 82% of patients, new arthritis observed in only 4 patients but myositis not found in any patient.
In current study, 99% of SLE patients had positive ANA, it was speckled in 59%, homogenous in 40% and both speckled and homogenous observed in only 1 patient. Anti dsDNA and anti nucleosome were common antibodies detected (56%, 50%) followed by anti sm and anti RNP (41%), then anti histone detected in 19% of our patients, anti RO 60 detected also in 40% of our patients.
Antiphospholipid antibodies observed in thrombocytopenic patients in current study as, lupus anticoagulant in 23% of patients, B2 glycoproteins IgM in 22% of patients, anticardiolipin IgM in 14%, B2 glycoproteins IgG in 13%, and anticardiolipin IgG in 11%. We found in our study that there was negative and significant correlation between platelet count and both anticardiolipin IgM titer and B2glycoprotein IgM titre (p= 0.01, 0.05 respectively), and there was negative high significant correlation between platelet count and both lupus titer and anticardiolipin IgG titer. Platelet count also negative but non significant correlated with B2glycoprotein IgG titer (p= 0.195), but no correlation was found between serum aPL levels and activity or chronicity index scores in renal biopsies, SLEDAI-2K which was similar to previous results as that obtained by Chock et al. (2019).
Conclusion
Our findings from this study pooling together a large number of studies, indicate that there is substantial evidence that aPL are strongly associated with increased risk of thrombocytopenia in SLE patients. We have identified aPL profiles – and especially LA and IgM isotypes – as biomarkers for the risk stratification of thrombocytopenia in SLE patients. Finally, for everyday practice, in aPL positive patients with SLE, platelet count monitoring should be performed. In SLE patients with thrombocytopenia and aPL, risk stratification according to different aPL profiles may guide clinical management.