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Systemic lupus erythroematosis (SLE) is a systemic autoimmune disease with multisystemic involvement. The condition has several phenotypes, with varying clinical presentations from mild mucocutaneous manifestations to multiorgan and severe central nervous system involvement. Several immunopathogenic pathways play a role in the development of SLE. Despite recent advances in technology and understanding of the pathological basis and risk factors for SLE, the exact pathogenesis is still not well known. Diagnosis of SLE can be challenging, and while several classification criteria have been posed, their utility in the clinical setting is still a matter of debate. Management of SLE is dictated by organ system involvement. Despite several agents shown to be efficacious in treating SLE, the disease still poses significant morbidity and mortality risks in patients[1].
Haematological abnormalities are common in systemic lupus erythroematosis. Anemia is found in about 50% of patients.
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Causes of anemia in SLE:
Anemia due to chronic disease is the most frequent in patients with SLE, representing approximately one-third of the cases [2].
Iron deficiency anemia is also a common cause, usually caused by blood loss (menorrhagia or gastrointestinal bleeding) [3].
Autoimmune hemolytic anemia (AIHA) a classification criteria for SLE [4]. The mechanism is thought to be caused by the destruction of red blood cells through warm or cold antibodies [5]. Patients with AIHA may present with symptoms of anemia or hemolysis or symptoms of an underlying disorder. Severe hemolysis may lead to hepatosplenomegaly, hemoglobinuria, and signs of heart failure [6]. Maanaging patients with AIHA may be challenging because specific therapy should be individualized in accordance with the disease manifestations and its severity [7].
Hemopoietic failure is the suspected to be the result of an immunologically damaged bone marrow (BM) .
Overall, hypocellularity, morphological dysplasia, increased fibrosis, and BM necrosis were common findings in patients with SLE with hemocytopenias, suggesting a primary BM involvement in pathogenesis of the disease, probably mediated by auto-antibodies, immune complexes, and immunopotent T cells [8, 9].
Solid proof of the participation of humoral immune mechanisms in hemopoietic dysfunction was obtained from patients with SLE with aplastic anemia, a BM failure syndrome of a definite immune pathogenesis [10-12].
In these cases, complement dependent or independent autoantibodies were found to suppress erythroid and granulocytic colony formation of BM progenitor cells [10-12].
Targeted by autoantibodies, the progenitor BM cells lead to various syndromes of hemopoietic failure, such as aplastic anaemia, hypoplasia of myeloid line, amegakaryocytic thrombocytopenia, and the extremely rare pure red cell aplasia (PRCA) [13-19].
The presence of the inhibitory autoantibody is typically related to SLE activity and can be suppressed by successful treatment-that is, by immunosuppression. However, PRCA can occur in the absence of disease activity or even precede the appearance of SLE [15].
In our study we will search for the most common causes of anemia in SLE in our environment ,focusing on the most common causes of refractory anemia in SLE.
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67 participants in 1 patient group
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Data sourced from clinicaltrials.gov
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