Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus (SLE) is an autoimmune heterogenous disease, meaning it is caused by many genes and alleles and variations of those genes. According to the Journal of Rare Diseases,SLE is characterized by the presence of autoantibodies against nuclear antigens (1). An estimated 1 per 1000 individuals are affected overall, qualifying SLE as a rare disease. Females are more affected at a female to male ratio of 10:1. Researchers believe that, as many females become susceptible during pregnancy, the hormone estrogen is involved in the etiopathogenesis (1). The etiopathogenesis of SLE is very complicated and involves a variety of factors such as genetics, environmental factors, and immune deficiencies. The genetic factors causing SLE is not entirely understood, although it is known that it is not a single gene contributing to SLE, but variations of many genes due to damages, improper splicing, deficiencies, and duplications. An individual can also be predisposed
The most prevalent hematological disorders that are exhibited in SLE are Anemia, Leukopenia, and Thrombocytopenia. Anemia is defined as hemoglobin levels of less than 13.5 grams per deciliter (g/dl) for men, and 12 g/dl for women. Anemia accounts for 13% of the total causes of hematological defects in SLE. The three most common types of Anemia are Anemia of Chronic Disease (ACD) which accounts for 37.7% of Anemia in hematologic SLE patients, Iron Deficiency Anemia (IDA) which accounts for 35%, and Autoimmune Hemolytic Anemia (AIHA) which accounts for 14.4%. Other cases of Anemia, such as pure red cell aplasia (autoantibodies against erythroblasts), pernicious anemia, and aplastic anemia (autoantibodies against bone marrow precursors) constitute for the remaining percentage. ACD is the most common type of Anemia in general, and is classified as a suppressed production of red blood cells secondary to chronic