myocardial infarction) can be exacerbated in SLE but mostly these are secondary to accelerated atheroscle-rosis and other risks i.e.
Although it is almost common in SLE that there are deposits of immunoglobulin in the glomeruli but only one half of the patients present with the features of clinical nephritis (Ben Menachem et al 2010).
Pulmonary manifestations of SLE may manifest acu-tely or indolently that include many complications such as serositis which can affect both cardiac and pulmonary systems and cardiac and pulmonary serosi-tis often coexist.
The most common ocular manifes-tation of SLE is kerato-conjunctivitis sicca (KCS) that occurs in approximately 25% of patients (Arevalo et al 2002).
Patients with SLE have a complex array of abnormali-ties of immune system.
Management of SLE often depends on disease severity and disease manifestations (Hahn et al 2005).
Conventional therapy: Conventionally patients of SLE are treated with non-steroidal anti-inflammatory anti-malarial glucocorticoids and immunosuppressive drugs including cyclophosphamide azathioprine me-thotrexate and Mycophenolate mofetil.
New potential drugs for SLE therapy are as follows.
LN which is one of the life threatening complications of SLE is associated with kidney failure that needs treatment with dialysis.
IVIG treatment is effective for treating moderate to severe SLE and IVIG can be used as an adjuvant therapy (Netta et al 2014).
Ocrelizumab: A humanized anti-CD20 monoclonal antibody has also been evaluated in SLE (Chaichian et al 2013).
Antibody against CD22: B cell depletion using CD22 as a target has been studied as a potential therapy in SLE. Epratuzumab is a humanized monoclonal antibody against CD22.