Pathophysiology of Systemic Lupus Erythematosus p2
Pathophysiology
Systemic lupus
erythematosus (SLE) is an autoimmune connective tissue disorder that affects
multiple systems of the body (Huether& McCance, 2008). The muscles, as well as the central and peripheral
nervous systems are affected in those with SLE. It is important to understand
that there could be several different clinical presentations of SLE (Huether& McCance, 2008). When lupus affects the
central nervous system (CNS), the diagnosis present challenges, however; the
disease is often treatable. Since the pathophysiology of SLE is still not
completely understood, it is difficult to determine the exact causes. Several
genes that affect our body’s immune function, specifically the human leukocyte
antigen (HLA), add to the susceptibility of this clinical disease. Lewis &
Heitkemper (2004) discuss how certain medications (phenytoin, hydralazine, procainamide,
and isoniazid) potentially produce drug-induced lupus, however; this disorder
differs from the classic SLE autoantibody profile. The autoimmune reaction of
SLE affects many sites throughout the body through various mechanisms (Lewis
& Heitkemper, 2004). These mechanisms include deposition of immune
complexes, effects of cytokins and other chemical neuromodulators, direct
attack by autoantibodies or activated leukocytes, and several others (Lewis
& Heitkemper, 2004). As previously stated, SLE can affect non-neurologic
organs of the body as well as the nervous system. Non-neurological orgals that
are affected include the renal glomeruli, joints, pleural or pericardial
serosa, integument, cardiac or vascular endothelium, the cardiac valves,
etcetera (Huether & McCance, 2008).
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