Association Between Neuropathy and Some Autoantibodies in Systemic Lupus Erythematosus (SLE) Patients

Systemic lupus erythematosus (SLE) is a chronic, inflammatory,autoimmune disease that is characterized by multisystemic involvement with diverse clinical presentation . Peripheral neuropathy is a well-documented clinical manifestation of systemic lupus erythematosus (SLE) , with a prevalence rate ranging from 2% to 27.8% . Several lines of evidence link the risk of neuropathy with the antiphospholipid antibody and rheumatoid factor , as well as neuropsychiatric lupus with anti-Ro . Some evidence links anti-ganglioside antibodies with neuropathy , but other studies do not . Peripheral neuropathy may be slowly progressive or acutely devastating . Lupus nephritis (LN), a more definite and specific subgroup of lupus, is a major cause of morbidity and mortality in SLE and can affect up to 60% of SLE patients. Furthermore, the presence of peripheral neuropathy in LN patients may be relevant for improving their lives . Such complex situation poses a therapeutic challenge. The clinical presentation of PN relies upon the diameter of the affected nerve, the sort of demyelinating or axonal lesions, and their acute or chronic occurrence . Routine nerve conduction studies just mirror the activity of the fast conducting myelinated A nerve fibers, which are physiologically irrelevant to pain. Hence, quantitative sensory testing can evaluate small nerve fiber function The pathogenesis of SLE-related neuropathy is obscure, and the few pathological studies of the peripheral nerves in SLE have revealed axonal degeneration, inflammatory changes, and vasculitis . The major inflammatory mediators released from immune cells act on sensory neurons, inducing peripheral sensitization and hyperalgesic phenomena. In addition, after damage, this natural inflammatory response could encourage the pathogenetic activity of antineural autoantibodies, in addition to ischemic vascular mechanism, by vasa nervorum vascularitis or by microthrombi linked to antiphospholipid antibodies. The other legitimate mechanisms are immunologic cause by a direct aggression by antibodies, entraining obliteration of the peripheral nerve component. Furthermore, the PN has not been well prescribed in SLE in terms of onset, severity, clinical associations, and electrophysiological characteristics.. Therefore, we are going to characterize PN in SLE with respect to the patient's clinical lupus properties, serologic markers, disease activity, and electrophysiological data