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AB0495 Cutaneous Silent Period in Patients with Systemic Lupus Erythematosus without Neuropathic Symptoms
  1. O.N. Pamuk1,
  2. A. Tekatas1,2,
  3. D.D. Tekatas1,
  4. Y. Dogu2,
  5. V. Akdemir2
  1. 1Rheumatology
  2. 2Neurology, Trakya University Medical Faculty, Edirne, Turkey


Background Small fiber neuropathy (SFN) is a peripheral nerve disorder affecting specifically small myelinated A Delta fibers and unmyelinated C fibers. SFN is one of the common causes of neuropathic pain syndrome, however it can not be shown in conventional nerve conduction studies, making it difficult to diagnose. It was suggested that Cutaneous Silent Period (CSP) can be used as an objective method for evaluating small nerve fibers.

Objectives Evaluating small nerve fibers in patients with systemic lupus erythematosus (SLE) using CSP and assesssing the relationship between clinical signs, autoantibodies and neuropathic pain score.

Methods 51 SLE (48 female, 3 male, mean age:39.9±9.4), and 46 healthy control subjects (42 females, 4 males, mean age: 40±9.2) were included the study. Patients having risk factors for peripheral neuropathy were excluded. Electrophysiologic recordings were performed both on patients and the control group using nerve conduction studies and CSP. Values (latency and duration) gahered by using CSP from lower and upper extremities were recorded. Clinical features were extracted from medical charts.

Results The mean level of upper and lower extremity latencies were significantly higher in patients with SLE than in healthy control subjects (p<0.001). In addition, the mean duration of upper and lower extremity were significantly shorter in SLE patients than in controls (p<0.001). The mean upper latency is significantly higher in active SLE patients (SLEDAI score ≥6) when compared to inactive patients (85.4±14.9 vs. 78.6±8.4, p=0.023). The mean level of upper latency of active SLE patients tended to be higher (117.3±22 vs. 108.3±13.9, p=0.08). In SLE patients with nephritis, the mean level of lower extremity latency was significantly higher than in SLE patients without nephritis (119.4±20.2 vs. 107.6±14.3, p=0.028). Other EMG measures (NCS) were similar in patients with and without nephritis (all p values >0.05). When patients with anti-dsDNA positive were compared to the anti-dsDNA negative, it was observed that there was a tendency a lower duration of upper extremity in former group (31.2±8.2 vs. 35.2±7.5, p=0.08). Other measures were similar in patients with and without anti-dsDNA (all p values >0.05). The mean level of latency and duration were similar in SLE patients with and without hypocomplementemia, arthritis, photosensitivity, serositis, CNS involvement and other ENA antibodies. Age, treatment with antimalarials, steroids, immunsuppressives (azathioprine, cyclophosphamid), hemogram parameters had no effect on the NCS or CSP results. Also, LANNS score was not associated with any clinical parameters and NCS or CSP measure.In SLE patients, SLEDAI scores correlated with upper (r=0.36, p=0.009) and lower extremity latency (r=-0.38, p=0.008). The level of lower extremity latency also correlated with ESR (r=0.34, p=0.01) and disease duration (r=0.30, p=0.03).

Conclusions We detected marked small nerve fiber damage in both lower and upper extremities in SLE patients using CSP. However, patients must be observed in the long term, because a correlation with neuropathic pain score was not found.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.4019

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