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Intraepidermal Nerve Fiber Densities in Chronic Inflammatory Autoimmune Diseases
Lasse G. Gøransson, MD;
Johan G. Brun, MD, PhD;
Erna Harboe, MD;
Svein I. Mellgren, MD, PhD;
Roald Omdal, MD, PhD
Arch Neurol. 2006;63:1410-1413.
Background Some patients with systemic lupus erythematosus have selective loss of small-diameter nerve fibers, while larger nerve fibers are unaffected.
Objective To determine intraepidermal nerve fiber densities in patients with different chronic inflammatory autoimmune diseases.
Design Cross-sectional study.
Setting Stavanger University Hospital, Stavanger, and Haukeland University Hospital, Haukeland, Norway.
Patients Sixty patients with systemic lupus erythematosus (SLE) (mean ± SD age, 43.2 ± 13.5 years), 61 patients with primary Sjögren syndrome (age, 57.1 ± 14.7 years), and 52 patients with rheumatoid arthritis (age, 57.4 ± 12.3 years) were compared with 106 healthy subjects (age, 49.0 ± 19.6 years).
Interventions Skin biopsy specimens.
Main Outcome Measures To evaluate small-diameter nerve fiber loss, intraepidermal nerve fiber densities were measured in skin punch biopsy specimens obtained from the distal part of the leg.
Results The mean ± SD densities were 7.5 ± 3.8 fibers/mm in patients with SLE, 9.2 ± 3.8 fibers/mm in primary Sjögren syndrome, and 10.9 ± 5.4 fibers/mm in rheumatoid arthritis vs 12.4 ± 4.6 fibers/mm in healthy subjects. Densities were significantly less in patients with SLE vs patients with rheumatoid arthritis and vs healthy subjects (P<.001 for both), as well as in patients with primary Sjögren syndrome vs healthy subjects (P<.001). Eight patients (13%) with SLE, 2 patients (3%) with primary Sjögren syndrome, and 2 patients (4%) with rheumatoid arthritis had densities below the lower reference limit of 3.4 fibers/mm, consistent with small-diameter nerve fiber neuropathy.
Conclusion The degree of loss of small-diameter nerve fibers differs among patients with these chronic inflammatory autoimmune diseases, likely reflecting differences in pathogenesis and organ affinity of the individual disease entities.
Author Affiliations: Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger (Drs Gøransson, Harboe, and Omdal); Institute of Internal Medicine (Drs Gøransson and Omdal) and Section of Rheumatology, Institute of Medicine (Dr Brun), University of Bergen, Bergen; Department of Rheumatology, Haukeland University Hospital, Haukeland (Dr Brun); and Institute of Clinical Medicine, University of Tromsø, and Department of Neurology, University Hospital of North Norway, Tromsø (Dr Mellgren), Norway.
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Arch Neurol 2006;63:1612-1615.
ABSTRACT
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