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Utility of TWEAK to assess neuropsychiatric disease activity in systemic lupus erhytematosus

2015; SAGE Publishing; Volume: 25; Issue: 4 Linguagem: Inglês

10.1177/0961203315610206

1477-0962

Hilda Fragoso-Loyo, Yemil Atisha‐Fregoso, Carlos A. Núñez‐Álvarez, Luis Llorente,

Protein Tyrosine Phosphatases

Objective The purpose of this study was to assess the utility of tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) in serum and cerebrospinal fluid (CSF) as a biomarker in neuropsychiatric systemic lupus erythematosus (NPSLE). Methods Thirty three NPSLE patients were evaluated at hospitalization and six months later. As controls, five SLE patients with septic meningitis, 51 hospitalized SLE patients without a history of neuropsychiatric (NP) manifestations and without infections, 16 SLE patients without NP manifestations (surgical-SLE), four patients with primary neuropsychiatric disorders, and 25 patients with non-autoimmune diseases were also studied. Serum and CSF samples were drawn at hospitalization, except non-NPSLE patients, in whom only serum was studied, and six months later in 19 NPSLE and 27 non-NPSLE patients. Serum and CSF TWEAK levels were measured by ELISA; values are expressed in pg/mL. Results The mean ± SD age of NPSLE patients was 31 ± 13.1 years, which was similar across study groups ( p = 0.54). TWEAK levels in serum were not different across the study groups. In CSF, TWEAK levels were higher in NPSLE, surgical-SLE and primary neuropsychiatric groups than in non-autoimmune patients: median (IQR) 159.2 (94.1–374.9), 172.3 (125.3–421.9), 371.3 (143–543) vs 122.1 (76.1–212.4), respectively; all p < 0.05. Six months later, when the neuropsychiatric manifestations were clinically in remission, serum or CSF TWEAK did not vary from baseline in NPSLE patients. Conclusions TWEAK levels are slightly elevated in CSF in SLE patients compared with non-autoimmune controls, irrespective of the presence of NP manifestations. TWEAK levels in serum and CSF do not seem to be a useful biomarker of CNS involvement in SLE.