OBJECTIVE: The objective of this study was to define the cytokine and chemokine profiles in cerebrospinal fluid (CSF) from patients with headache as neuropsychiatric systemic lupus erythematosus (NPSLE). METHODS: In a post hoc analysis, seven patients hospitalized because of headache were included. Patients were evaluated at hospitalization and 6 months later and a CSF sample was obtained. As controls, CSF from 27 patients with other NPSLE syndromes, 16 SLE patients without a history of NP manifestations (non-NPSLE) and 25 patients with non-autoimmune diseases were studied. Soluble molecules including cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-α and IFN-γ) and chemokines [monocyte chemotactic protein-1, RANTES (regulated on activation normal T cell expressed and secreted), IL-8, monokine induced by IFN-γ (MIG), and IFN-γ-induced protein 10 (IP-10)] were measured with the use of cytometric bead array kits or luminometry. RESULTS: Patients with headache had increased CSF values in the following molecules compared with non-NPSLE and non-autoimmune diseases patients, respectively: IL-6 (208.5, 3.0, 3.0 pg/ml, P < 0.004 and P < 0.001), IL-8 (406.6, 30.0, 19.7 pg/ml, P < 0.05 and P < 0.004), IP-10 (4673, 329.7, 113.6 pg/ml, P = 0.02 and P < 0.002), RANTES (7.5, 2.5, 2.2 pg/ml, P < 0.003 for both) and MIG (944.7, 11.4, 3.5 pg/ml, P = 0.02 and P = 0.001). No clear difference was observed between patients with headache and other NPSLE. Higher levels of inflammatory molecules were found in patients with headache from intracranial hypertension and intractable non-specific headache than patients with migraine. Six months later, when the headache had resolved, all the elevated molecule levels had decreased significantly. CONCLUSION: Headache from intracranial hypertension and intractable non-specific headache, but not migraine, share the inflammatory profile in CSF observed in other NPSLE syndromes.
OBJECTIVE: The objective of this study was to define the cytokine and chemokine profiles in cerebrospinal fluid (CSF) from patients with headache as neuropsychiatric systemic lupus erythematosus (NPSLE). METHODS: In a post hoc analysis, seven patients hospitalized because of headache were included. Patients were evaluated at hospitalization and 6 months later and a CSF sample was obtained. As controls, CSF from 27 patients with other NPSLE syndromes, 16 SLEpatients without a history of NP manifestations (non-NPSLE) and 25 patients with non-autoimmune diseases were studied. Soluble molecules including cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-α and IFN-γ) and chemokines [monocyte chemotactic protein-1, RANTES (regulated on activation normal T cell expressed and secreted), IL-8, monokine induced by IFN-γ (MIG), and IFN-γ-induced protein 10 (IP-10)] were measured with the use of cytometric bead array kits or luminometry. RESULTS:Patients with headache had increased CSF values in the following molecules compared with non-NPSLE and non-autoimmune diseasespatients, respectively: IL-6 (208.5, 3.0, 3.0 pg/ml, P < 0.004 and P < 0.001), IL-8 (406.6, 30.0, 19.7 pg/ml, P < 0.05 and P < 0.004), IP-10 (4673, 329.7, 113.6 pg/ml, P = 0.02 and P < 0.002), RANTES (7.5, 2.5, 2.2 pg/ml, P < 0.003 for both) and MIG (944.7, 11.4, 3.5 pg/ml, P = 0.02 and P = 0.001). No clear difference was observed between patients with headache and other NPSLE. Higher levels of inflammatory molecules were found in patients with headache from intracranial hypertension and intractable non-specific headache than patients with migraine. Six months later, when the headache had resolved, all the elevated molecule levels had decreased significantly. CONCLUSION:Headache from intracranial hypertension and intractable non-specific headache, but not migraine, share the inflammatory profile in CSF observed in other NPSLE syndromes.