INTERLEUKIN-6 LEVELS IN THE CEREBROSPINAL-FLUID AND SERUM OF PATIENTSWITH GUILLAIN-BARRE-SYNDROME AND CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY

Clinical and experimental findings suggest that humoral factors, such as anti-peripheral nerve antibodies and cytokines, may be implicated i n the immunopathogenesis of Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Interleukin- 6 (IL-6) is a multifunctional cytokine that promotes immunoglobulin sy nthesis by B lymphocytes. Increased IL-6 release is associated with au toantibody production in a number of immune-mediated and neoplastic di sorders. To investigate the possible involvement of abnormal IL-6 rele ase in inflammatory polyneuropathies, we assayed IL-6 levels in the ce rebrospinal fluid (CSF) and serum of 23 patients with acute GBS and se ven with CIDP. We also studied 69 patients with other non-inflammatory neurological diseases (NIND), 25 with other inflammatory neurological diseases (IND), four with brain tumors (BT), and 15 normal donors (se rum alone) as controls. We found detectable levels of IL-6 in the CSF of 57% of GBS, 43% of CIDP, 60% of IND, 75% of BT, and 4% of NIND. In GBS patients, no correlation was found between CSF IL-6 values and oth er laboratory or clinical parameters, such as CSF total protein, CSF a lbumin, CSF IgG, CSF/serum albumin ratio, functional disability score, and time elapsed from disease onset. Serum IL-6 levels were increased in six of 23 (26%) GBS, in one of 39 (3%) NIND, and in one of seven ( 14%) IND, but in none of the CIDP or BT patients. There was no correla tion between serum and CSF IL-6 values, but cytokine levels in GBS ser a correlated with time elapsed from clinical onset. In addition, we me asured anti-GM1 IgG and IgM levels in the CSF and sera of GBS and CIDP patients to study the possible association of these autoantibodies wi th increased IL-6 secretion. In both CSF and sera of GBS or CIDP patie nts, increased anti-GM1 antibody levels were not associated with eleva ted IL-6. We conclude that elevated IL-6 levels are frequently detecte d in the CSF of patients with inflammatory polyneuropathies, especiall y GBS. The presence of a heightened IL-6 release, however, is not requ ired for the production of anti-GM1 antibodies in GBS and CIDP patient s. Additional studies may clarify whether testing CSF IL-6 levels in t he early phase of GBS would help in defining the inflammatory nature o f the polyneuropathy, prompting a faster choice of plasma exchange tre atment.