Serum and cerebrospinal fluid S100B concentrations in patients with neurocysticercosis

Author(s)

J.E. Lima ^[1] ; R. Walz ^[2] ; A. Tort ^[3] ; D. Souza ^[4] ; L. Portela ^[5] ; M.M. Bianchin ^[6] ; O.M. Takayanagui ^[7] ; J.P. Leite ^[8]

Affiliation

^[1] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Neurologia - Brasil

^[2] Hospital Governador Celso Ramos. Universidade Federal de Santa Catarina e Centro de Cirurgia de Epilepsia. Departamento de Clínica Médica - Brasil

^[3] Universidade Federal do Rio Grande do Sul. Departamento de Bioquímica - Brasil

^[4] Universidade Federal do Rio Grande do Sul. Departamento de Bioquímica - Brasil

^[5] Universidade Federal do Rio Grande do Sul. Departamento de Bioquímica - Brasil

^[6] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Neurologia - Brasil

^[7] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Neurologia - Brasil

^[8] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Neurologia - Brasil

• Document type: Journal article
• Source: Brazilian Journal of Medical and Biological Research; v. 39, n. 1, p. 129-135, 2006-01-00.

Abstract

The clinical manifestations of neurocysticercosis (NC) are varied and depend on the number and location of cysts, as well as on the host immune response. Symptoms usually occur in NC when cysticerci enter a degenerative course associated with an inflammatory response. The expression of brain damage markers may be expected to increase during this phase. S100B is a calcium-binding protein produced and released predominantly by astrocytes that has been used as a marker of reactive gliosis and astrocytic death in many pathological conditions. The aim of the present study was to investigate the levels of S100B in patients in different phases of NC evolution. Cerebrospinal fluid and serum S100B concentrations were measured in 25 patients with NC: 14 patients with degenerative cysts (D), 8 patients with viable cysts (V) and 3 patients with inactive cysts. All NC patients, except 1, had five or less cysts. In most of them, symptoms had been present for at least 1 month before sample collection. Samples from 8 normal controls (C) were also assayed. The albumin quotient was used to estimate the blood-brain barrier permeability. There were no significant differences in serum (P = 0.5) or cerebrospinal fluid (P = 0.91) S100B levels among the V, D, and C groups. These findings suggest that parenchymal changes associated with a relatively small number of degenerating cysts probably have a negligible impact on glial tissue. (AU)