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We evaluated S-100 levels in paired cerebrospinal fluid (CSF) and serum samples in a group of 135 patients referred to the German Creutzfeldt-Jakob disease (CJD) surveillance unit from June 1993 to May 1995. The patients were seen in a prospective case control study. The diagnosis of probable CJD during life was made in any patient presenting with rapidly progressive dementia of less than 2 years' duration, typical periodic sharp wave complexes (PSWCs) in the EEG and at least two of the following findings: myoclonus, visual/or cerebellar symptoms, pyramidal and/or extrapyramidal signs and/or akinetic mutism. Patients presenting with the above clinical signs and symptoms but without PSWCs were classified as possible, while those with a dementia of a duration exceeding 2 years and without PSWCs were classified as other. S-100 was determined in paired CSF and serum samples by a commercially available enzyme-linked immunosorbent assay. In a group of 76 patients with definite and probable CJD, S-100 concentration (median 25 ng/ml, range 2-117) in CSF was significantly higher (P < 0.0001) than in 32 patients diagnosed as other (median 4 ng/ml, range 1-19). Serum levels of S-100 were below 0.5 ng/ml in all groups. At a cut-off of 8 ng/ml an optimum sensitivity of 84.2% with a specificity of 90.6% for the diagnosis of CJD by the determination of S-100 in CSF is obtained. S-100 levels exceeding 8 ng/ml in CSF support the diagnosis of CJD in any patient presenting with rapidly progressive dementia.

Summary. The MDRl gene product P-glycoprotein (P-gp), a transmembrane efflux pump, is expressed in many normal tissues including subpopulations of normal peripheral blood. To test the potential impact of cigarette smoke and/or a variety of lipophilic industrial solvents present in paint and varnish, P-gp expression in unsorted peripheral blood cells of 51 healthy volunteers was measured by means of immuno-cytochemistry and daunorubicin uptake studies. 10 of these volunteers were heavy smokers and 10 were working as painters or sprayers, and consequently in regular and intense contact with industrial solvents. Cigarette smoke had no impact with regard to increased P-gp expression and function. However, extensive contact with industrial solvents of lipophilic origin was shown to cause a significant increase in the level of P-gp expression (P