AIM: To evaluate the penetration of ceftriaxone into the cerebrospinal fluid (CSF) in patients with invasive bacterial infection and to define correlation between the penetration and laboratory markers of inflammation. MATERIAL AND METHODS: Levels of ceftriaxone in the serum and CSF of 17 patients with purulent meningitis were examined. Serum concentrations of ceftriaxone before and after its administration were measured in 9 patients (18 samples, 52.9 %) by microbiological assay based on the agar diffusion test. In all patients, the CSF/serum quotient for ceftriaxone was calculated and correlated with laboratory markers of inflammation (C-reactive protein, fibrinogen and neutrophils). The CSF from nine patients with positive culture for bacteria was used for a modified bactericidal test. RESULTS: Ceftriaxone levels in the serum before and after administration (31.2 mg/l -/+ SD 12.29 and 300.0 mg/l -/+ SD 125.9, respectively) were different (p = 0.000156). The decrease of ceftriaxone levels in the CSF was gradual. There was also a significant difference between the levels of inflammatory markers and CSF/serum quotient of ceftriaxone. Patients with the values higher than 0.1 had higher CRP serum levels (p = 0.00192), fibrinogen serum levels (p = 0.0178) as well as neutrophil count in the CSF (p = 0.0112). However, no inflammatory markers (or their combinations) predicted the extent of penetration of ceftriaxone into the CSF. CONCLUSION: High serum concentration of ceftriaxone causes higher penetration through the inflamed blood-brain barrier. Higher antibiotic penetration correlated with the extent of systemic inflammatory response. However, no inflammatory marker predicted the rate of ceftriaxone crossing the blood-brain barrier. Ceftriaxone penetration, with a 24-hour regimen of administration, remains reliable and efficient therapy of purulent meningitis.
AIM: To evaluate the penetration of ceftriaxone into the cerebrospinal fluid (CSF) in patients with invasive bacterial infection and to define correlation between the penetration and laboratory markers of inflammation. MATERIAL AND METHODS: Levels of ceftriaxone in the serum and CSF of 17 patients with purulent meningitis were examined. Serum concentrations of ceftriaxone before and after its administration were measured in 9 patients (18 samples, 52.9 %) by microbiological assay based on the agar diffusion test. In all patients, the CSF/serum quotient for ceftriaxone was calculated and correlated with laboratory markers of inflammation (C-reactive protein, fibrinogen and neutrophils). The CSF from nine patients with positive culture for bacteria was used for a modified bactericidal test. RESULTS:Ceftriaxone levels in the serum before and after administration (31.2 mg/l -/+ SD 12.29 and 300.0 mg/l -/+ SD 125.9, respectively) were different (p = 0.000156). The decrease of ceftriaxone levels in the CSF was gradual. There was also a significant difference between the levels of inflammatory markers and CSF/serum quotient of ceftriaxone. Patients with the values higher than 0.1 had higher CRP serum levels (p = 0.00192), fibrinogen serum levels (p = 0.0178) as well as neutrophil count in the CSF (p = 0.0112). However, no inflammatory markers (or their combinations) predicted the extent of penetration of ceftriaxone into the CSF. CONCLUSION: High serum concentration of ceftriaxone causes higher penetration through the inflamed blood-brain barrier. Higher antibiotic penetration correlated with the extent of systemic inflammatory response. However, no inflammatory marker predicted the rate of ceftriaxone crossing the blood-brain barrier. Ceftriaxone penetration, with a 24-hour regimen of administration, remains reliable and efficient therapy of purulent meningitis.