Cortisol levels in cerebrospinal fluid correlate with severity and bacterial origin of meningitis

Holub, Michal; Beran, Ondřej; Džupová, Olga; Hnyková, Jarmila; Lacinová, Z; Příhodová, J.; Procházka, Bohumír; Helcl, M.

doi:10.1186/cc5729

Cited by 37 publications

(28 citation statements)

References 33 publications

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“…The finding of higher Cort concentrations in bacterial infections in comparison to viral infections is in accordance with our earlier observations in patients with meningitis; cortisol levels in CSF were significantly higher in patients with bacterial meningitis in comparison to patients with viral meningitis. It is worth noting that cortisol levels of 46.1 nmol/l in CSF had 82% sensitivity and 100% specificity for the diagnosis of bacterial meningitis [24]. The importance of S-Cort observed in this study for the distinction between bacterial and viral infections has not yet been described.…”

Section: Discussionmentioning

confidence: 62%

Evaluation of potential biomarkers for the discrimination of bacterial and viral infections

et al. 2011

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Section: Discussionmentioning

confidence: 62%

Evaluation of potential biomarkers for the discrimination of bacterial and viral infections

et al. 2011

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“…Similar elevations and effects on outcome have been reported in a variety of neurological conditions, including septic shock, bacterial meningitis, post-traumatic stress disorder, Alzheimer disease, depression, and multiple sclerosis. [47][48][49][50][51][52] This study further extends previous work 33,34 by systematically attempting to elucidate the origins and implications behind endogenous hormone profiles after TBI. This goal was accomplished by identifying temporal CSF hormone profiles, investigating correlations between serum and CSF hormone levels, and examining injury-specific relationships between CSF progesterone and cortisol levels.…”

Section: Discussionmentioning

confidence: 66%

“…43 In addition to hormone transport kinetics and BBB permeability, injury and inflammation may also reduce the ability of brain cells to metabolize sterol molecules, as is noted in the context of meningitis, 48 perhaps leading to further sustained increases in CSF cortisol in the setting of TBI. Moreover, because severe illness and/or chronic stress greatly reduces corticosteroid-binding globulin (CBG) production, there is an increased percentage of free cortisol readily available to cross the BBB and enter the injured brain.…”

Section: Mechanism Of Injury (# %)mentioning

confidence: 99%

Cerebrospinal Fluid Cortisol and Progesterone Profiles and Outcomes Prognostication after Severe Traumatic Brain Injury

Santarsieri

Niyonkuru

McCullough

et al. 2014

Journal of Neurotrauma

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Despite significant advances in the management of head trauma, there remains a lack of pharmacological treatment options for traumatic brain injury (TBI). While progesterone clinical trials have shown promise, corticosteroid trials have failed. The purpose of this study was to (1) characterize endogenous cerebrospinal fluid (CSF) progesterone and cortisol levels after TBI, (2) determine relationships between CSF and serum profiles, and (3) assess the utility of these hormones as predictors of long-term outcomes. We evaluated 130 adults with severe TBI. Serum samples (n = 538) and CSF samples (n = 746) were collected for 6 days post-injury, analyzed for cortisol and progesterone, and compared with healthy controls (n = 13). Hormone data were linked with clinical data, including Glasgow Outcome Scale (GOS) scores at 6 and 12 months. Group based trajectory (TRAJ) analysis was used to develop temporal hormone profiles delineating distinct subpopulations. Compared with controls, CSF cortisol levels were significantly and persistently elevated during the first week after TBI, and high CSF cortisol levels were associated with poor outcome. As a precursor to cortisol, progesterone mediated these effects. Serum and CSF levels for both cortisol and progesterone were strongly correlated after TBI relative to controls, possibly because of blood-brain barrier disruption. Also, differentially impaired hormone transport and metabolism mechanisms after TBI, potential de novo synthesis of steroids within the brain, and the complex interplay of cortisol and pro-inflammatory cytokines may explain these acute hormone profiles and, when taken together, may help shed light on why corticosteroid trials have previously failed and why progesterone treatment after TBI may be beneficial.

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“…Multiple chemokines have been reported to be upregulated in the CSF of patients with pneumococcal meningitis, including MIP-1delta (CCL15), NAP-2 (CXCL7), MIF, MCP-2 (CCL8), PARC (CCL18), MIP-3␣ (CCL20) (226), ENA-78 (CXCL5), GRO-␣ (CXCL-1) (455, 553), IL-8 (CXCL-8) (201,363,455,493,553), MCP-1 (CCL2), MIP-1␣ (CCL3), and MIP-1␤ (CCL4) (455). In animal models of pneumococcal meningitis, additional chemokines have been identified by protein arrays for brain tissue, including MIP-1␥ (CCL9), MIP-2 (CXCL-2), lymphotactin (XCL-1), TCA-3 (CCL1), eotaxin (CCL11), MCP-5 (CCL12), eotaxin-2 (CCL24), TECK (CCL25), PF-4 (CXCL4), CRG-2 (CXCL10), SDF-1␣ (CXCL12), BLC (CXCL13), and CXCL16 (246).…”

Section: Chemokinesmentioning

confidence: 99%

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

et al. 2011

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SUMMARY Pneumococcal meningitis continues to be associated with high rates of mortality and long-term neurological sequelae. The most common route of infection starts by nasopharyngeal colonization by Streptococcus pneumoniae , which must avoid mucosal entrapment and evade the host immune system after local activation. During invasive disease, pneumococcal epithelial adhesion is followed by bloodstream invasion and activation of the complement and coagulation systems. The release of inflammatory mediators facilitates pneumococcal crossing of the blood-brain barrier into the brain, where the bacteria multiply freely and trigger activation of circulating antigen-presenting cells and resident microglial cells. The resulting massive inflammation leads to further neutrophil recruitment and inflammation, resulting in the well-known features of bacterial meningitis, including cerebrospinal fluid pleocytosis, cochlear damage, cerebral edema, hydrocephalus, and cerebrovascular complications. Experimental animal models continue to further our understanding of the pathophysiology of pneumococcal meningitis and provide the platform for the development of new adjuvant treatments and antimicrobial therapy. This review discusses the most recent views on the pathophysiology of pneumococcal meningitis, as well as potential targets for (adjunctive) therapy.

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Cortisol levels in cerebrospinal fluid correlate with severity and bacterial origin of meningitis

Cited by 37 publications

References 33 publications

Evaluation of potential biomarkers for the discrimination of bacterial and viral infections

Evaluation of potential biomarkers for the discrimination of bacterial and viral infections

Cerebrospinal Fluid Cortisol and Progesterone Profiles and Outcomes Prognostication after Severe Traumatic Brain Injury

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

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