Cerebrospinal fluid and serum IL-8, CCL2, and ICAM-1 concentrations in astrocytic brain tumor patients.

BACKGROUND: The aim of the study was the evaluation of serum and CSF concentrations of CCL2, IL-8, and sICAM-1 in patients with astrocytic tumors as compared to a group of non-tumoral patients. METHODS: Chemokine concentrations were measured using the ELISA method. RESULTS: Regardless of the parameter tested and the patient group (brain tumor or non-tumoral patients), statistical differences (P < 0.05) were found between concentrations obtained in CSF compared to values obtained in serum for all proteins tested. CSF IL-8 concentrations were significantly elevated in CNS tumor patients as compared to non-tumoral individuals (P = 0.000); serum CCL2 and sICAM-1 concentrations were significantly decreased in CNS tumors in comparison with the comparative group (P = 0.002 and P = 0.026, respectively). Among proteins tested in the serum, a higher area under the ROC curve (AUC) revealed CCL2 compared to sICAM-1 in differentiating subjects with CNS brain tumors from non-tumoral subjects. AUC for CSF IL-8 was higher than for its index (CSF IL-8/serum IL-8). CONCLUSIONS: For individual biomarkers (IL-8 and CCL2, sICAM-1), measured in CNS brain tumor patients, the appropriate material, respectively CSF or serum, should be chosen and quantitatively tested. Increased cerebrospinal fluid IL-8 with decreased serum CCL2 create a pattern of biomarkers, which may be helpful in the management of CNS astrocytic brain tumors.

[Brain temperature in patients with central nervous system lesions]. / Temperatura mózgu u chorych operowanych z powodu uszkodzen osrodkowego ukladu nerwowego.

The knowledge of human brain temperature is still very limited. In this report we investigated the relationship between brain and trunk temperature in neurosurgical patients during normothermia and fever. Another problem addressed was that of possible gradients of temperature within the brain. We carried out direct recordings of temperature in 63 operated, neurosurgical patients with a variety of intracranial pathologies. Flexible, teflon-coated thermocouples were placed intracranially during neurosurgical procedures. Oesophageal, rectal and tympanic temperatures were also monitored. An error of up to 1.3 degrees C is to be expected in single cases if brain temperature is deduced from the rectal or oesophageal temperature. Mean differences between brain temperature and core body temperature measured in the rectum or in the oesophagus, were between 0 to 0.3 degree C. Tympanic temperature (Tty) improved the approximation of brain temperature (Tbr) to within the mean difference between Tbr-Tty close to 0 degree C. Nevertheless Tty also differed from Tbr by as much as 1 degree C in single cases. Brain temperature was the highest body temperature measured, either in normothermia or in fever. Temperature gradients were proved to exist between the warmer brain interior and cooler surface, with maximal differences in temperature reaching 0.6 degree C. This temperature gradient tended to increase along with the rise in intracranial pressure and deterioration of the level of consciousness. Our results suggest that conclusions regarding brain temperature drawn on the basis of other core temperatures, may lead to significant errors, and intracranial temperature measurement is desirable in neurosurgical intensive care. Temperature gradients within the brain may exacerbate its biochemical injury during ischaemia and fever--a combination seen frequently in neurosurgical patients. This may be particularly so, since brain temperature in fever is the highest body temperature in a high proportion of these patients.

No specific brain protection against thermal stress in fever.

Knowledge about human brain temperature is still very limited, despite evidence demonstrating the critical influence of mild increases in temperature on the ischaemic brain. It has been suggested that in passive and exercise hyperthermia the brain may be protected against thermal damage by a mechanism of selective brain cooling (SBC). It is said to bring about suppression of the temperature of the brain, rendering it significantly lower than trunk and arterial blood temperature. Yet very little is known about the possible role of this mechanism in fever, a condition fundamentally different from "physiological" hyperthermia, especially when it occurs in brain-damaged patients. In our investigation we retrospectively analysed the results of direct recordings of cerebral temperature within the subdural space (Tsd) and within the brain parenchyma (Tbr-16 cases) in 63 unanaesthetized patients following neurosurgical procedures, including 23 with fever > 38 degrees C. The difference between trunk temperature, measured in the rectum (Tre) or in the oesophagus (Tes), and the intracranial temperature, were calculated in all subjects. A statistically significant reduction of these differences, in step with increasing fever, would be compatible with demonstrating a process of selective brain cooling. The offsets Tre-Tsd, Tre-Tbr, and Tes-Tsd were plotted against Tre over a wide range of body temperature and near zero correlation was found. This finding suggests that brain temperature in fever was not selectively suppressed by any specific thermolytic mechanism and that dissipation of the main bulk of cerebral metabolic heat both in normothermia and in fever depends on heat uptake by arterial blood. The results suggest that the brain in fever can be seriously jeopardized by heat stress and no specific cooling mechanism exists, to reduce it below body temperature in feverish neurosurgical patients. Tbr and/or Tsd remained the highest body temperature in 14 out of the 23 patients during fever.