PMID- 9254084
OWN - NLM
STAT- MEDLINE
DCOM- 19971002
LR  - 20220316
IS  - 0022-3085 (Print)
IS  - 0022-3085 (Linking)
VI  - 87
IP  - 2
DP  - 1997 Aug
TI  - Cerebrospinal fluid interleukin-1 receptor antagonist and tumor necrosis 
      factor-alpha following subarachnoid hemorrhage.
PG  - 215-20
AB  - Subarachnoid hemorrhage (SAH) causes an inflammatory reaction and may lead to 
      ischemic brain damage. Experimental ischemia has been shown to be connected with 
      the alarm-reaction cytokines interleukin-1 receptor antagonist (IL-1Ra) and tumor 
      necrosis factor-alpha (TNF alpha). Increased levels of these cytokines, however, 
      have not been detected thus far in patients following an SAH event. For this 
      reason daily cerebrospinal fluid (CSF) samples were collected from 22 
      consecutively enrolled patients with SAH and from 10 non-SAH patients (controls). 
      The CSF samples were studied using immunoassays for IL-1Ra and TNF alpha to 
      investigate whether an SAH caused increased cytokine levels. The mean IL-1Ra 
      levels were significantly higher in patients with SAH who were in poor clinical 
      condition on admission than in those who were in good condition (318 pg/ml vs. 82 
      pg/ml, p < 0.02). The IL-1Ra levels increased during delayed ischemic episodes 
      and after surgery in patients who were in poor clinical condition. Significant 
      increases in IL-1Ra and TNF alpha were detected during Days 4 through 10 in 
      patients suffering from SAH who eventually had a poor outcome (p < 0.05). 
      Patients with good outcomes and control patients had low levels of these 
      cytokines. The levels of IL-1Ra increased after surgery in patients with Hunt and 
      Hess Grades III through V, but not in those with Grade I or II. This finding 
      indicates that patients in poor clinical condition have a labile biochemical 
      state in the brain that is reflected in increased cytokine levels following the 
      surgical trauma. Both IL-1Ra and TNF alpha are known to induce fever, malaise, 
      leukocytosis, and nitric oxide synthesis and to mediate ischemic and traumatic 
      brain injuries. The present study shows that levels of these cytokines increase 
      after SAH occurs and that high cytokine levels correlate with brain damage. It is 
      therefore likely that fever, leukocytosis, and nitric oxide synthesis are also 
      mediated by IL-1 in patients suffering from SAH and it is probable that the 
      inflammatory mediators contribute to brain damage.
FAU - Mathiesen, T
AU  - Mathiesen T
AD  - Department of Neurosurgery, Karolinska Hospital, Stockholm, Sweden.
FAU - Edner, G
AU  - Edner G
FAU - Ulfarsson, E
AU  - Ulfarsson E
FAU - Andersson, B
AU  - Andersson B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosurg
JT  - Journal of neurosurgery
JID - 0253357
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Female
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Male
MH  - Middle Aged
MH  - Sialoglycoproteins/*cerebrospinal fluid
MH  - Subarachnoid Hemorrhage/*cerebrospinal fluid
MH  - Tumor Necrosis Factor-alpha/*cerebrospinal fluid
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - 10.3171/jns.1997.87.2.0215 [doi]
PST - ppublish
SO  - J Neurosurg. 1997 Aug;87(2):215-20. doi: 10.3171/jns.1997.87.2.0215.