Cerebrospinal fluid macrophage migration inhibitory factor: a potential predictor of cerebral vasospasm and clinical outcome after aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 133 (6) ◽  
pp. 1786-1791 ◽  
Author(s):  
Kevin Kwan ◽  
Orseola Arapi ◽  
Katherine E. Wagner ◽  
Julia Schneider ◽  
Heustein L. Sy ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Significant Difference

OBJECTIVEIn patients with aneurysmal subarachnoid hemorrhage (aSAH), poor outcomes have been shown to be correlated with subsequent cerebral vasospasm (CV) and delayed cerebral ischemia (DCI). The identification of novel biomarkers may aid in the prediction of which patients are vulnerable to developing vasospasm, cerebral ischemia, and neurological deterioration.METHODSIn this prospective clinical study at North Shore University Hospital, patients with aSAH or normal pressure hydrocephalus (NPH) with external ventricular drains were enrolled. The concentration of macrophage migration inhibitory factor (MIF) in CSF was assessed for correlation with CV or DCI, the primary outcome measures.RESULTSTwenty-five patients were enrolled in the aSAH group and 9 were enrolled in the NPH group. There was a significant increase in aggregate CSF MIF concentration in patients with aSAH versus those with NPH (24.4 ± 19.2 vs 2.3 ± 1.1 ng/ml, p < 0.0002). Incidence of the day of peak MIF concentration significantly correlated with the onset of clinical vasospasm (rho = 0.778, p < 0.0010). MIF concentrations were significantly elevated in patients with versus those without evidence of DCI (18.7 ± 4.93 vs 8.86 ± 1.28 ng/ml, respectively, p < 0.0025). There was a significant difference in MIF concentrations between patients with infection versus those without infection (16.43 ± 4.21 vs 8.5 ± 1.22 ng/ml, respectively, p < 0.0119).CONCLUSIONSPreliminary evidence from this study suggests that CSF concentrations of MIF are correlated with CV and DCI. These results, however, could be confounded in the presence of clinical infection. A study with a larger patient sample size is necessary to corroborate these findings.

scholarly journals Blood free Radicals Concentration Determined by Electron Paramagnetic Resonance Spectroscopy and Delayed Cerebral Ischemia Occurrence in Patients with Aneurysmal Subarachnoid Hemorrhage

2017 ◽  
Vol 75 (3-4) ◽  
pp. 351-358 ◽  
Author(s):  
Grzywna Ewelina ◽  
Stachura Krzysztof ◽  
Moskala Marek ◽  
Kruczala Krzysztof
Keyword(s):  
Electron Paramagnetic Resonance ◽  
Free Radicals ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Paramagnetic Resonance ◽  
Significant Difference ◽  
Electron Paramagnetic

Abstract Pathophysiology of delayed cerebral ischemia and cerebral vasospasm following aneurysmal subarachnoid hemorrhage is still poorly recognized, however free radicals are postulated as one of the crucial players. This study was designed to scrutinize whether the concentration of free radicals in the peripheral venous blood is related to the occurrence of delayed cerebral ischemia associated with cerebral vasospasm. Twenty-four aneurysmal subarachnoid hemorrhage patients and seven patients with unruptured intracranial aneurysm (control group) have been studied. Free radicals in patients’ blood have been detected by the electron paramagnetic resonance (CMH.HCl spin probe, 150 K, ELEXSYS E500 spectrometer) on admission and at least 72 h from disease onset. Delayed cerebral ischemia monitoring was performed by daily neurological follow-up and transcranial color coded Doppler. Delayed cerebral ischemia observed in six aneurysmal subarachnoid hemorrhage patients was accompanied by cerebral vasospasm in all six cases. No statistically significant difference in average free radicals concentration between controls and study subgroups was noticed on admission (p = .3; Kruskal–Wallis test). After 72 h free radicals concentration in delayed cerebral ischemia patients (3.19 ± 1.52 mmol/l) differed significantly from the concentration in aneurysmal subarachnoid hemorrhage patients without delayed cerebral ischemia (0.65 ± 0.37 mmol/l) (p = .012; Mann–Whitney test). These findings are consistent with our assumptions and seem to confirm the role of free radicals in delayed cerebral ischemia development. Preliminary results presented above are promising and we need perform further investigation to establish whether blood free radicals concentration may serve as the biomarker of delayed cerebral ischemia associated with cerebral vasospasm.

scholarly journals Macrophage migration inhibitory factor expression is increased in pituitary adenoma cell nuclei

2003 ◽  
Vol 176 (1) ◽  
pp. 103-110 ◽  
Author(s):  
ME Pyle ◽  
M Korbonits ◽  
M Gueorguiev ◽  
S Jordan ◽  
B Kola ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Migration Inhibitory Factor ◽  
Pituitary Adenomas ◽  
Normal Tissue ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Inflammatory Factor ◽  
Macrophage Migration ◽  
Cell Nuclei ◽  
Significant Difference

Macrophage migration inhibitory factor (MIF) is an essential regulator of the macrophage responses to endotoxin. MIF also has the ability to override the anti-inflammatory actions of glucocorticoids during an immune response, and is thus an important pro-inflammatory factor. The presence of MIF in cells of the anterior pituitary has been described, and high levels of MIF in other rapidly proliferating tIssues have also been demonstrated. It has been hypothesised that MIF release from these cells is influenced by the hypothalamo-pituitary-adrenal axis, and that ACTH and MIF are released simultaneously to exert counter-regulatory effects on cortisol. However, another intracellular role for MIF has also been suggested as it has been shown that MIF exerts an effect on the inhibitory cell cycle control protein p27 through an interaction with Jab1, a protein implicated in p27 degradation. We studied MIF expression in different normal and adenomatous human pituitary samples using immunohistochemistry and RT-PCR. There was evidence of co-immunoprecipitation of MIF with Jab1, suggesting an interaction of the two proteins. Our results showed that there is increased expression of MIF protein in the nuclei of all pituitary adenomas compared with normal tIssue (P=0.0067), but there was no statistically significant difference in nuclear MIF expression between the different adenoma types. Nuclear MIF expression correlated positively with p27 and its phosphorylated form in normal tIssue (P=0.0028 and P<0.0001); however, this relationship was not seen in the adenoma samples. Cytoplasmic expression of MIF was found to be variable both in normal and adenomatous samples, with no consistent pattern. MIF mRNA was demonstrated to be present in all tumour and normal samples studied. Somatotroph tumours showed higher MIF mRNA expression compared with normal pituitary or other types of adenomas. In conclusion, MIF is expressed in cell nuclei in pituitary adenomas to a greater extent than in normal pituitary tIssue. We speculate that it may play a role in the control of the cell cycle, but whether its higher level in adenomas is a cause or a consequence of the tumorigenic process remains to be clarified.

scholarly journals Anesthesia modality does not affect clinical outcomes of intra-arterial vasodilator treatment in patients with symptomatic cerebral vasospasms

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 417
Author(s):  
Corinne Fischer ◽  
Sonja Vulcu ◽  
Johannes Goldberg ◽  
Franca Wagner ◽  
Belén Rodriguez ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
General Anesthesia ◽  
Clinical Outcomes ◽  
Cerebral Vasospasm ◽  
Conscious Sedation ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Vasodilator Therapy ◽  
Significant Difference ◽  
Vasodilator Treatment

Background: Delayed cerebral ischemia and cerebral vasospasm remain the leading causes of poor outcome in survivors of aneurysmal subarachnoid hemorrhage. Refractory cerebral vasospasms can be treated with endovascular vasodilator therapy, which can either be performed in conscious sedation or general anesthesia. The aim of this study is to compare the effect of the anesthesia modality on long-term clinical outcomes in patients undergoing endovascular vasodilator therapy due to cerebral vasospasm and hypoperfusion. Methods: Modified Rankin Scale (mRS) scores were retrospectively analyzed at time of discharge from the hospital and six months after aneurysmal subarachnoid hemorrhage. Additionally, National Institutes of Health Stroke Scale (NIHSS) was assessed 24 hours before, immediately before, immediately after, and 24 hours after endovascular vasodilator therapy, and at discharge and six months. Interventional parameters such as duration of intervention, choice and dosage of vasodilator and number of arteries treated were also recorded. Results: A total of 98 patients were included in this analysis and separated into patients who had interventions in conscious sedation, general anesthesia and a mix of both. Neither mRS at discharge nor at six months showed a significant difference for functionally independent outcomes (mRS 0-2) between groups. NIHSS before endovascular vasodilator therapy was significantly higher in patients receiving interventions in general anesthesia but did not differ anymore between groups six months after the initial bleed. Conclusion: This study did not observe a difference in outcome whether patients underwent endovascular vasodilator therapy in general anesthesia or conscious sedation for refractory cerebral vasospasms. Hence, the choice should be made for each patient individually.

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