Evaluation of VCAM-1 and ICAM-1 concentration and values of global tests concerning the coagulation system of patients suffering from subarachnoid haemorrage

Michał Wiciński 2  ,  
Anna Czeczuk 4,  
Department of Neurosurgery and Neurotraumatology, University Hospital No. 2, Bydgoszcz, Poland
Department of Pharmacology and Therapeutics, Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz
Department of Natural Sciences, Faculty of Physical Education and Sport, Biała Podlaska, Poland
Department of Physical Education, Faculty of Physical Education and Sport, Biała Podlaska, Poland
Ann Agric Environ Med 2016;23(4):654–659
The term ‘subarachnoid haemorrhage’ (SAH) stands for bleeding into the subarachnoid space, regardless of its source. It may be of primary character when the source of bleeding is situated within the subarachnoid space. Subarachnoid haemorrhage is often described as spontaneous bleeding, mainly in order to differentiate it from post-traumatic bleeding.

The aim of the study was to evaluate the concentration of ICAM-1 and VCAM-1 in the blood of patients in the early phase following subarachnoid haemorrhage in terms of searching for markers useful in subarachnoid bleeding diagnostics and monitoring a patient’s clinical state.

Material and Methods:
The study comprised 85 patients (47 women, 38 men), aged 29–81 (average 53±12 years), suffering from subarachnoid haemorrhage. The control group comprised 45 healthy people selected according to gender and age corresponding with the experimental group.

The study revealed that the concentration of ICAM-1 and VCAM-1 was significantly higher in patients suffering from subarachnoid haemorrhage. Additionally, the concentration of fibrinogen decreased, aPTT was shorter and the concentration of D-dimers increased. The studied parameters did not differ with respect to the age or gender of the patients. It was stated that according to the Hunt and Hess scale, the concentration of ICAM-1 was considerably higher in the group of patients in the most severe neurological state, compared to other patients. It was also observed that the concentration of fibrinogen was significantly higher, aPTT was shorter, and the concentration of D-dimers increased in the afore-mentioned group.

Evaluation of the concentration of adhesion molecules, as well as values of global tests concerning the coagulation system, may serve as a useful diagnostic tool for SAH.

Michał Wiciński   
Department of Pharmacology and Therapeutics, Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz
1. Kidwell CS, Chalela JA, Saver JL, Starkman S, Hill MD, Demchuk AM, et al. Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA 2004; 292(15): 1823–1830.
2. Anand N, Stead LG. Neuron-specific enolase as a marker for acute ischemic stroke: a systematic review. Cerebrovasc Dis. 2005; 20(4): 213–219.
3. Galis ZS, Khatri JJ. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circ Res. 2002; 90(3): 251–262.
4. Marchi N, Cavaglia M, Fazio V, Bhudia S, Hallene K, Janigro D. Peripheral markers of blood-brain barrier damage. Clin Chim Acta 2004; 342(1–2): 1–12.
5. Stolpe A, Saag PT. Intercellular adhesion molecule-1. J Mol Med. 1996; 74(1): 13–33.
6. Acevedo A, del Pozo MA, Arroyo AG, Sánchez-Mateos P, González-Amaro R, Sánchez-Madrid F. Distribution of ICAM-3 bearing cells in normal human tissues. Expression of a novel counter-receptor for LFA-1 in epidermal Langerhans cells. Am J Pathol. 1993; 143(3): 774–783.
7. Rothlein R, Mainolfi EA, Czajkowski M, Marlin SD. A form of circulating ICAM-1 in human serum. J Immunol. 1991; 147(11): 3788–3793.
8. Seth R, Raymond FD, Makgoba MW. Circulatig ICAM-1 isoforms: diagnostic prospects for inflammatory and immune disorders. Lancet 1991; 338(8759): 83–84.
9. Sligh JE, Ballantyne CM, Rich SS, Hawkins HK, Smith CW, Bradley A, et al. Inflammatory and immune responses are impaired in mice deficient in intracellular adhesion molecule-1 deficient mice. Proc Natl Acad Sci USA. 1993; 90(18): 8529–8533.
10. Shimizu Y, Newman W, Tanaka Y, Shaw S. Lymphocyte interactions with endothelial cells. Immunol Today. 1992; 13(3): 106–112.
11. Pepinsky B, Hession C, Chen LL, Moy P, Burkly L, Jakubowsky A, et al. Structure/function studies on vascular cell adhesion molecule-1. J Biol Chem. 1992; 267(25): 17820–17826.
12. Handa Y, Kabuto M, Kobayashi H, Kawano H, Takeuchi H, Hayashi M. The correlation between immunological reaction in the arterial wall and the time course of the development of cerebral vasospasm in a primate model. Neurosurgery. 1991; 28(4): 542–549.
13. Kraus J, Gerriets T, Leis S, Stolz E, Oschmann P, Heckmann JG. Time course of VCAM-1 and ICAM-1 in CSF in patients with basal ganglia haemorrhage. Acta Neurol Scand. 2007; 116(1): 49–55.
14. Sessler CN, Windsor AC, Schwartz M, Watson L, Fisher BJ, Sugerman HJ, et al. Circulating ICAM-1 is increased in septic shock. Am J Respir Crit Care Med. 1995; 151(5): 1420–1427.
15. Bavbek M, Polin R, Kwan AL, Arthur AS, Kassell NF, Lee KS. Monoclonal antibodies against ICAM-1 and CD18 attenuate cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits. Stroke. 1998; 29(9): 1930–1936.
16. Tanne D, Haim M, Boyko V, Goldbourt U, Reshef T, Matetzky S, et al. Soluble intercellular adhesion molecule-1 and risk of future ischemic stroke: a nested case-control study from the Bezafibrate Infarction Prevention (BIP) study cohort. Stroke 2002; 33(9): 2182–2186.
17. Sobel RA, Mitchell ME, Fondren G. Intercellular adhesion molecule-1 (ICAM-1) in cellular immune reactions in the human central nervous system. Am J Pathol. 1990; 136(6): 1309–1316.
18. Khurana VG, Besser M. Pathophysiological basis of cerebral vasospasm following aneurysmal subarachnoid haemorrhage. J Clin Neurosci. 1997; 4(2): 122–131.
19. Wijdicks EF, Kallmes DF, Manno EM, Fulgham JR, Piepgras DG. Subarachnoid hemorrhage. Neurointensive care and aneurysm repair. Mayo Clin Proc. 2005; 80(4): 550–559.
20. Blann A, Kumar P, Krupinski J, McCollum C, Beevers DG, Lip GY. Soluble intercellular adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 and von Willebrand factor in stroke. Blood Coagul Fibrinolysis. 1999; 10(5): 277–284.
21. Kałuża J, Krupiński J, Kumar P, Kumar S, Wang JM. VCAM-1 expression on reactive and tumour astrocytes. Folia Histochem Cytobiol. 1994; 32(1): 17–20.
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