Relationship of spontaneous subarachnoid haemorrhage and cerebral aneurysm to serum Visfatin and Nesfatin-1 levels

Objectives: Visfatin and nesfatin are recently discovered peptides that play a role in various metabolic reactions exhibiting inflammatory and neuroprotective effects, and their levels are known to increase in cerebral ischaemia and haematomas. Inflammation plays a role in the development of aneurysm, and spontaneous subarachnoid haemorrhage (SAH) is typically caused by rupture of the aneurysmal sac because of the increased inflammation. In the present study, we investigated the relationship between serum visfatin and nesfatin levels and the clinical and radiological findings in patients with SAH. Patients and Method: Overall, 62 patients with spontaneous SAH who were followed-up in our clinic between September 2018 and July 2019 and 35 healthy patients who presented to our outpatient clinic with complaints of back, lumbar and neck pain were included in the study. ELISA method was used to study the visfatin and nesfatin levels in the serum samples of both groups. The visfatin and nesfatin levels of patients with spontaneous SAH were compared with the healthy population. In addition, the relationship between visfatin and nesfatin levels and the radiological and clinical findings of patients with spontaneous SAH were also investigated. All findings were evaluated statistically. Results: The median nesfatin and mean visfatin levels were higher in patients with SAH compared with the control group. The median nesfatin and mean visfatin levels were higher in patients with aneurysm than those without aneurysm. A positive correlation was observed between aneurysm length and nesfatin and visfatin levels. In patients with perimesencephalic haemorrhage, the mean visfatin level was determined to be lower compared with patients with classical aneurysmatic SAH, and the median nesfatin level did not differ significantly. The cut-off value of nesfatin for predicting SAH in patients compared with controls was > 598.4 with 82.8 % sensitivity and 80 % specificity (P < 0.001). The cut-off value of visfatin for predicting SAH was > 10.3 with 85.3 % sensitivity and 91.4 % specificity (P < 0.001). The diagnostic performance of visfatin and nesfatin levels was similar in predicting SAH. Conclusion: In the present study, we demonstrated that the presence of aneurysm, size of aneurysm, number of aneurysms correlate with visfatin and nesfatin levels in patients with SAH, and visfatin and nesfatin may be biomarkers for predicting SAH and presence of aneurysm. Nonetheless, future studies can include patients with unruptured aneurysm and investigate their serum visfatin and nesfatin levels to prove whether visfatin and nesfatin can serve as biomarkers in the follow-up of these patients.