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Procalcitonin Levels in Migraine Patients

Published online by Cambridge University Press:  02 December 2014

Hale Turan ,
Bahriye Horasanli ,
Murat Ugur  and
Hande Arslan
Hale Turan*
Affiliation:
Department of Infectious Diseases and Clinical Microbiology Department, Baskent University Faculty of Medicine, Selçuklu, Konya
Bahriye Horasanli
Affiliation:
Neurology Department, Baskent University Faculty of Medicine, Selçuklu, Konya
Murat Ugur
Affiliation:
Emergency Department, Baskent University Faculty of Medicine, Selçuklu, Konya
Hande Arslan
Affiliation:
Department of Infectious Diseases and Clinical Microbiology, Bahçelievler, Ankara, Turkey
*
Baskent University Faculty of Medicine, Department of Infectious Diseases and Clinical Microbiology Department, Hocacihan mahallesi. Saray caddesi No:1, Selçuklu 42080, Konya, Turkey
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Abstract:

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Objectives:

Migraine is a risk factor for ischemic stroke. Sterile vascular inflammation may develop during migraine attacks. This study aims to investigate procalcitonin (PCT) levels amongst migraine patients as they are important markers for infection and sepsis, but can also be found at elevated levels in various cases of inflammation.

Methods:

Eighty adult migraine patients participated in our study. Patients were initially separated into two main groups; Group-1 consisted of 34 patients who had migraines during the attack period. Group-2 consisted of 46 patients during the period in-between attacks. Afterwards, patients were further divided into four subgroups based on their aura status; Group-1a Migraine without aura, 27 patients during attack period, Group-1b Migraine with aura, 7 patients during attack period, Group-2a Migraine without aura, 40 patients during the period in-between attacks, Group-2b Migraine with aura, 6 patients during the period in-between attacks.

Results:

Average PCT levels in patients during attack periods were found to be higher than the average PCT levels of patients during the period in-between attacks. These elevated levels were determined to be statistically significant(p<0.01). Serum PCT levels of the patients with migraine without aura during the attack period were significantly higher than those of patients during the period in-between attacks(p<0.01).

Conclusions:

Based on significantly high levels of PCT, our results support the idea that sterile inflammation plays a role in migraine pathogenesis. Further studies are necessary to understand whether PCT is a marker for ischemic stroke risk in patients who go through frequent migraine attacks.

Résumé:

Résumé:Objectifs:

La migraine est un facteur de risque de l'accident vasculaire cérébral ischémique. Une inflammation vasculaire stérile peut survenir pendant les crises de migraine. Le but de cette étude était de déterminer chez des patients migraineux les niveaux de procalcitonine (PCT), un marqueur important de l'infection et de la septicémie, qui peut également être élevé dans l'inflammation due à des causes variées.

Méthodes:

Quatre-vingt patients migraineux adultes ont participé à notre étude. Les patients ont été répartis en deux groupes: dans le groupe 1, composé de 34 patients, le taux de PCT était mesuré pendant les crises; dans le groupe 2, composé de 46 patients, le taux de PCT était mesuré entre les crises. Chaque groupe était ensuite subdivisé en deux sous-groupes selon l'absence ou la présence d'une aura: le groupe 1a, composé de 27 patients sans aura et le groupe 1b, composé de 7 patients avec aura ; le groupe 2a, composé de 40 patients sans aura et le groupe 2b, composé de 6 patients avec aura.

Résultats:

Les taux moyens de PCT mesurés pendant les crises étaient plus élevés que les taux moyens mesurés entre les crises et la différence était significative au point de vue statistique (p < 0,01). Les niveaux sériques de PCT des patients avec migraine sans aura étaient significativement plus élevés pendant les crises qu'entre les crises (p < 0,01).

Conclusions:

Nos résultats, soit des taux significativement plus élevés de PCT, sont en faveur de l'hypothèse selon laquelle l'inflammation stérile jouerait un rôle dans la pathogenèse de la migraine. Il faudra des études plus poussées pour déterminer si la PCT est un marqueur du risque d'accident vasculaire cérébral chez les patients dont les crises de migraine sont fréquentes.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 38 , Issue 1 , January 2011 , pp. 124 - 128
Copyright
Copyright © Canadian Neurological Sciences Federation 2011

References

1 Bousser, MG, Welch, KM. Relation between migraine and stroke. Lancet Neurol. 2005;4:533–42.Google Scholar
2 Vanmolkot, FH, de Hoon, JN. Increased C-reactive protein in young adult patients with migraine. Cephalalgia. 2007;27:843–6.CrossRefGoogle ScholarPubMed
3 Moskowitz, MA, Cutrer, FM. Sumatriptan: a receptor-targeted for migraine. Ann Rev Med. 1993;44:145–54.Google Scholar
4 Buzzi, MG, Moskowitz, MA. The antimigraine drug, sumatriptan (GR43175) selectively blocks neurogenic plasma extravasation from blood vessels in dura mater. Br J Pharmacol. 1990;99:202–6.Google Scholar
5 Bolay, H, Reuter, U, Dunn, AK, Huang, Z, Boas, DA, Moskowitz, MA. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med. 2002;8:136–42.Google Scholar
6 Waeber, C, Moskowitz, MA. Migraine as an inflammatory disorder. Neurology. 2005;64:9–15.Google Scholar
7 Lindsberg, PJ, Grau, AJ. Inflammation and infections as risk factors for ischemic stroke. Stroke. 2003;34:2518–32.Google Scholar
8 Welch, KM. Stroke and migraine—the spectrum of cause and effect. Funct Neurol. 2003;18:121–6.Google ScholarPubMed
9 Welch, KM, Brandes, AW, Salerno, L, Brandes, JL. C-reactive protein may be increased in migraine patients who present with complex clinical features. Headache. 2006;46:197–9.Google Scholar
10 Yasunari, K, Maeda, K, Nakamura, M. Oxidative stress in leukocytes is a possible link between blood pressure, blood glucose, and Creactive protein. Hypertension. 2002;39:777–80.CrossRefGoogle Scholar
11 Ridker, PM, Cushman, M, Stampfer, MJ, Tracy, RP, Hennekens, CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Eng J Med. 1997;336:973–9.Google Scholar
12 Becker, KL, Snider, R, Nylen, ES. Procalcitonin assay in systemic inflammation, infection, and sepsis: clinical utility and limitations. Crit Care Med. 2008;36(3):941–52.Google Scholar
13 Miyakis, S, Georgakopoulos, P, Kiagia, M, et al. Serial serum procalcitonin changes in the prognosis of acute stroke. Clin Chim Acta. 2004;350:237–9.Google Scholar
14 Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia. 1988;8:1–96.Google Scholar
15 Johnson, AM, Rohlfs, EM, Silverman, LM. Proteins. In: Burtis, CA, Ashwoodd, ER, editors. Tietz textbook of clinical chemistry. Philadelphia: WB Saunders; 1999. p. 493.Google Scholar
16 Biasucci, LM, Biasillo, G, Stefanelli, A. Procalcitonin and acute coronary syndromes; a new biomarker for an old disease. Intern Emerg Med. 2009;4:363–5.Google Scholar
17 van Dijk, EJ, Prins, ND, Vermeer, SE, et al. C-reactive protein and cerebral small-vessel disease: the Rotterdam Scan Study. Circulation. 2005;112:900–5.CrossRefGoogle ScholarPubMed
18 Choudhuri, R, Cui, L, Yong, C, et al. Cortical spreading depression and gene regulation: relevance to migraine. Ann Neurol. 2002;51:499–506.CrossRefGoogle ScholarPubMed
19 Pearson, TA, Mensah, GA, Alexander, RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499–511.CrossRefGoogle Scholar
20 Gudmundsson, LS, Aspelund, T, Scher, AI, et al. C-reactive protein in migraine sufferers similar to that of non-migraineurs: The Reykjavik Study. Cephalalgia. 2009;29:1301–10.Google Scholar
21 Di Napoli, M, Schwanniger, M, Cappelli, R, et al. Evaluation of Creactive protein measurement for assessing the risk and prognosis in ischemic stroke: a statement for health care professionals from the CRP Pooling Project members. Stroke. 2005;36:1316–29.Google Scholar
22 Sentürk, T, Cordan, J, Bardan, J, et al. Procalcitonin in patients with acute coronary syndrome: correlation with high-sensitive Creactive protein, prognosis, and severity of coronary artery disease. Acta Cardiol. 2007;62:135–41.Google Scholar
23 Lassen, LH, Jacobsen, VB, Haderslev, PA, et al. Involvement of calcitonin gene-related peptide in migraine: regional cerebral blood flow and blood flow velocity in migraine patients. J Headache Pain. 2008;9:151–7.Google Scholar
24 Lassen, LH, Haderslev, PA, Jacobsen, VB, Iversen, HK, Sperling, B, Olesen, J. CGRP may play a causative role in migraine. Cephalalgia. 2002;22:54–61.Google Scholar
25 Becker, KL, Nylen, ES, White, JC, Muller, B, Snider, RH Jr. Procalcitonin and the calcitonin gene family of peptides in inflammation, infection and sepsis: a journey from calcitonin back to its precursors. J Clin Endocrinol Metabol. 2004;84:1512–25.Google Scholar
26 Schneider, HG, Lam, QT. Procalcitonin for the clinical laboratory: a review. Pathology. 2007;39(4):383–90.Google Scholar