Ayşe ÖZDEMİR, Rahsan ILİKCİ SAGKAN, Ali Yavuz KARAHAN, BANU ORDAHAN

Evaluation of salivary alpha-amylase activity after stroke

This study aimed to investigate the levels of sAA (Salivary Alpha-Amylase) in stroke patients. The H0 hypothesis of the study was established as the increase in sAA activity after stroke is not statistically significant when compared with the normal healthy population of the similar age group. Patients and Methods: This research is a case-control study. Forty-two patients who had a stroke during the period of February-November 2018 in the Department of Physical Medicine and Rehabilitation in Turkey and 40 healthy volunteers were included in the study. Saliva samples were collected within the first seven days after stroke. Saliva samples were taken by passive dilution (drool) technique with the standard method at certain hours. The concentration in U/mL of sAA in the samples is then calculated by comparing optical densities (OD) of the samples to the standard curve. Results: In the stroke group, a total of 42 patients and a total of 40 patients as volunteers were evaluated. The mean age was 69.4 ± 6.1 in the stroke group and 69.6 ± 6.4 in the healthy volunteers. The mean functional independence criterion in the stroke group was 64.7 ± 18.4. The sAA levels were found to be 142.18 ± 42.15 U / mL in the stroke group and 103.69 ± 36.52 U / mL in the healthy volunteers. There were statistically significant difference levels of the sAA between the two groups (p: 0.012). Conclusion: The levels of sAA in stroke patients were not clearly investigated in the literature, and the results indicate that patients with stroke have higher sAA activity compared to healthy subjects. The relationships between autonomic dysfunction and high sAA activity in stroke patients are new topics to be investigated.

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Manwani B, Liu F, Scranton V, et al. Differential effects of aging and sex on stroke-induced inflammation across the lifespan. Experimental Neurol. 2013;249:120–31.

Yılmaz N, Mandıroğlu S, Alemdaroğlu E, et al. Axillary nerve involvement in hemiplegia. Aegean J Med Sci. 2019;2:19-25.

Ordahan B, Karahan AY, Basaran A, et al. Impact of exercises administered to stroke patients with balance trainer on rehabilitation results: a randomized controlled study. Hippokratia. 2015;19:125–30.

Dorrance AM. and Fink G. Effects of Stroke on the Autonomic Nervous System. Compr Physiol. 2015;5:1241-63.

Pires PW, Dams Ramos CM, Matin N, Dorrance AM. The effects of hypertension on the cerebral circulation. Am J Physiol Heart Circ Physiol. 2013;304:H1598-614.

Hart MN, Heistad DD, Brody MJ. Effect of chronic hypertension and sympathetic denervation on wall/lumen ratio of cerebral vessels. Hypertension. 1980;2: 419-23.

Sadoshima S, Busija D, Brody M, et al. Sympathetic nerves protect against stroke in stroke-prone hypertensive rats. A preliminary report. Hypertension. 1981;3:I124-7.

Öztürk Turan Ç, Uysal E. Karotid arter darlığında 3D-TOF MR ve kontrastlı MR Anjiografi ile DSA bulgularının karşılaştırılması. Aegean J Med Sci. 2018;1:43-9.

Suzuki N, Hardebo JE, Kahrstrom J, et al. Selective electrical stimulation of postganglionic cerebrovascular parasympathetic nerve fibers originating from the sphenopalatine ganglion enhances cortical blood flow in the rat. J Cereb Blood Flow Metab. 1990;10:383-91.

10. Myers MG, Norris JW, Hachinski VC, et al. Cardiac sequelae of acute stroke. Stroke. 1982;13:838-42.

11. Kirschbaum C, Hellhammer DH. Salivary cortisol in psychoneuroendocrine research: recent developments and applications. Psychoneuroendocrinology. 1994;19:313–33.

12. Nater UM, Rohleder M. Salivary alpha-amylase as a non-invasive biomarker for the sympathetic nervous system: Current state of research; Psychoneuroendocrinology. 2009;34:486-96.

13. Gordis EB, Granger DA, Susman EJ, et al. Salivary alpha amylase–cortisol asymmetry in maltreated youth. Hormones Behavior. 2008;53:96-103.

14. Fuentes M, Tecles F, Gutiérrez A, et al. Validation of an automated method for salivary alpha-amylase measurements in pigs (sus scrofa domesticus) and its application as a stress biomarker. J Veterinary Diagn Investigation. 2011;23:282-7.

15. Strahler J, Kirschbaum C, Rohleder N. Association of blood pressure and antihypertensive drugs with diurnal alpha-amylase activity. Int J Psychophysiol. 2011;81:31-7.

16. Lakshmi PV, Sridevi E, Sai Sankar AJ, et al. Diagnostic perspective of saliva in insulin dependent diabetes mellitus children: An in vivo study. Contemp Clin Dent. 2015;6:443–7.

17. Küçükdeveci AA, Yavuzer G, Elhan AH, et al. Adaptation of the functional independence measure for use in Turkey. Clin Rehabil. 2001;15:311-9.

18. Şahan M, Satar S, Koç AF, ve ark. İskemik İnme ve Akut Faz Reaktanları. Arsiv. 2010;19:85.

19. Utku U. Stroke: Definition, Etiology, Classification and risk Factors. Turk J Phys Med Rehab. 2007;53:1-3.

20. Becker KJ, Kindrick DL, Lester MP, et al. Sensitization to brain antigens after stroke is augmented by lipopolysaccharide. J Cereb Blood Flow Metab 2005;25:1634-44.

21. Colivicchi F, Bassi A, Santini M, et al. Prognostic implications of right-sided insular damage, cardiac autonomic derangement, and arrhythmias after acute ischemic stroke. Stroke. 2005;36:1710-5.

22. Korpelainen JT, Sotaniemi KA, Huikuri HV, et al. Abnormal heart rate variability as a manifestation of autonomic dysfunction in hemispheric brain infarction. Stroke. 1996;27:2059-63.

23. Sander D, Winbeck K, Klingelhofer J, et al. Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke. Neurology. 2001;57:833-8.

24. Prosser J, MacGregor L, Lees KR, et al. Predictors of early cardiac morbidity and mortality after ischemic stroke. Stroke. 2007:38;2295-302.

25. McCance AJ. Assessment of sympathoneural activity in clinical research. Life Sciences. 1991;48:713-21.

26. Malliani A, Montano N. Heart rate variability as a clinical tool. Ital Heart J. 2002;3:439-45. 27. Myers MG, Norris JW, Hachniski VC, et al. Plasma norepinephrine in stroke. Stroke. 1981;12:200-4.

28. Ozdemir A, Erel O. Thiol-Disulphide Balance: Could Be a New Marker for Thyroid Cancer? J Cancer Therapy. 2018;9:598-604.

29. Deutsch O, Fleissig Y, Zaks B, et al. An approach to remove alpha amylase for proteomic analysis of low abundance biomarkers in human saliva. Wiley Online Library. 2008;29:4150–7.

30. Yamaquchi M, Dequshi M, Wakasuqi J, et al. Hand-heldmonitor of sympathetic nervous system using salivary amylase activity and its validation by driver fatigue assessment. Biosens&Bioelectron. 2006;21:1007-14.

31. Scannapieco FA, Solomon L, Wadenya RO. Emergence in human dental plaque and host distrubution of amylase-binding streptoccocci. J Dent Res. 2004;73:1627-35.

32. Anderson LC, Garrett JR, Johnson DA, et al. Influence of circulating catecholamines on protein secretion into rat parotid saliva during parasympathetic stimulation. J. Physiol.1984:352:163-71.

33. Rohleder N, Nater UM, Wolf JM, et al. Psychosocialstress-induced activation of salivary alpha amylase: an indicator of sympatheti cactivity. Ann N Y Acad Sci. 2004;1032:258-63.

34. Poggi Davis E, Granger AD. Developmental differences in infant salivary alpha-amylase and cortisol responses to stress. Psychoneuroendocrinology. 2009;34:795-804.

35. Sander D, Klingelhofer J. Changes of circadian blood pressure patterns and cardiovascular parameters indicate lateralization of sympathetic activation following hemispheric brain infarction. J Neurol. 1995;242:313-8..

36. Strittmatter M, Meyer S, Fischer C, et al. Locationdependent patterns in cardio-autonomic dysfunction in ischaemic stroke. Eur Neurol. 2003;50:30-8.

37. Meyer S, Strittmatter M, Fischer C, Georg T, Schmitz B. Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex. Neuroreport. 2004;15:357-61.

38. Nater UM, Rohleder N, Schlotz W, et al. Determinants of the diurnal course of salivary alpha-amylase. Psychoneuroendocrinology. 2007;32:392-401.

39. Fábián TK, Fejérdy P, Csermely P. Saliva in health and disease, chemical biology of. Wıley encyclopedıa of chemıcal bıology, John Wiley & Sons, Inc; 2007. p. 1-10.

40. Ochiai A, Harada K, Hashimoto K, et al. α-Amylase is a potential growth inhibitor of Porphyromonas gingivalis, a periodontal pathogenic bacterium. J Periodont Res. 2014;49:62-8.

41. Çakır Edis, E. Aspirasyon Pnömonisi, Derleme, Güncel Göğüs Hastalıkları Serisi. 2014;2:52-8.

42. Yılmaz FH, Yılmaz İ, Uysal Aladağ B, et al. Aspirasyon Pnömonisi –Olgu sunumu. Genel Tıp Derg. 2014;24:6-8.

43. Karahan AY, Kucuksen S, Yilmaz H, et al. Effects of rehabilitation services on anxiety, depression, care-giving burden and perceived social support of stroke caregivers. Acta Medica (Hradec Kralove). 2014;57:68-72.

44. Abu-Hasan M, Elmallah M, Neal D, et al. Salivary Amylase Level in Bronchoalveolar Fluid as a Marker of Chronic Pulmonary Aspiration in Children. Pediatr Allergy Immunol Pulmonol. 2014;27:115-9.