[Primary vasculitis of internal carotid and vertebral arteries: a role of cytokines, transforming growth factor beta 1 and basic fibroblast growth factor].

Autor:	Kalashnikova LA; Research Center of Neurology, Moscow, Russia., Legenko MS; Research Center of Neurology, Moscow, Russia., Shabalina AA; Research Center of Neurology, Moscow, Russia., Dobrynina LA; Research Center of Neurology, Moscow, Russia., Shamtieva KV; Research Center of Neurology, Moscow, Russia., Kostyreva MV; Research Center of Neurology, Moscow, Russia., Dreval MV; Research Center of Neurology, Moscow, Russia., Lesnykh TA; Research Center of Neurology, Moscow, Russia.
Jazyk:	ruština
Zdroj:	Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova [Zh Nevrol Psikhiatr Im S S Korsakova] 2021; Vol. 121 (7), pp. 14-21.
DOI:	10.17116/jnevro202112107114
Abstrakt:	Objective: To study clinical/laboratory signs of primary vasculitis (PV) of the internal carotid artery (ICA) and vertebral artery (VA). Material and Methods: We examined 31 patients (23 men, 74%, mean age - 36.2±5.7 years) with ICA/VA PV verified by vessel wall contrast enhancement on black blood MRI (T1-weighted fat and blood suppressed sequences with- and without contrast injection) at the Research Center of Neurology (Moscow) from January 2012 to September 2019. Systemic vasculitis was excluded in all cases. Interleukins (IL-1β, IL-2, IL-6, IL-17), TNF-a, transforming growth factor beta 1 (TGF-β1) and basic fibroblast growth factor (bFGF) were analyzed by ELISA in 25 patients. Control group consisted of 21 healthy volunteers (12 men, 57%; mean age - 35.3±10.2 years). Results: Clinical manifestations of ICA/VA PV included: ischemic stroke (IS) (94%), which combined with transient ischemic attacks (TIA) in 35%; isolated TIA (3%); Tolosa-Hunt syndrome (3%). Recurrent strokes were observed in 41% of patients on average in 5.3±2.1 months. Carotid artery was involved in 77%, VA - in 16%, both arteries - in 7%. Concomitant involvement of ICA/VA branches was in 19% patients. The level of arterial damage was follows: Intracranial part of arteries involved in 55%, intra-extracranial - in 35%, extracranial - in 10%. Bilateral involvement was found in 26%. Headache/neck pain in the acute IS period was observed in 21%. IS severity (NIHSS) was as follows: moderate (59%), mild (34%), moderately severe (7%). Disability after 3 months according to mRankin scale was as follows: mild (72%) moderate (21%), none (7%). The laboratory study revealed an increased levels of IL-6 (8.19±3.89 pg/ml vs 4.7±1.48 in control, p =0.000), IL-2 (5.64±1.82 pg/ml vs 4.30±1.65, p =0.013), TNF-a (36.9±33.66 pg/ml vs 12.68±5.93, p =0.000), TGF β1 (2.77±1.60 pg/ml vs 1.63±0.64, p =0.006) and bFGF (417.67±132.68 pg/ml vs 335.71±105.08, p =0.018). The levels of IL-1β and IL-17 did not differ significantly from the control. Conclusion: ICA/VA PV has a number of clinical peculiarities. Proinflammatory cytokines produced by Th17 and Th1 CD4+ lymphocytes as well as bFGF and TGR-β1 play a role in its pathogenesis. Normal levels of IL-1β and IL-17 suggest that they are not significant in the development of isolated inflammation in ICA/PA, in contrast to systemic inflammation in giant cell arteritis, in which, according to literature data, their level increases. Isolated ICA/PA inflammation seems to be caused by transaxonal (trigeminal nerve, upper-cervical roots, autonomic nerves) spread of pathogens that initiate immune inflammation in the ICA/PA wall.
Databáze:	MEDLINE
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