Alfa-1 Antitripsin Eksikliğinde Migren Nedenselliği

Year 2024, , 179 - 182, 30.08.2024

Esra Demir Unal

https://doi.org/10.18678/dtfd.1447131

Abstract

Alfa1-antitripsin (A1AT), çeşitli inflamatuar durumlarda anti-inflamatuar ve immünomodülatör etkilerle ilişkili antiproteaz aktivitesine sahip bir anti-inflamatuar aracıdır. A1AT eksikliği (A1ATE), akciğer hastalığı (amfizem ve bronşektazi), karaciğer hastalığı (kronik hepatit, siroz ve hepatoma) ve cilt hastalıkları (pannikülit) gibi çeşitli hiperinflamatuar hastalıklarla ilişkilendirilmiştir. Auralı migren, etyopatogenezinde kortikal yayılan depresyon ve glial hiperinflamasyonla ilişkili nöroimmünolojik aktivasyon ve nöroinflamasyonla ilişkili olan yaygın migren alt tiplerinden biri olup şimdiye kadar açıklanan ana mekanizmalar, proinflamatuar mediatörlerin hiperinflamasyonu, trigeminal sinir liflerinin duyarlılığı ve ağrıyla konjuge glial hücrelerin aktivasyonudur. Bu vaka raporunda, sistemik hiperinflamatuar süreçlerin santral yansımalarını gösteren etioradiopatogenetik mekanizmalar üzerinden auralı migren ve A1ATE'nin nedensel bir perspektifi sunulmuş ve periferik hiperinflamatuar durumların migren etiyolojisindeki önemi incelenmiştir.

Keywords

Alfa-1 antitripsin eksikliği, kortikal yayılan depresyon, hepatoserebral yollar, migren, nöroimmün aktivasyon, nöroinflamasyon

Migraine Causality in Alpha-1 Antitrypsin Deficiency

Abstract

Alpha1-antitrypsin (A1AT) is an anti-inflammatory mediator with antiprotease activity associated with anti-inflammatory and immunomodulatory effects in various inflammatory conditions. A1AT deficiency (A1ATD) has been associated with various hyperinflammatory diseases, such as lung disease (emphysema and bronchiectasis), liver disease (chronic hepatitis, cirrhosis, and hepatoma), and skin diseases (panniculitis). Migraine with aura is one of the common migraine subtypes associated with neuroimmunologic activation and neuroinflammation which is associated with cortical spreading depression and glial hyperinflammation in etioradiopathogenesis, and the main mechanisms explained so far are hyperinflammation of pro-inflammatory mediators, sensitivity of trigeminal nerve fibers and pain-conjugated glial cells activation. In this case report, a causative perspective of migraine with aura and A1ATD was presented through etioradiopathogenetics mechanisms that show the central reflections of systemic hyperinflammatory processes, and the importance of peripheral hyperinflammatory conditions in migraine etiology was examined.

Keywords

Alpha-1 antitrypsin deficiency, cortical spreading depression, hepatocerebral pathways, migraine, neuroimmune activation, neuroinflammation

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