Clinical Neurosciences Department, College of Medicine, King Faisal University, Hofuf, Saudi Arabia.
Department of Pharmacology, Toxicology and Medicine, Medical Faculty, College of Medicine, Al-Mustansiriyah University, PO Box 14132, Baghdad, Iraq.
Acta Neurol Belg. 2024 Jun;124(3):755-766. doi: 10.1007/s13760-023-02354-3. Epub 2023 Aug 16.
Acromegaly is an endocrine disorder due to the excess production of growth hormone (GH) from the anterior pituitary gland after closed epiphyseal growth plates. Acromegaly is mainly caused by benign GH-secreting pituitary adenoma. Acute ischemic stroke (AIS) is one of the most common cardiovascular complications. It ranks second after ischemic heart disease (IHD) as a cause of disability and death in high-income countries globally. Thus, this review aimed to elucidate the possible link between acromegaly and the development of AIS. The local effects of acromegaly in the development of AIS are related to the development of pituitary adenoma and associated surgical and radiotherapies. Pituitary adenoma triggers the development of AIS through different mechanisms, particularly aneurysmal formation, associated thrombosis, and alteration of cerebral microcirculation. Cardiovascular complications and mortality were higher in patients with pituitary adenoma. The systemic effect of acromegaly-induced cardio-metabolic disorders may increase the risk for the development of AIS. Additionally, acromegaly contributes to the development of endothelial dysfunction (ED), inflammatory and oxidative stress, and induction of thrombosis that increases the risk for the development of AIS. Moreover, activated signaling pathways, including activator of transcription 3 (STAT3), nuclear factor kappa B (NF-κB), nod-like receptor pyrin 3 (NLRP3) inflammasome, and mitogen-activated protein kinase (MAPK) in acromegaly may induce systemic inflammation with the development of cardiovascular complications mainly AIS. Taken together, acromegaly triggers the development of AIS through local and systemic effects by inducing the formation of a cerebral vessel aneurysm, the release of pro-inflammatory cytokines, the development of oxidative stress, ED, and thrombosis correspondingly.
肢端肥大症是一种内分泌疾病，由于生长激素（GH）在前垂体过度产生，闭合的骺板生长板后。肢端肥大症主要由良性生长激素分泌性垂体腺瘤引起。急性缺血性脑卒中（AIS）是最常见的心血管并发症之一。它在全球高收入国家的残疾和死亡原因中仅次于缺血性心脏病（IHD），排名第二。因此，本综述旨在阐明肢端肥大症与 AIS 发展之间的可能联系。肢端肥大症在 AIS 发展中的局部作用与垂体腺瘤的发展以及相关的手术和放射治疗有关。垂体腺瘤通过不同的机制触发 AIS 的发展，特别是动脉瘤形成、相关血栓形成和脑微循环改变。患有垂体腺瘤的患者心血管并发症和死亡率更高。肢端肥大症引起的心血管代谢紊乱的全身效应可能会增加发生 AIS 的风险。此外，肢端肥大症导致内皮功能障碍（ED）、炎症和氧化应激的发展以及血栓形成的诱导，从而增加发生 AIS 的风险。此外，在肢端肥大症中，包括转录激活因子 3（STAT3）、核因子 kappa B（NF-κB）、NOD 样受体 pyrin 3（NLRP3）炎性小体和丝裂原活化蛋白激酶（MAPK）在内的激活信号通路可能会引发全身炎症，从而导致心血管并发症的发展，主要是 AIS。总之，肢端肥大症通过诱导脑血管动脉瘤形成、促炎细胞因子释放、氧化应激、ED 和血栓形成的发展，通过局部和全身作用触发 AIS 的发展。
