Wumier Wuerken, Abulizi Alimasi, Wu Pengfei, Jinsihan Najiahai, Wang Yongxin, Duysenbi Serick, Wang Zengliang
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, 830000, China.
Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, No. 137, Li Yu Shan Road, Xinshi District, Urumqi, 830000, China.
Acta Parasitol. 2025 Jan 24;70(1):33. doi: 10.1007/s11686-024-00943-7.
Alveolar echinococcosis (AE) is an infrequent zoonosis caused by Echinococcus multilocularis with a high degree of disability and mortality. Metastatic cerebral alveolar echinococcosis (CAE) is very rare and the lesions could lead to severe perilesional brain edema (PLBE) and subsequent uncontrollable intracranial hypertension. In this study, we sought to determine the expression of edema-associated factors in CAE lesions and their associations with PLBE. We retrospectively evaluated the clinical data of 18 CAE patients who received craniotomy. Severity of PLBE was described by edema index (EI). Archived specimens were processed for immunohistochemistry to detect tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor A (VEGF-A) and microvessel density (MVD) in CAE lesions. Expression intensity of CAE lesions was quantified by integral optical density (IOD) or count and was compared to the control group. The results showed TNF-α and VEGF-A were significantly expressed in CAE lesions (p < 0.001), their levels were positively correlated with PLBE (TNF-α: r = 0.701, p = 0.001; VEGF-A: r = 0.803, p < 0.001). The MVD of CAE lesions had a similar expression with normal brain tissue, and it was positively correlated with PLBE and VEGF-A (PLBE: r = 0.849, p < 0.001; VEGF-A: r = 0.687, p = 0.002). In conclusion, we speculated the upregulation of TNF-α and VEGF-A induced the formation of PLBE. Besides, though there was no extra increase of MVD, it was still regulated by VEGF-A and provided a better anatomical basis for the formation of PLBE and further promoted it.
肺泡型棘球蚴病（AE）是一种由多房棘球绦虫引起的罕见人畜共患病，具有高度的致残率和死亡率。转移性脑肺泡型棘球蚴病（CAE）极为罕见，其病灶可导致严重的病灶周围脑水肿（PLBE）及随后难以控制的颅内高压。在本研究中，我们试图确定CAE病灶中水肿相关因子的表达及其与PLBE的关联。我们回顾性评估了18例行开颅手术的CAE患者的临床资料。PLBE的严重程度通过水肿指数（EI）来描述。对存档标本进行免疫组织化学处理，以检测CAE病灶中的肿瘤坏死因子α（TNF-α）、血管内皮生长因子A（VEGF-A）和微血管密度（MVD）。通过积分光密度（IOD）或计数对CAE病灶的表达强度进行定量，并与对照组进行比较。结果显示，TNF-α和VEGF-A在CAE病灶中显著表达（p < 0.001），它们的水平与PLBE呈正相关（TNF-α：r = 0.701，p = 0.001；VEGF-A：r = 0.803，p < 0.001）。CAE病灶的MVD与正常脑组织有相似的表达，且与PLBE和VEGF-A呈正相关（PLBE：r = 0.849，p < 0.001；VEGF-A：r = 0.687，p = 0.002）。总之，我们推测TNF-α和VEGF-A的上调诱导了PLBE的形成。此外，虽然MVD没有额外增加，但它仍受VEGF-A调节，为PLBE的形成提供了更好的解剖学基础并进一步促进了其形成。
