Artikel
Ischemia induced inflammation in arteriovenous malformations
Ischämie induzierte Entzündungsreaktion in arteriovenösen Malformationen
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Autoren
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Jan Rodemerk
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Marvin Darkwah Oppong
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Andreas Junker
- Universitätsklinikum Essen, Neuropathologie, Essen, Deutschland
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Cornelius Deuschl
- Universitätsklinikum Essen, Institut für Diagnostische und Interventionelle Radiologie und Neuroradiologie, Essen, Deutschland
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Michael Forsting
- Universitätsklinikum Essen, Institut für Diagnostische und Interventionelle Radiologie und Neuroradiologie, Essen, Deutschland
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Yuan Zhu
- Universitätsklinikum Essen, Molekulare Neurochirurgie, Essen, Deutschland
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Anne-Kathrin Uerschels
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Philipp Dammann
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Ramazan Jabbarli
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Ulrich Sure
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
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Karsten H. Wrede
- Universitätsklinikum Essen, Klinik für Neurochirurgie und Wirbelsäulenchirurgie, Essen, Deutschland
| Veröffentlicht: | 25. Mai 2022 |
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Gliederung
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Objective: Arteriovenous malformations’ (AVMs) pathophysiology of development, growth, and rupture is only partially understood. However, inflammation is known to play an essential role in many vascular diseases. This feasibility study aimed to investigate the expression of enzymes [COX-2 (Cyclooxygenase 2) and NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3)] in the AVM nidus that are essential in their inflammatory pathway. Moreover, to determine generally which inflammatory pathways influence the pathophysiology of AVMs.
Methods: The study group comprised 21 patients with partly thrombosed arteriovenous malformation. The cohort included ten ruptured and 11 unruptured AVMs, which had all been treated microsurgically. The Formaldehyde-fixed and paraffin-embedded samples were immunohistochemically stained with a monoclonal antibody against COX-2 and NLRP3 (Dako, Santa Clara, CA; Clone: CX-294; ABCAM, Cambridge, MA, ab214185). We correlated MRI and clinical data with immunohistochemistry, using the Trainable Weka Segmentation algorithm for analysis.
Results: A total of 21 patients (7 male) with ruptured (n = 8) and unruptured (n = 13) with AVMs were included into the study. In 81%, elastic fibers were lost in the AVM nidus, and in 52%, iron deposition in the wall structures is reported. The median AVM volume was 2240 mm³ (IQR: 924 – 8372 mm³). Moreover, proportion of NLRP3 positive cells was significantly higher (26.23 % - 83.95 %), compared to COX-2 positive cells (0.25 % - 14.94 %, p < 0.0001, Figure 1 [Fig. 1]). Ruptured AVM had no higher expression of NLRP3 (p = 0.39) or COX-2 (p = 0.44), compared to non-ruptured AVMs. Further, no patient characteristics could be reported that showed significant correlations to the enzyme expression.
Conclusion: The inflammatory process in AVMs seems to be mainly associated with ischemic (NLRP3) and not with mechanical (COX-2) driven inflammatory pathways. No direct associations between NLRP3 or COX-2 expression and radiological, standard histopathological, or patient characteristics were found in this cohort.
