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Aetiopathogenesis

 

Acetylcholinesterase-associated inflammation in patients with giant cell arteritis. Evaluation by histology and 11C-donepezil PET/CT


1, 2, 3, 4, 5, 6, 7, 8

 

  1. Department of Rheumatology, Aarhus University Hospital, Denmark.
  2. Department of Rheumatology and Department of Clinical Medicine, Aarhus University Hospital, Denmark.
  3. Department of Rheumatology and Department of Clinical Medicine, Aarhus University Hospital, Denmark.
  4. Department of Rheumatology, Aarhus University Hospital, Denmark.
  5. Department of Clinical Medicine and Department of Histopathology, Aarhus University Hospital, Denmark.
  6. Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Denmark.
  7. Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Denmark.
  8. Department of Rheumatology and Department of Clinical Medicine, Aarhus University Hospital, Denmark. ellen.hauge@aarhus.rm.dk

CER11754
2019 Vol.37, N°2 ,Suppl.117
PI 0020, PF 0025
Aetiopathogenesis

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PMID: 31162030 [PubMed]

Received: 19/09/2018
Accepted : 17/12/2018
In Press: 21/05/2019
Published: 21/05/2019

Abstract

OBJECTIVES:
To investigate the in-situ expression of acetylcholinesterase (AChE) in the inflamed vessel wall of patients with biopsy-positive giant cell arteritis (GCA) as compared to biopsy-negative non-GCA patients, and to evaluate the in-vivo expression of AChE in patients with large-vessel GCA (LVGCA) by 11C-donepezil (AChE inhibitor) positron emission tomography/computed tomography (PET/CT).
METHODS:
Twenty-four biopsy-positive GCA and 44 biopsy-negative non-GCA patients were included for AChE histology. Immunohistochemical methods were used to determine the AChE expression. The histological inflammation and the AChE expression were assessed by an experienced pathologist on a 3-point scale. Two patients with newly diagnosed 18F-fluorodeoxyglucose (18F-FDG) PET/CT verified LVGCA were included for 11C-donepezil PET/CT. PET images were assessed by an experienced nuclear medicine physician.
RESULTS:
AChE was expressed in all 24 positive temporal artery biopsies, 10/24 showed high AChE expression (grade 2) and 14/24 showed moderate AChE expression (grade 1). No AChE expression was observed outside the media smooth muscle cells (grade 0) in any of the biopsy-negative non-GCA patients. The AChE expression was in 86% agreement with the histological inflammation. The AChE expression was not associated with any clinical or biochemical findings. In both LV-GCA patients, PET/CT revealed extensive vascular FDG uptake but no 11C-donepezil uptake.
CONCLUSIONS:
AChE is highly expressed in the inflamed vessel wall of patients with GCA. Although, 11C-donepezil PET/CT showed no vascular uptake in the FDG PET/CT verified LV-GCA patients, histological findings raise the possibility that AChE can be used in the development of new diagnostic and disease monitoring tools for GCA.

Rheumatology Article