Universidade Federal do Estado do Rio de Janeiro, PPGNeuro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro, Departamento de Radiologia, Serviço de Medicina Nuclear, Rio de Janeiro, Brazil.
PLoS Negl Trop Dis. 2023 Jun 5;17(6):e0011383. doi: 10.1371/journal.pntd.0011383. eCollection 2023 Jun.
Leprosy is caused by multiple interactions between Mycobacterium leprae (M. leprae) and the host's peripheral nerve cells. M. leprae primarily invades Schwann cells, causing nerve damage and consequent development of disabilities. Despite its long history, the pathophysiological mechanisms of nerve damage in the lepromatous pole of leprosy remain poorly understood. This study used the findings of 18F-FDG PET/CT on the peripheral nerves of eight lepromatous patients to evaluate the degree of glucose uptake by peripheral nerves and compared them with clinical, electrophysiological, and histopathological evaluations.
Eight patients with lepromatous leprosy were included in this study. Six patients were evaluated up to three months after leprosy diagnosis using neurological examination, nerve conduction study, 18F-FDG PET/CT, and nerve biopsy. Two others were evaluated during an episode of acute neuritis, with clinical, neurophysiological, and PET-CT examinations to compare the images with the first six.
Initially, six patients already had signs of peripheral nerve injury, regardless of symptoms; however, they did not present with signs of neuritis, and there was little or no uptake of 18F-FDG in the clinically and electrophysiologically affected nerves. Two patients with signs of acute neuritis had 18F-FDG uptake in the affected nerves.
18F-FDG uptake correlates with clinical neuritis in lepromatous leprosy patients but not in silent neuritis patients. 18F-FDG PET-CT could be a useful tool to confirm neuritis, especially in cases that are difficult to diagnose, such as for the differential diagnosis between a new episode of neuritis and chronic neuropathy.
麻风病是由麻风分枝杆菌（M. leprae）与宿主周围神经细胞的多重相互作用引起的。M. leprae 主要侵犯施万细胞，导致神经损伤，继而导致残疾。尽管历史悠久，但麻风病瘤型患者周围神经损伤的病理生理机制仍知之甚少。本研究使用 18F-FDG PET/CT 检测 8 例瘤型麻风患者周围神经的葡萄糖摄取情况，并与临床、电生理和组织病理学评估进行比较。
本研究纳入 8 例瘤型麻风患者。6 例患者在麻风病诊断后 3 个月内进行神经检查、神经传导研究、18F-FDG PET/CT 和神经活检评估。另外 2 例在急性神经炎发作时进行评估，进行临床、神经生理学和 PET-CT 检查，将图像与前 6 例进行比较。
最初，6 例患者已有周围神经损伤的迹象，尽管没有症状，但没有神经炎的迹象，且在临床上和电生理学上受影响的神经中 18F-FDG 的摄取很少或没有。2 例有急性神经炎表现的患者在受累神经中有 18F-FDG 摄取。
18F-FDG 摄取与瘤型麻风患者的临床神经炎相关，但与无症状神经炎患者无关。18F-FDG PET-CT 可能是一种有用的工具，可以确认神经炎，尤其是在难以诊断的情况下，例如新发神经炎与慢性神经病的鉴别诊断。
