Evidencing leprosy neuronal inflammation by 18-Fluoro-deoxy-glucose

Abstract

Background 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. Methods 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. Results 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. Conclusions 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.

Cytokines profile in pure neural leprosy

“…IL-10 has also been described in the lepromatous pole of leprosy ( 2 ). This suggests that patients with PNL these patients may have a form of the disease related to the multibacillary forms, when silent neuritis plays an important role ( 23 ).…”

“…It has been proposed that M. leprae induces Schwann cell death by a pathway that involves proinflammatory cytokines, and TNF-a has already been identified in the nerve biopsies of patients with neuritis (10). TNF-a has been related to demyelination and axonal degeneration as well as immune cell recruitment to the injury site and, in leprosy, it has been detected in reactional states (3).…”

“…Neural damage and neuritis may occur in both types of leprosy reactions (6, 9). It is still unknown whether the damage to the peripheral nerve is caused by the M. leprae itself or the inflammatory response that it causes (10). It has been suggested that both mechanisms play a role in the clinical spectrum of the disease (11).…”