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

• Published in: PLoS neglected tropical diseases Vol. 17; no. 6; p. e0011383
• Main Authors: Penna, Patricia Sola, De Souza, Sergio Augusto Lopes, De Lacerda, Paulo Gustavo Limeira Nobre, Rodrigues Pitta, Izabela Jardim, Spitz, Clarissa Neves, Sales, Anna Maria, Lara, Flavio Alves, De Souza, Ana Caroline Siquara, Sarno, Euzenir Nunes, Pinheiro, Roberta Olmo, Jardim, Marcia Rodrigues
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01-06-2023; Public Library of Science (PLoS)
• Subjects: Asymptomatic; Biology and Life Sciences; Biopsy; Care and treatment; Cells; Computed tomography; Damage; Diagnosis; Differential diagnosis; Disabilities; Electrophysiology; Fluorine isotopes; Glucose; Histopathology; Inflammation; Laboratories; Leprosy; Medicine and Health Sciences; Nerve conduction; Nerves; Neuritis; Neuropathy; Outpatient care facilities; Patients; Peripheral nerves; Peripheral neuropathy; Physical Sciences; Positron emission; Positron emission tomography; Schwann cells; Skin; Social Sciences; Symptoms; Tomography; Tropical diseases; Uptake; Brazil; Rio de Janeiro Brazil
• ISSN: 1935-2735; 1935-2727; 1935-2735
• DOI: 10.1371/journal.pntd.0011383

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.