02791nas a2200337   4500000000100000008004100001260003700042653002400079653005700103653001200160653002800172653002600200100001300226700001700239700002000256700002300276700001300299700001300312700001200325700001700337700001300354700001600367700001400383700001300397245007200410856009900482300001300581490000700594520183800601022001402439       2023                            d  bPublic Library of Science (PLoS)10aInfectious Diseases10aPublic Health, Environmental and Occupational Health10aLeprosy10a18-Fluoro-deoxy-glucose10aneuronal inflammation1 aPenna PS1 aDe Souza SAL1 aDe Lacerda PGLN1 aRodrigues Pitta IJ1 aSpitz CN1 aSales AM1 aLara FA1 aDe Souza ACS1 aSarno EN1 aPinheiro RO1 aJardim MR1 aAdams LB00aEvidencing leprosy neuronal inflammation by 18-Fluoro-deoxy-glucose  uhttps://journals.plos.org/plosntds/article/file?id=10.1371/journal.pntd.0011383&type=printable  ae00113830 v173 a<p><strong>Background:</strong> 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.</p>

<p><strong>Methods:</strong> 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.</p>

<p><strong>Results:</strong> 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.</p>

<p><strong>Conclusions:</strong> 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.</p>
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