Evidence map›Paper›PMID 37276237›Full record

ArticlePLoS neglected tropical diseases2023

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

Patricia Sola Penna, Sergio Augusto Lopes De Souza, Paulo Gustavo Limeira Nobre De Lacerda, Izabela Jardim Rodrigues Pitta, Clarissa Neves Spitz, Anna Maria Sales, Flavio Alves Lara, Ana Caroline Siquara De Souza, Euzenir Nunes Sarno, Roberta Olmo Pinheiro and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Cytokines profile in pure neural leprosy.Frontiers in immunology · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Patricia Sola PennaUniversidade Federal do Estado do Rio de Janeiro, PPGNeuro, Rio de Janeiro, Brazil.ORCID 0000-0003-1773-2358
Sergio Augusto Lopes De SouzaUniversidade Federal do Rio de Janeiro, Departamento de Radiologia, Serviço de Medicina Nuclear, Rio de Janeiro, Brazil.
Paulo Gustavo Limeira Nobre De LacerdaUniversidade Federal do Rio de Janeiro, Departamento de Radiologia, Serviço de Medicina Nuclear, Rio de Janeiro, Brazil.
Izabela Jardim Rodrigues PittaInstituto Oswaldo Cruz, Laboratório de Hanseníase (LAHAN), Rio de Janeiro, Brazil.
Clarissa Neves SpitzUniversidade Federal do Estado do Rio de Janeiro, PPGNeuro, Rio de Janeiro, Brazil.
Anna Maria SalesInstituto Oswaldo Cruz, Laboratório de Hanseníase (LAHAN), Rio de Janeiro, Brazil.
Flavio Alves LaraInstituto Oswaldo Cruz, Laboratório de Microbiologia Celular (LAMICEL), Rio de Janeiro, Brazil.
Ana Caroline Siquara De SouzaUniversidade Federal do Estado do Rio de Janeiro, PPGNeuro, Rio de Janeiro, Brazil.
Euzenir Nunes SarnoInstituto Oswaldo Cruz, Laboratório de Hanseníase (LAHAN), Rio de Janeiro, Brazil.
Roberta Olmo PinheiroInstituto Oswaldo Cruz, Laboratório de Hanseníase (LAHAN), Rio de Janeiro, Brazil.
Marcia Rodrigues JardimUniversidade Federal do Estado do Rio de Janeiro, PPGNeuro, Rio de Janeiro, Brazil.
Fundação Oswaldo Cruz · BRUniversidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BRUniversidade Federal do Estado do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLeprosy 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.

methodsEight 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.

resultsInitially, 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.

conclusions18F-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.

Indexed as

LeprosyLeprosy, LepromatousNeuritisPeripheral Nervous System DiseasesFluorodeoxyglucose F18GlucoseHumansInflammationMycobacterium lepraePositron Emission Tomography Computed TomographyFluorodeoxyglucose F18Glucose

Identifiers

PMID37276237
PMCPMC10270593
OpenAlexW4379469044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.