SynthesisJournal of neurology2025
Peripheral neuropathies associated with anti-tnf-α treatments: a systematic review and proposed recommendations.
Synthesis in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Severity of Cardiovascular Autonomic Neuropathy Is Linked to Increasing Levels of Circulating Proinflammatory Cytokines.Diabetes, obesity & metabolism · 2026Observational
- Monophasic multifocal motor neuropathy with concomitant central nervous system demyelination following anti-TNFα therapy.Journal of neurology · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is growing evidence that anti-TNF-α therapies may trigger immune-mediated polyneuropathies. However, the clinical spectrum, therapeutic strategies, and long-term outcomes remain insufficiently defined. This systematic review aims to address these gaps by collecting published case-reports and describing two additional cases of anti-TNF-α-induced neuropathy.
methodsA total of 99 cases from the literature and two from our center were included (n = 101). Clinical, neurophysiological, therapeutic, and outcome data were summarized. Predictors of poor neurological outcomes were identified using univariate and multivariate logistic regression.
resultsNinety percent of neuropathies typically developed within the first 24 months of treatment (median: 6 (IQR: 3-14) months), with Infliximab as the most frequently implicated agent (63.4%). Motor impairment, either isolated (29.7%) or with sensory symptoms (55.4%), was the predominant presentation. Neurophysiological studies showed conduction blocks (41%) or demyelination (39%). TNF-α therapy was discontinued in 94.8% of cases, and rescue immunotherapy was used in 73%. Complete recovery occurred in 39.6%, while 31.7% developed a chronic inflammatory demyelinating polyneuropathy-like phenotype. Univariate analysis identified sensory-motor involvement, demyelination, and conduction blocks as predictors of poor outcome; multivariate analysis confirmed sensory-motor involvement as an independent predictor (OR = 5.14; 95% CI: 1.24-21.34; p = 0.024). Symptom recurrence was evident in 7 re-exposed patients, while no relapse was observed in 2 patients who underwent dose reduction or different anti-TNF-α drug.
conclusionsAnti-TNF-α therapy can induce neuropathies characterized predominantly by motor symptoms and demyelinating features, frequently resulting in chronic neurological impairment despite drug withdrawn and immunomodulatory therapy. Drug rechallenge should be approached cautiously, and close monitoring is warranted if rechallenge is considered.
Indexed as
Identifiers
40447953What OpenQuestion holds
Registered trials
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.