Cerebral MRI lesions and anti-tumor necrosis factor-alpha therapy

Winkelmann, Alexander; Patejdl, Robert; Wagner, Sabine; Benecke, Reiner; Zettl, Uwe K.

doi:10.1007/s00415-008-6020-z

Cited by 27 publications

(16 citation statements)

References 31 publications

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“…Moreover, clinicians should also be alert to distinguish symptoms suggestive of CNS demyelination, and in cases of high clinical suspicion, brain MRI scan should be performed even prior to treatment initiation [10, 18, 24]. Furthermore, in case of emerging demyelination during treatment, TNF α antagonists should be discontinued and close clinical and MRI monitoring should follow [12, 36].…”

Section: Discussionmentioning

confidence: 99%

Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association? Report of Four Cases and Review of the Literature

Andreadou

Kemanetzoglou

Brokalaki

et al. 2013

Case Reports in Neurological Medicine

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Tumor necrosis factor antagonists (anti-TNFa) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported and literature data suggest a potential role of anti-TNFa in the induction of demyelination of the CNS. We present four patients treated with anti-TNFa who developed symptoms suggestive of CNS demyelination. The first patient, a 17-year-old male who received etanercept for psoriatic arthritis for eight months, presented with dysesthesias up to T4 level. The second patient, a 30-year-old male treated with adalimumab for three years due to ankylosing spondylitis, presented with right unilateral tinnitus. The third case, a 47-year-old female, received etanercept for four years because of psoriatic arthritis and developed persistent headache and left-sided face and head numbness. Finally, the fourth patient, a 57-years-old female treated with etanercept for six years due to ankylosing spondylitis, presented with difficulty in speech, swallowing, and ptosis of the right corner of the mouth. In all cases, brain MRI showed lesions suggestive of demyelination, while positive oligoclonal bands were detected in the CSF. Anti-TNFa treatments were discontinued and patients showed clinical improvement with pulsed intravenous corticosteroid therapy. CNS demyelination following anti-TNFa treatment represents a relatively rare but potential serious complication. Close follow-up and MRI monitoring of these patients is mandatory to elucidate whether the clinical manifestations represent adverse events occurring during anti-TNFa therapy or a first demyelinating episode.

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Section: Discussionmentioning

confidence: 99%

Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association? Report of Four Cases and Review of the Literature

Andreadou

Kemanetzoglou

Brokalaki

et al. 2013

Case Reports in Neurological Medicine

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“…Compared to placebo control patients, lenercept-treated individuals experienced higher occurrence of relapse and increased neurological deficit (1999). Moreover, anti-TNF-α agents used to treat other inflammatory diseases such as psoriatic arthritis, ankylosing spondylitis, and rheumatoid arthritis have also been associated with demyelination that closely resembles that observed in multiple sclerosis (Mohan et al 2001;Titelbaum et al 2005;Winkelmann et al 2008). The ineffectiveness of anti-TNF-α therapy in MS may be a consequence of divergent roles for the TNF receptors, considering that blocking TNF-RI in mouse models dampens disease severity, while suppressing TNF-RII, the receptor that induces remyelination and harbors immunosuppressive properties, results in exacerbated disease (Arnett et al 2001;Kassiotis and Kollias 2001).…”

Section: Multiple Sclerosismentioning

confidence: 98%

Tumor Necrosis Factor-alpha and the Roles it Plays in Homeostatic and Degenerative Processes Within the Central Nervous System

Montgomery

Bowers

2011

J Neuroimmune Pharmacol

304

181

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Tumor Necrosis Factor-alpha (TNF-α) is a prototypic pro-inflammatory cytokine involved in the innate immune response. TNF-α ligation and downstream signaling with one of its cognate receptors, TNF-RI or TNF-RII, modulates fundamental processes in the brain including synapse formation and regulation, neurogenesis, regeneration, and general maintenance of the central nervous system (CNS). During states of chronic neuroinflammation, extensive experimental evidence implicates TNF-α as a key mediator in disease progression, gliosis, demyelination, inflammation, blood-brain-barrier deterioration, and cell death. This review explores the complex roles of TNF-α in the CNS under normal physiologic conditions and during neurodegeneration. We focus our discussion on Multiple Sclerosis, Parkinson's disease, and Alzheimer's disease, relaying the outcomes of preclinical and clinical testing of TNF-α directed therapeutic strategies, and arguing that despite the wealth of functions attributed to this central cytokine, surprisingly little is known about the cell type- and stage-specific roles of TNF-α in these debilitating disorders.

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“…Suspected MS following anti-TNF- α treatment in patients with family history of MS was reported in many cases [14, 18] which recommended that anti-TNF- α should be avoided in such patients and advocated requesting cerebral MRI before treatment initiation in patients with high risk of MS [21, 22]. …”

Section: Discussionmentioning

confidence: 99%

Adalimumab Induced or Provoked MS in Patient with Autoimmune Uveitis: A Case Report and Review of the Literature

Alsukhni

Jriekh

Aboras

2016

Case Reports in Medicine

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Anti-tumor necrosis factor α (anti-TNF-α) agents have been widely used in the field of autoimmune diseases and have proved decisive efficacy and relative safety. Data concerning their adverse effects has been lately describing central nervous system (CNS) demyelination process at escalating basis. Case Presentation. A 23-year-old male with autoimmune uveitis and a family history of multiple sclerosis (MS) developed two neurological attacks, after Adalimumab infusion, simultaneously with several cerebral lesions on magnetic resonance imaging (MRI). Hence the diagnosis of Adalimumab induced MS was suspected. Conclusion. This case is reported to tell physicians to be cautious when using anti-TNF-α in patients with family history of MS and to reconsider the risk of MS in patients with autoimmune diseases.

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Cerebral MRI lesions and anti-tumor necrosis factor-alpha therapy

Cited by 27 publications

References 31 publications

Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association? Report of Four Cases and Review of the Literature

Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association? Report of Four Cases and Review of the Literature

Tumor Necrosis Factor-alpha and the Roles it Plays in Homeostatic and Degenerative Processes Within the Central Nervous System

Adalimumab Induced or Provoked MS in Patient with Autoimmune Uveitis: A Case Report and Review of the Literature

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