Occurrence of demyelinating diseases after anti-TNFα treatment of inflammatory bowel disease: A Danish Crohn Colitis Database study

Andersen, Nynne Nyboe; Caspersen, Sarah; Jess, Tine; Munkholm, Pia

doi:10.1016/j.crohns.2008.04.001

Cited by 22 publications

(26 citation statements)

References 24 publications

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“…41 Several reports suggest a temporal relationship between starting treatment with infliximab and the development of WML or MS, or with the worsening of MS. 34,35,42 However, among 500 CD patients treated with infliximab in the Mayo clinic experience, only one patient developed lesions consistent with demyelination. 43 Further, Andersen et al 44 did not find an increased risk of MS development in IBD patients who were treated with biological agents when compared to those who were treated with non-biological agents. Indeed, a definite causal relationship based on currently available evidence is difficult to establish: however, caution continues to be advised when prescribing these drugs in IBD, and treated patients should be counseled and closely monitored for the development of neurological symptoms and MRI abnormalities.…”

Section: Ibd and Cns White Matter Lesions (Wml)mentioning

confidence: 99%

Multiple sclerosis and inflammatory bowel diseases: what we know and what we would need to know!

et al. 2012

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Multiple sclerosis (MS) is a demyelinating disorder of the central nervous system (CNS) but the causes have not been defined. The disease process appears to involve interplay between environmental factors and certain susceptibility genes. It is likely that the identification of the exact etiological mechanisms will permit the development of preventive and curative treatments. Evaluation of several diseases found to be more often associated than by chance alone may reveal clues to the etiology of those disorders. An association between MS and inflammatory bowel diseases (IBD) was suggested by the observation of an increased incidence of IBD among MS patients. A problem in the interpretation of the data rests, in part, with the observation that abnormal findings in brain magnetic resonance imaging (MRI) may be reported as MS in IBD patients. Defining the limits between incidental MRI findings and findings compatible with MS has resulted in further exploration of this possible association.

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Section: Ibd and Cns White Matter Lesions (Wml)mentioning

confidence: 99%

Multiple sclerosis and inflammatory bowel diseases: what we know and what we would need to know!

et al. 2012

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“…This is not an unexpected finding, as it is known that MS predominantly affects women in their forties and fifties [23]. As mentioned above, IBD and MS share similar age and geographical distributions, and thus the possibility of common causative environmental factors needs to be thoroughly investigated [17,24].…”

Section: Methodsmentioning

confidence: 77%

“…All patients presented upper or lower limp paresthesias, one of them experienced muscle pain and another one lower limb weakness. Three of them were treated with infliximab and one with adalimumab [24]. Similarly, Lees et al have found 5 patients with CD complicated with central, axonal or peripheral demyelination in a retrospective analysis of 199 IBD patients treated with anti-TNF-a (infliximab, adalimumab, natalizumab) between 1999 and 2007 in Edinburgh [44].…”

Section: Methodsmentioning

confidence: 96%

Inflammatory bowel disease and demyelination: more than just a coincidence?

Katsanos

Κατσάνος

2014

Expert Review of Clinical Immunology

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Infliximab and other anti-TNF-α agents have been implicated for drug-induced demyelination in patients with inflammatory bowel diseases (IBDs). We evaluated existing data from MEDLINE and EMBASE and conducted a narrative review to investigate further the aforementioned association. Our literature search highlighted 34 case reports, 3 case-control studies, 1 prospective and 7 retrospective cohort studies published in English. Available data suggest that IBD patients can manifest demyelinating events in both central and peripheral nervous system, however, they are still insufficient to conclude whether anti-TNF-α therapies are an independent risk factor for demyelination. Prospective cohort studies with internal control groups are needed to estimate the true incidence of demyelinating disorders in patients with IBD and to elucidate if anti-TNF-α therapy increases further the risk of demyelination.

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“…It is important to recognize that in such trials, a previous history or a concurrent demyelinating disorder is considered an exclusion criterium. However, the risk of developing MS after anti-TNF therapy may not be higher than the baseline risk of MS being associated with IBD [4]. TNF is considered to be involved in the pathogenesis of MS and it is somewhat paradoxical that the lenercept Multiple Sclerosis study reported clinical worsening of MS [8], halting further development of anti-TNF strategies in MS. TNF is a pleotropic cytokine which signals via TNF receptor 1 (TNFR1) and TNFR2; while signaling via TNFR1 results in demyelination, it is generally accepted that signaling via TNFR2 may be required for remyelination of nerve fibers [9].…”

Section: Demyelinating Disease and Anti-tnf Therapymentioning

confidence: 99%

“…There needs to be awareness of this when interpreting new onset of MS in a patient treated with immunosuppressant therapies especially anti-TNF therapy. In the Danish Crohn Colitis Database study, the risk of developing MS after anti-TNF therapy did not exceed this baseline risk of MS in IBD patients [4]. Autoimmune diseases cluster together and may manifest for the first time masquerading as a side effect of therapy.…”

Section: Introductionmentioning

confidence: 99%

Biologic Therapies: Lessons from Multiple Sclerosis

Ghosh

2012

Dig Dis

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New evidence points to a possible association of multiple sclerosis (MS) with IBD. Tumour necrosis factor (TNF) is involved in the pathogenesis of MS. Paradoxically, administration of anti-TNF monoclonal antibodies to IBD patients has led to exacerbation of MS or triggered demyelination. TNF receptor 1 (TNFR1) mediates demyelination and TNFR2 mediates remyelination, suggesting that a more selective approach to TNF antagonism may be required for an anti-TNF strategy to be effective in MS. Conversely, interferon treatment for MS may worsen IBD. Anti-lymphocyte trafficking strategies such as alpha4 integrin blockers are effective in both these diseases. Recent advances in small molecule development in this area may provide further effective therapies. Common inflammatory cytokine and signaling pathways may be shared between MS and IBD, such as TNF, interleukin (IL)-12/23, IL-17, CD40 and STAT3. However, in contrast to Crohn’s disease, ustekinumab has not shown efficacy in MS. Vitamin D deficiency is a hot topic in both diseases. Several drugs developed for MS, e.g. glatiramer acetate, are also being studied in IBDs. As in rheumatoid arthritis, MS also serves as an example of a chronic relapsing inflammatory disease where disease modification is the goal of treatment based on objective evidence derived from imaging, in turn providing examples of how to conduct IBD studies in future.

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Occurrence of demyelinating diseases after anti-TNFα treatment of inflammatory bowel disease: A Danish Crohn Colitis Database study

Abstract: The literature review revealed an up to four-fold increased risk of demyelinating diseases, in particular MS, in IBD patients in general. The risk of developing MS in the anti-TNFα treated Danish cohort did apparently not exceed this risk.

Cited by 22 publications

References 24 publications

Multiple sclerosis and inflammatory bowel diseases: what we know and what we would need to know!

Multiple sclerosis and inflammatory bowel diseases: what we know and what we would need to know!

Inflammatory bowel disease and demyelination: more than just a coincidence?

Biologic Therapies: Lessons from Multiple Sclerosis

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