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October 27, 2009; 73 (17) Clinical/Scientific Notes

OCULAR TOXOPLASMOSIS DURING NATALIZUMAB TREATMENT

Chiara Zecca, Fabio Nessi, Enos Bernasconi, Claudio Gobbi
First published September 23, 2009, DOI: https://doi.org/10.1212/WNL.0b013e3181bd114f
Chiara Zecca
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Fabio Nessi
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Enos Bernasconi
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Claudio Gobbi
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OCULAR TOXOPLASMOSIS DURING NATALIZUMAB TREATMENT
Chiara Zecca, Fabio Nessi, Enos Bernasconi, Claudio Gobbi
Neurology Oct 2009, 73 (17) 1418-1419; DOI: 10.1212/WNL.0b013e3181bd114f

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This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.

Natalizumab (Tysabri®, Biogen-Dompé, Cambridge, MA) is the first selective adhesion-molecule inhibitor approved for the treatment of multiple sclerosis (MS). Although undoubtedly efficacious in clinical and radiologic control of MS, its use raised some concerns regarding the potential occurrence of opportunistic infection in the exposed population, referring in particular to progressive multifocal leukoencephalopathy (PML).1

Toxoplasma gondii (TG) is a protozoan parasite that infects up to a third of the world's immunocompetent population with usually mild or no symptoms. On the contrary, its reactivation is a threatening condition that affects immunocompromised subjects, namely persons with HIV, organ transplant recipients, people with neoplastic disease, or people on a prolonged steroid treatment.2,3

Here we discuss the reactivation of ocular toxoplasmosis (OT) during natalizumab treatment.

Case report.

The patient is a 28-year-old man with relapsing-remitting MS. His previous medical history includes alcohol abuse and no malignancies, signs of immunodeficiency, or temporary stays abroad.

He first visited our center in 2004 due to a right subacute sensory-motor syndrome. We performed brain MRI and CSF analysis along with screening for autoimmune, infectious, dysmetabolic, and thrombophilic diseases. All of them proved to be compatible with the diagnosis of clinically isolated syndrome suggestive for MS. After a high-dose steroid course followed by symptoms remission, he was treated with interferon beta 1b …

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