Cerebral toxoplasmosis in an MS patient receiving Fingolimod

Enríquez-Marulanda, Alejandro; Valderrama-Chaparro, Jaime Andrés; Parrado-Sánchez, Laura; Vélez, Juan D.; Granados, Ana; Orozco, Jorge; Quiñones, Jairo

doi:10.1016/j.msard.2017.05.004

Cited by 27 publications

(14 citation statements)

References 7 publications

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“…4c). Interestingly, the administration of SLB736 did not reduce the number of lymphocytes, which is a well-known adverse effect of FTY720 through its effect on S1PR1 39,40 (Fig. 4d).…”

Section: Resultsmentioning

confidence: 93%

A novel S1PR4 functional antagonist prevents nonalcoholic steatohepatitis by deactivating the NLRP3 inflammasome without causing lymphopenia

Lee

Koh

Hong

et al. 2020

Preprint

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Sphingosine 1-phosphate (S1P) receptors (S1PRs) are a group of G protein-coupled receptors that confer a broad range of functional effects in chronic inflammatory diseases and metabolic diseases. S1PRs may also be involved in the development of non-alcoholic steatohepatitis (NASH), but the specific subtypes involved and the mechanism of action are unclear. Here we show that the livers of various mouse models of NASH as well as Kupffer cells had a particularly strong expression of S1pr4. Accordingly, genetic depletion of S1pr4 protected the mice against hepatic inflammation and fibrosis. Moreover, SLB736, a novel selective functional antagonist of SIPR4 prevented diet-induced NASH in mice without lymphopenia. S1P increased the expression of S1pr4 in Kupffer cells and activated the NLRP3 inflammasome through PLC/IP3/IP3R-dependent [Ca++] signaling. SLB736 treatment or S1pr4 depletion in Kupffer cells inhibited LPS-mediated Ca++ release and deactivated the NLRP3 inflammasome. S1PR4 antagonism may be a novel therapeutic strategy for NASH.

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“…4c). Interestingly, the administration of SLB736 did not reduce the number of lymphocytes, which is a well-known adverse effect of FTY720 through its effect on S1PR1 39,40 (Fig. 4d).…”

Section: Resultsmentioning

confidence: 93%

A novel S1PR4 functional antagonist prevents nonalcoholic steatohepatitis by deactivating the NLRP3 inflammasome without causing lymphopenia

Lee

Koh

Hong

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Diagnosis is typically made indirectly, with serology, or directly, with techniques such as polymerase chain reaction looking for T. gondii DNA [9]. Immunosuppressant implicated in the development of cerebral toxoplasmosis includes cyclosporine, azathioprine, tacrolimus, and methylprednisolone [13][14][15][16] as well as rituximab [17,18], infliximab [19], fingolimod [20] and adalimumab [21]. First-line treatment includes a combination of pyrimethamine, leucovorin and sulfadiazine.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasma Gondii Encephalitis from Mycophenolate Mofetil: A Case Report and Review

Jl¹,

N²

2018

Arch Med

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Mycophenolate mofetil (MMF) is often used in the treatment of autoimmune diseases such as myasthenia gravis and the prevention of organ rejection after transplantation. Toxoplasma encephalitis (TE) is typically associated with human immunodeficiency virus (HIV) infection. We present a case of an HIV sero-negative woman who developed TE after long-term MMF therapy for the treatment of myasthenia gravis. TE can occur even with low doses of MMF. A high index of suspicion is needed for patients presenting with focal neurologic deficits given poor outcomes in the majority of reported cases. Prophylaxis against TE can be considered although further study is needed.

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“…Accurate identification of TE can be challenging in individuals who do not have HIV, including recipients of hematopoietic stem cell or solid organ transplants, and those who received immunomodulatory therapies, in whom a wide variety of bacterial and fungal pathogens are possible. An example of this challenge is an individual with multiple sclerosis (MS) who developed TE during treatment with fingolimod (189). Brain lesions resembled tumefactive MS and prompted intensification of MS treatment.…”

Section: How Clinicians Use Laboratory Tests In Their Diagnostic Algorithmsmentioning

confidence: 99%

Epidemiology, Pathophysiology, Diagnosis, and Management of Cerebral Toxoplasmosis

2020

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SUMMARY Toxoplasma gondii is known to infect a considerable number of mammalian and avian species and a substantial proportion of the world’s human population. The parasite has an impressive ability to disseminate within the host’s body and employs various tactics to overcome the highly regulatory blood-brain barrier and reside in the brain. In healthy individuals, T. gondii infection is largely tolerated without any obvious ill effects. However, primary infection in immunosuppressed patients can result in acute cerebral or systemic disease, and reactivation of latent tissue cysts can lead to a deadly outcome. It is imperative that treatment of life-threatening toxoplasmic encephalitis is timely and effective. Several therapeutic and prophylactic regimens have been used in clinical practice. Current approaches can control infection caused by the invasive and highly proliferative tachyzoites but cannot eliminate the dormant tissue cysts. Adverse events and other limitations are associated with the standard pyrimethamine-based therapy, and effective vaccines are unavailable. In this review, the epidemiology, economic impact, pathophysiology, diagnosis, and management of cerebral toxoplasmosis are discussed, and critical areas for future research are highlighted.

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Cerebral toxoplasmosis in an MS patient receiving Fingolimod

Cited by 27 publications

References 7 publications

A novel S1PR4 functional antagonist prevents nonalcoholic steatohepatitis by deactivating the NLRP3 inflammasome without causing lymphopenia

A novel S1PR4 functional antagonist prevents nonalcoholic steatohepatitis by deactivating the NLRP3 inflammasome without causing lymphopenia

Toxoplasma Gondii Encephalitis from Mycophenolate Mofetil: A Case Report and Review

Epidemiology, Pathophysiology, Diagnosis, and Management of Cerebral Toxoplasmosis

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