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In phase II clinical trial, fingolimod at a dose of 5.0mg (ten times higher than the currently approved dose) induced dyspnoea and decreased forced expiratory flow in some patients, probably trought an airways constriction S1P4-mediated. In phase III trials, respiratory adverse events associated with fingolimod treatment as dyspnoea, cough, oropharingeal pain and nasal congestion are reported with the same incidence of placebo. Here we report two cases of severe dyspnoea with alteration of the diffusion capacity of the lung associated with fingolimod treatment, which led to permanent treatment withdrawal.
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http://dx.doi.org/10.1016/j.msard.2016.06.005 | DOI Listing |
Ophthalmol Sci
July 2025
John F. Hardesty, MD Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri.
Purpose: Sphingosine-1-phosphate (S1P) plays a pivotal role in cells as a bioactive lipid mediator, with emerging evidence suggesting that it may play a role in retinal ganglion cell survival, axonal growth, retinal pigment epithelium (RPE) barrier function, and photoreceptor function. While previous studies have documented associated ophthalmic effects such as fingolimod-associated macular edema, the specific impact of S1P receptor modulators on inner and outer retinal layer thicknesses requires further elucidation.
Design: Retrospective case series.
Medicina (Kaunas)
August 2025
Department of Neurology, Faculty of Medicine, Dicle University, Diyarbakir 21090, Turkey.
: Multiple sclerosis (MS) is a chronic immune-mediated neurological disorder that primarily affects young adults and is frequently accompanied by psychiatric comorbidities such as depression and anxiety, both of which significantly diminish patients' quality of life (QoL). This study investigated the effect of two oral disease-modifying therapies (DMTs), fingolimod and cladribine, on mental health and QoL in patients with relapsing-remitting MS (RRMS). The aim of the study was to compare levels of depression, anxiety, and health-related quality of life (HRQoL) in RRMS patients treated with fingolimod or cladribine, and to evaluate their associations with clinical and radiological parameters.
View Article and Find Full Text PDFImmun Inflamm Dis
August 2025
Department of Rehabilitation Medicine, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China.
Background: Ischemic stroke frequently leads to white matter injury (WMI), significantly impairing neurological function and recovery. Microglia, the central nervous system's resident immune cells, play a dual role in poststroke pathology and repair. Their diverse activation states and interactions with other glial cells influence demyelination, remyelination, and overall WMI outcomes.
View Article and Find Full Text PDFMult Scler J Exp Transl Clin
August 2025
Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Background: Fingolimod was approved in 2010 for the treatment of relapsing-remitting multiple sclerosis, generally as second-line therapy. While its efficacy in reducing the relapse rate is well-recognized, the dermatologic complications of fingolimod remain unexplored. Herein, we aimed to report our experience with multiple sclerosis patients treated with fingolimod who underwent periodic dermatologic examinations.
View Article and Find Full Text PDFInt J Biol Sci
August 2025
Department of Cardiology, Zhongda Hospital, Southeast University, 87 Dingjiaqiao, Nanjing 210009, P.R. China.
Myocardial ischemia/reperfusion (MI/R) injury remains a major challenge in cardiovascular therapeutics, with pathogenesis closely associated with reactive oxygen species (ROS) accumulation and ferroptosis. While sphingosine-1-phosphate receptors (S1PRs) activation demonstrates cardioprotective potential against MI/R injury, its mechanistic relationship with redox homeostasis and ferroptotic pathways requires elucidation. Using hypoxia/reoxygenation (H/R)-treated cardiomyocytes, we investigated S1P-mediated regulation of , , and transcription through pharmacological inhibition of the S1PRs/Src/STAT3 signaling pathway.
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