Immunotherapy with monoclonal antibodies targeting cytotoxic T-lymphocyte antigen 4 (CTLA-4) or programmed cell death 1 (PD-1) has improved the survival of patients with metastatic melanoma. These agents carry a certain risk of adverse immune-related events. We present a patient with widely metastatic melanoma who was initially treated with ipilimumab and subsequently with nivolumab. After four infusions of nivolumab, he developed subacute multifocal central nervous system (CNS) demyelination. Nivolumab was discontinued and, despite immunosuppressive therapy, the largest lesion progressed significantly, whereas another lesion showed radiographic improvement. After further progression, the patient succumbed to his CNS lesions 4 months later. Autopsy revealed extensive demyelination, a mild multifocal T-cell-rich perivascular lymphoid infiltrate, abundant macrophages, and necrosis. There was no metastatic melanoma in the brain. CNS demyelination has not been described in association with nivolumab. We hypothesize that the combination therapy of ipilimumab and subsequent nivolumab accounted for the severity of the demyelinating process in this patient. This case, with comprehensive clinical, molecular, and neuropathologic characterization, illustrates the need for awareness of these potential CNS complications with the use of multiple checkpoint inhibitors.
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http://dx.doi.org/10.1158/2326-6066.CIR-15-0141 | DOI Listing |
Sci Rep
January 2025
Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.
As one of the most commonly used general anesthetics (GAs) in surgery, numerous studies have demonstrated the detrimental effects of sevoflurane exposure on myelination in the developing and elderly brain. However, the impact of sevoflurane exposure on intact myelin structure in the adult brain is barely discovered. Here, we show that repeated sevoflurane exposure, but not single exposure, causes hypomyelination and abnormal ultrastructure of myelin sheath in the prefrontal cortex (PFC) of adult male mice, which is considered as a critical brain region for general anesthesia mediated consciousness change.
View Article and Find Full Text PDFAJNR Am J Neuroradiol
January 2025
From the Department of Radiology (GMC, MM, YN, BJE), Department of Quantitative Health Sciences (PAD, MLK, JEEP), Department of Neurology (CBM, JAS, MWR, FSG, HKP, DHL, WOT), Department of Neurosurgery (TCB), Department of Laboratory Medicine and Pathology (RBJ), and Center for Multiple Sclerosis and Autoimmune Neurology (WOT), Mayo Clinic, Rochester, MN, USA; Dell Medical School (MFE), University of Texas, Austin, TX, USA.
Background And Purpose: Diagnosis of tumefactive demyelination can be challenging. The diagnosis of indeterminate brain lesions on MRI often requires tissue confirmation via brain biopsy. Noninvasive methods for accurate diagnosis of tumor and non-tumor etiologies allows for tailored therapy, optimal tumor control, and a reduced risk of iatrogenic morbidity and mortality.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Biophysics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Multiple sclerosis (MS) is a devastating autoimmune disease that leads to the destruction of the myelin sheath in the human central nervous system (CNS). Infection by viruses and bacteria has been found to be strongly associated with the onset of MS or its severity. We postulated that the immune system's attack on the myelin sheath could be triggered by viruses and bacteria antigens that resemble myelin sheath components.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
In multiple sclerosis (MS), microglia and macrophages within the central nervous system (CNS) play an important role in determining the balance among demyelination, neurodegeneration, and myelin repair. Phagocytic and regenerative functions of these CNS innate immune cells support remyelination, whereas chronic and maladaptive inflammatory activation promotes lesion expansion and disability, particularly in the progressive forms of MS. No currently approved drugs convincingly target microglia and macrophages within the CNS, contributing to the lack of therapies aimed at promoting remyelination and slowing disease progression for individuals with MS.
View Article and Find Full Text PDFCells
December 2024
Department of Neurology, Medical University of Lodz, Kosciuszki Street 4, 90-419 Lodz, Poland.
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) with a complex and not fully understood etiopathological background involving inflammatory and neurodegenerative processes. CHI3L1 has been implicated in pathological conditions such as inflammation, injury, and neurodegeneration, and is likely to play a role in the physiological development of the CNS. CHI3L1 is primarily produced by CNS macrophages, microglia, and activated astrocytes.
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