Clinical case A patient with chronic, painless, bilateral loss of vision, after significant intake of interferon (IFNα) and ribavirina due to liver transplant. Ocular fundus is normal. A suspected retrobulbar optic neuropathy is confirmed by a prolongation of the latency of the patient's visual evoked potential. There being no prior record of risk factors and with the patient's systemic analysis giving normal results, the clinical improvement and the electro-physiological tests conducted after the drug was withdrawn point to interferon as negatively affecting the bilateral optic nerve. Discussion Interferon-α is used in the treatment of viral and neoplastic illnesses. Currently the drug is formulated as Interferon alfa pegilado (IFNα-p) in order to reduce toxicity and increase tolerance. The most common secondary effects are flu symptoms, asthenia and weigh loss. Affected ocular tissue is rare and optic neuropathy is also an infrequent complication: retinopathy at the beginning of treatment is, however, more frequent. The most widely accepted hypothesis as to the cause of toxicity is the presence of circulating immune complexes. It is, therefore, essential for ophthalmologists to be aware of the toxicity of this drug in order to be able to withdraw it in good time, thus preventing potentially irreversible sight loss.
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http://dx.doi.org/10.1016/j.oftal.2012.09.007 | DOI Listing |
J Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Geriatric Medicine, Affiliated Hospital of Qingdao University, Qingdao, China.
Objective: This study aims to delineate the clinical features underlying the concurrent disease of neuromyelitis optica spectrum disorder (NMOSD) and myasthenia gravis (MG), and to identify efficacious therapeutic strategies.
Background: NMOSD and MG are uncommon autoimmune diseases that infrequently co-exist. Despite previous reports, a consensus on treating NMOSD concurrent with MG is lacking.
Front Endocrinol (Lausanne)
January 2025
No. 1 Teaching Hospital, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin, China.
Thyroid-associated ophthalmopathy (TAO), an autoimmune disease closely related to thyroid dysfunction, remains a challenging ophthalmic condition among adults. Its clinical manifestations are complex and diverse, and disease progression can lead to exophthalmos, diplopia, exposure keratitis, corneal ulceration, and compressive optic neuropathy, resulting in irreversible vision damage or even blindness. Traditional treatment methods for TAO, including glucocorticoids, immunosuppressants, and radiation therapy, often have limitations and side effects, making this disease problematic in ophthalmology.
View Article and Find Full Text PDFJ Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
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