Therapeutic plasma exchange for worsening multiple sclerosis: does it work?

Khatri, Bhupendra

doi:10.1586/eci.09.42

Cited by 3 publications

(4 citation statements)

References 9 publications

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“…TPE has been shown to accelerate the removal of natalizumab, accelerate the desaturation of the targeted alpha‐4‐integrin receptor, and restore leukocyte transmigration . Desaturation of the alpha‐4‐integrin occurs when plasma concentration of natalizumab is less than 1 µg/mL which is achieved 15 days after three sessions of TPE or 82 days after no TPE . When immunosuppression is rapidly reversed, an extreme immune response targeting the JC virus in the CNS occurs 2–6 weeks later and is termed immune reconstitution inflammatory syndrome (IRIS) .…”

Section: Natalizumab‐associated Progressive Multifocal Leukoencephalomentioning

confidence: 99%

Neurologic indications for therapeutic plasma exchange: 2013 update

Gwathmey

Balogun

Burns

2014

J of Clinical Apheresis

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Neurologists commonly use therapeutic plasma exchange (TPE) to treat a number of conditions. This concise review considers the most common neurologic indications for TPE. It focuses on Guillain-Barré syndrome and myasthenia gravis and also the role of TPE in chronic inflammatory demyelinating polyneuropathy, Lambert-Eaton syndrome, multiple sclerosis, neuromyelitis optica, paraproteinemic polyneuropathy, Sydenham's chorea, and natalizumab-associated progressive multifocal leukoencephalopathy. As with any treatment, the proven efficacy, cost, side effects, and availability must be considered before initiation of therapy.

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Section: Natalizumab‐associated Progressive Multifocal Leukoencephalomentioning

confidence: 99%

Neurologic indications for therapeutic plasma exchange: 2013 update

Gwathmey

Balogun

Burns

2014

J of Clinical Apheresis

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“…Desaturation of a4-integrin occurs when plasma concentration of natalizumab is less than 1 mg/ml, which is achieved 15 days after three sessions of PLEX or at 82 days without PLEX [18]. Suspension of natalizumab and plasma removal of the drug as early as possible is the essential step in the treatment of PML.…”

Section: Treatmentmentioning

confidence: 99%

Progressive multifocal leukoencephalopathy in patients with multiple sclerosis

Baldwin¹,

Hogg

2013

Current Opinion in Neurology

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There continues to be significant gaps in our understanding of PML pathogenesis and its relationship with therapeutic immunosuppression. There have been advances made in our ability to treat multiple sclerosis, although these have come with the unintended risk of PML. Fortunately, natalizumab-associated PML remains a rare entity compared to multiple sclerosis-associated disability, and the risk may be mitigated with appropriate patient selection, accurate and rapid diagnosis, and aggressive treatment strategies.

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“…The utility of this procedure includes the removal of antibodies, alloantibodies, immune complexes, monoclonal proteins, toxins and cytokines, and it involves the replenishment of a specific plasma factor containing 5% albumin. PP has been successfully used in several immune-mediated neurological disorders, including Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and myasthenia gravis [14][15][16][17][18]. Less common neurological diseases in which plasmapheresis has afforded beneficial effects are paraneoplastic polyneuropathies, neuromyelitis optica (also known as Devic's disease), motor neuron disease, polymyositis, and multifocal motor neuropathy [18].…”

Section: Introductionmentioning

confidence: 99%

“…PP can be a therapeutic strategy to remove or reduce the substances that are considered pathogenically responsible, e.g., Aβ peptides in AD from the blood, by changing their transportation through the blood-brain barrier, thereby limiting their accumulation in the brain. In the case of MS, eliminating pathogenic humoral factors from the blood [14], including suspected auto-antibodies directed against the myelin sheath, is needed in some patients with steroid refractory relapses [15], or in patients that develop neutralizing antibodies to interferon-beta (IFN-β), which are associated with reduced bioactivity and efficacy of IFN-β [19,20]. There is extensive literature related to the use of plasma exchange in relapsing and remitting multiple sclerosis, and its use as a temporary treatment of acute relapses in steroid-unresponsive MS patients has been recently reviewed [15,16].…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Plasmapheresis with Albumin Replacement in Alzheimer’s Disease and Chronic Progressive Multiple Sclerosis: A Review

Navarro-Martínez

Cauli

2020

Pharmaceuticals

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Background: Reducing the burden of beta-amyloid accumulation and toxic autoimmunity-related proteins, one of the recognized pathophysiological markers of chronic and common neurological disorders such as Alzheimer’s disease (AD) and multiple sclerosis (MS), may be a valid alternative therapy to reduce their accumulation in the brain and thus reduce the progression of these disorders. The objective of this review was to evaluate the efficacy of plasmapheresis (PP) in AD and chronic progressive MS patients (in terms of improving clinical symptoms) and to analyze its safety and protocols. Methods: Articles related to this topic and published without time limitations in the Medline, and Cochrane databases were reviewed. Results: In AD patients, PP reduced amyloid beta (Aβ) levels in the brain, accompanied by a tendency towards cognitive stabilization, and improved language and verbal fluency. In regards to structural and functional brain changes, PP reduced brain volume and favored the stabilization, or absence, of the progression of perfusion. In chronic progressive form of MS patients, PP improved neurological deficits in 20–70% of patients with a chronic progressive form of MS, and restored interferon (IFN) responsiveness, which was not accompanied by any image change in brain plaques. Conclusions: Therapeutic plasmapheresis with albumin replacement is a promising strategy for reducing Aβ mediated toxicity and slowing the progression of the disorder. Some patients with chronic progressive forms of MS show improvement in neurological deficits. The features of AD and MS patients who benefit most from this approach need further research.

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Therapeutic plasma exchange for worsening multiple sclerosis: does it work?

Cited by 3 publications

References 9 publications

Neurologic indications for therapeutic plasma exchange: 2013 update

Neurologic indications for therapeutic plasma exchange: 2013 update

Progressive multifocal leukoencephalopathy in patients with multiple sclerosis

Therapeutic Plasmapheresis with Albumin Replacement in Alzheimer’s Disease and Chronic Progressive Multiple Sclerosis: A Review

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