Autoimmune Comorbid Conditions in Multiple Sclerosis

US Neurology ◽  
2011 ◽  
Vol 07 (02) ◽  
pp. 132 ◽  
Author(s):  
Regina Berkovich ◽  
Dawood Subhani ◽  
Lawrence Steinman ◽  
◽  
◽  
...  

Autoimmune comorbidities occur frequently in multiple sclerosis (MS). They may arise as a consequence of a genetic susceptibility to autoimmunity. Certain pathological mechanisms are common to several autoimmune conditions. In the presence of comorbid autoimmune conditions, certain MS therapeutics may be preferable to others. Autoimmune comorbidity associated with MS could be a factor in predicting response to specific MS therapeutics. Treatment with interferon beta has been reported to precipitate immune-mediated abnormalities or to exacerbate existing autoimmune diseases. In comparison, there are fewer reported cases of treatment-associated comorbidities linked with autoimmune disease in patients taking glatiramer acetate. Knowledge of the factors influencing autoimmune comorbidities may provide insights into the complex pathogenesis of MS and help inform treatment choices.

2007 ◽  
Vol 13 (8) ◽  
pp. 1071-1075 ◽  
Author(s):  
D.R. Jeffery

Multiple sclerosis (MS) is thought to be an autoimmune disease in which activated T-cells initiate a macrophage mediated destruction of CNS myelin. Bone marrow transplantation (BMT) is currently being evaluated in the treatment of MS in patients with aggressive disease activity. Autologous BMT could potentially reset the immune response to myelin antigens leading to immune tolerance and decreased disease activity. Allogeneic transplantation could reconstitute the immune system potentially arresting the progression of autoimmune disease. The purpose of this paper is to report a patient with MS who underwent allogeneic BMT for chronic myelogenous leukemia (CML) and showed continued evidence of active demyelinating disease by clinical and radiologic criteria over a period of two years. While this is only a single case report with inherent limitations, it suggests that the immune mediated destruction of CNS myelin in MS may not be prevented or aborted by immune system reconstitution, and is consistent with the idea that immune mediated tissue destruction in MS could be targeted against an abnormal antigen. Multiple Sclerosis 2007; 13: 1071—1075. http://msj.sagepub.com


2018 ◽  
Vol 80 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Mirla Avila ◽  
Arpana Bansal ◽  
John Culberson ◽  
Alan N. Peiris

Multiple sclerosis (MS) is a chronic inflammatory demyelination disorder with an immune-mediated pathophysiology that affects the central nervous system (CNS). Like other autoimmune conditions, it has a predilection for female gender. This suggests a gender bias and a possible hormonal association. Inflammation and demyelination are hallmarks of MS. Oligodendrocytes are the myelinating cells of the CNS and these continue to be generated by oligodendrocyte precursor cells (OPCs). The process of remyelination represents a major form of plasticity in the developing adult CNS. Remyelination does occur in MS, but the process is largely inadequate and/or incomplete. Current treatment strategies primarily focus on reducing inflammation or immunosuppression, but there is a need for more extensive research on re-myelination as a possible mechanism of treatment. Previous studies have shown that pregnancy leads to an increase in OPC proliferation, oligodendrocyte generation and the number of myelinated axons in the maternal CNS. Studies have also suggested that this remyelination is possibly mediated by estriol. Sex hormones in particular have been shown to have an immuno-protective effect in TH1-driven autoimmunity diseases. The aim of our article is to review the available research on sex hormone-specific immune modulatory effects, assess its remyelination potential in MS, and suggest a future path for more extensive research on sex hormone as a target for therapeutics in MS.


2020 ◽  
Vol 8 (1) ◽  
pp. e000356 ◽  
Author(s):  
Patrick Boland ◽  
Anna C Pavlick ◽  
Jeffrey Weber ◽  
Sabina Sandigursky

In the past 10 years, immune checkpoint inhibitors (ICIs) have become an additional pillar of cancer therapy by activating the immune system to treat a number of different malignancies. Many patients receiving ICIs develop immune-related adverse events (irAEs) that mimic some features of classical autoimmune diseases. Unfortunately, patients with underlying autoimmune conditions, many of whom have an increased risk for malignancy, have been excluded from clinical trials of ICIs due to a concern that they will have an increased risk of irAEs. Retrospective data from patients with autoimmune diseases and concomitant malignancy treated with ICIs are encouraging and suggest that ICIs may be tolerated safely in patients with specific autoimmune diseases, but there are no prospective data to guide management. In this manuscript, we review the relationship between pre-existing autoimmune disease and irAEs from checkpoint inhibitors. In addition, we assess the likelihood of autoimmune disease exacerbations in patients with pre-existing autoimmunity receiving ICI.


2015 ◽  
Vol 45 (16) ◽  
pp. 3559-3569 ◽  
Author(s):  
N. W. Andersson ◽  
L. N. Gustafsson ◽  
N. Okkels ◽  
F. Taha ◽  
S. W. Cole ◽  
...  

Background.Autoimmune diseases are associated with substantial morbidity and mortality, yet the etiology remains unclear. Depression has been implicated as a risk factor for various immune-related disorders but little is known about the risk of autoimmune disease. This study examined the association between depression and the risk of autoimmune disease, and investigated the temporal and dose-response nature of these relationships.Method.A prospective population-based study including approximately 1.1 million people was conducted using linked Danish registries. Depression and autoimmune diseases were diagnosed by physicians and documented in medical records. In total, 145 217 individuals with depression were identified between 1995 and 2012. Survival analyses were used to estimate the relative risk of autoimmune disease among those with, compared to without, depression. Analyses were adjusted for gender, age, and co-morbid mental disorders.Results.Depression was associated with a significantly increased risk of autoimmune disease [incidence rate ratio (IRR) 1.25, 95% CI 1.19–1.31], compared to those without a history of depression. Results suggest a general increased risk of autoimmune diseases following the onset of depression during first year (IRR 1.29, 95% CI 1.05–1.58), which remained elevated for the ensuing 11 years and beyond (IRR 1.53, 95% CI 1.34–1.76). Findings did not support a dose-response relationship.Conclusions.Depression appears to be associated with an increased risk of a range of autoimmune diseases. Depression may play a role in the etiology of certain autoimmune conditions. If replicated, findings could highlight additional clinical implications in the treatment and management of depression. Future studies are needed to investigate the possible social, genetic, and neurobiological underpinnings of these relationships.


Author(s):  
Nazanin Ershadinia ◽  
Nader Mortazavinia ◽  
Sepideh Babaniamansour ◽  
Mahdi Najafi-Nesheli ◽  
Parto Babaniamansour ◽  
...  

Background: Multiple sclerosis (MS) is one of the most common autoimmune diseases worldwide and various autoimmune comorbidities are reported with MS. The objective of this study is to estimate the prevalence of the autoimmune diseases’ comorbidity in patients with MS. Methods: In this cross-sectional study, we investigated a group of patients with MS in terms of age, gender, duration of MS, presence of simultaneous autoimmune diseases, such as Graves’ disease, Hashimoto’s thyroiditis, type 1 diabetes mellitus (DM), and systemic lupus erythematous (SLE). Results: This study included 1215 patients with MS, of which 70.8% were women. The mean age of participants was 33.70 ± 27.63 years. 55 patients (4.5%) had at least one autoimmune disease. The most common comorbidity was for Hashimoto’s thyroiditis (30 patients). The frequency of simultaneous autoimmune disease was higher in women. Mean age (P = 0.01), mean duration of MS (P = 0.03), and mean age on MS diagnosis (P = 0.02) were significantly higher in simultaneous MS and other autoimmune diseases. Conclusion: Our study revealed that the probability of autoimmune diseases co-occurrence in patients with MS could be higher in older patients, in longer duration of disease, and also in patients with higher age at time of MS diagnosis.


2002 ◽  
Vol 8 (6) ◽  
pp. 534-536 ◽  
Author(s):  
A Altintas ◽  
Y Alici ◽  
M Melikoğlu ◽  
A Siva

Interferon beta (IFN-β) is the most widely prescribed disease-modifying drug for multiple sclerosis (MS). Therapy with IFN-βmay be associated with a number of adverse reactions. The development or exacerbation of other autoimmune diseases is a rare but reported side effect of IFN-βtherapy. In this case report, we present clinical and laboratory findings of two MS patients who developed arthritis during IFN-β1b treatment, probably of autoimmune origin.


2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Éric Toussirot ◽  
Matthieu Béreau ◽  
Marie Bossert ◽  
Imad Malkoun ◽  
Anne Lohse

Interferon beta (IFN-β) is the first line therapy of relapsing-remitting multiple sclerosis. IFN-βis a cytokine that can contribute to the development of systemic autoimmune disease including psoriasis. The development or the exacerbation of psoriasis during IFN-βtreatment has been previously observed. We report the occurrence of arthritis and dactylitis in a multiple sclerosis patient with preexisting psoriasis diagnosed as a psoriatic arthritis. The IL-23/Th17 pathway is involved in psoriasis and psoriatic arthritis and it has been suggested that IFN-βtherapy in patients with Th17-mediated disease may be detrimental. Together with previous similar reports, our case suggests that IFN-βshould certainly be used with caution in patients with concomitant systemic autoimmune disease with IL-23/Th17 involvement.


2021 ◽  
Author(s):  
Erik Schaeffner ◽  
Julia Edgar ◽  
Maria Lehning ◽  
Judith Strauss ◽  
Mar Bosch-Queralt ◽  
...  

Axonal degeneration determines the clinical outcome of multiple sclerosis (MS), and is thought to result from exposure of denuded axons to immune-mediated damage. We challenge this view after finding in MS and its mouse models that myelin itself increases the risk of axons to degenerate under inflammatory conditions. We propose a model for demyelinating diseases in which for axons that remain myelinated, and thus shielded from the extracellular milieu, dependence from oligodendroglial support turns fatal in an autoimmune disease environment.


2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Bharath Wootla ◽  
Makoto Eriguchi ◽  
Moses Rodriguez

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) with varied clinical presentations and heterogeneous histopathological features. The underlying immunological abnormalities in MS lead to various neurological and autoimmune manifestations. There is strong evidence that MS is, at least in part, an immune-mediated disease. There is less evidence that MS is a classical autoimmune disease, even though many authors state this in the description of the disease. We show the evidence that both supports and refutes the autoimmune hypothesis. In addition, we present an alternate hypothesis based on virus infection to explain the pathogenesis of MS.


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