Therapeutic Considerations for Disease Progression in Multiple Sclerosis

Frohman, Elliot M.; Stüve, Olaf; Havrdová, Eva; Corboy, John R.; Achiron, Anat; Zivadinov, Robert; Sørensen, Per Soelberg; Phillips, J. Theodore; Weinshenker, Brian; Hawker, Kathleen; Hartung, Hans Peter; Steinman, Lawrence; Zamvil, Scott S.; Cree, Bruce A.C.; Hauser, Stephen; Weiner, Howard L.; Racke, Michael K.; Filippi, Massimo

doi:10.1001/archneur.62.10.1519

Cited by 39 publications

(30 citation statements)

References 119 publications

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“…Costs were obtained from the published literature and were inflated to 2005 U.S. dollars, where necessary, by the medical component of the Consumer Price Index. 70 The annual acquisition cost of SC GA and each b-interferon was calculated using wholesale acquisition costs (WACs), 32 days supply per prescription, the recommended dosing schedule, patient compliance (assumed 70% in basecase model [71][72][73] ), patient copayment ($25 per prescription in base-case model), and the proportion of patients discontinuing therapy as reported in clinical trials (see Table 1). …”

Section: Costsmentioning

confidence: 99%

Cost-effectiveness of Four Immunomodulatory Therapies for Relapsing-Remitting Multiple Sclerosis: A Markov Model Based on Long-term Clinical Data

Bell¹,

Graham²,

Earnshaw³

et al. 2007

JMCP

118

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Section: Costsmentioning

confidence: 99%

Cost-effectiveness of Four Immunomodulatory Therapies for Relapsing-Remitting Multiple Sclerosis: A Markov Model Based on Long-term Clinical Data

Bell¹,

Graham²,

Earnshaw³

et al. 2007

JMCP

118

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show abstract

“…Interferon-b (IFN-b) is the mainstay of diseasemodifying therapy for patients with relapsing-remitting MS [96]. The mechanism by which IFN-b exerts beneficial disease-modifying effects in MS remains unclear but, among other mechanisms, may involve suppression of T cell activation [97,98]; inhibition of IFN-g-induced MHC class II expression on endothelial cells [99]; a decrease in TNF-a and increase in IL-6 production [100]; an increase of B7-H1 (PD-L1) on monocytes and DCs [101]; up-regulation of monocyte-derived HLA-G [102]; an increase of the costimulatory molecules CD80, CD86 and CD40 on monocytes [103]; inhibition of matrix metalloproteinases [104,105], leading to reduced T cell migration [106]; induction of TGF-b1 and its receptor [107]; and inhibition of iNOS expression [108].…”

Section: Interferon-b and Trp Catabolism In Msmentioning

confidence: 99%

Tryptophan degradation in autoimmune diseases

Opitz

Wick

Steinman

et al. 2007

Cell. Mol. Life Sci.

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Recent evidence points to tryptophan (Trp) degradation as a potent immunosuppressive mechanism involved in the maintenance of immunological tolerance. Both Trp depletion and downstream Trp catabolites (TCs) appear to synergistically confer protection against excessive inflammation. In this review, we give an overview of the immunosuppressive properties of Trp degradation with special focus on TCs. Constitutive and inducible Trp degradation in different cell types and tissues of human and murine origin is summarized. We address the influence of Trp degradation on different aspects of autoimmune disorders such as multiple sclerosis. Possible therapeutic approaches for autoimmune disorders targeting Trp degradation are presented, and key issues relevant for the development of such therapeutic strategies are discussed.

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“…2,3 Perhaps one of the most contentious issues in MS therapeutic decision-making concerns whether to switch to an alternative class of DMA, or instead to add a second agent to the first.…”

Section: Disease Progression: a Pretext For Using Chronic Corticostermentioning

confidence: 99%

Corticosteroids for Multiple Sclerosis: II. Application for Disease-Modifying Effects

et al. 2007

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Summary:Physicians who treat multiple sclerosis (MS) face the challenge of patients exhibiting ongoing disease activity, including exacerbations, loss of functional capabilities, intellectual decline, and radiologic progression, despite being on a disease-modifying agent (DMA). After searching for factors that might at least in part explain these changes-such as nonadherent drug-taking behavior, or the presence of interferon-neutralizing antibodies-some providers may ultimately decide to switch the patient to another DMA. In most circumstances, patients likely derive only partial effects from these agents, even in the absence of compromising factors. Thus, a number of factors must be considered in order to intensify the treatment regimen in response to disease progression. In the context of an inadequate treatment response to a DMA, some clinicians will convert the patient to an alternative therapy, and others will instead use a second agent in combination with the first (the so-called platform agent). In the first of this two-part series, we explored the use of anti-inflammatory CS and ACTH to treat MS exacerbations. Although we underscored the limited availability of evidence-based studies to support specific regimens for this purpose, there is an even greater paucity of data to support the routine use of these agents in order to achieve chronic disease-modifying effects in those who continue to deteriorate clinically, radiographically, or both. Without doubt, a number of factors influence the formulation of combination treatment plan for MS. Nevertheless, we will focus on the rationale and practical schemes that can be considered for using corticosteroids (CS) (and perhaps even ACTH) in an attempt to modify various domains of ongoing disease activity.

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Therapeutic Considerations for Disease Progression in Multiple Sclerosis

Cited by 39 publications

References 119 publications

Cost-effectiveness of Four Immunomodulatory Therapies for Relapsing-Remitting Multiple Sclerosis: A Markov Model Based on Long-term Clinical Data

Cost-effectiveness of Four Immunomodulatory Therapies for Relapsing-Remitting Multiple Sclerosis: A Markov Model Based on Long-term Clinical Data

Tryptophan degradation in autoimmune diseases

Corticosteroids for Multiple Sclerosis: II. Application for Disease-Modifying Effects

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