| pubmed-article:15261565 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0008976 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0010583 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0034107 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0205177 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C2349943 | lld:lifeskim |
| pubmed-article:15261565 | lifeskim:mentions | umls-concept:C0439611 | lld:lifeskim |
| pubmed-article:15261565 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15261565 | pubmed:dateCreated | 2004-7-20 | lld:pubmed |
| pubmed-article:15261565 | pubmed:abstractText | This was a randomized, single-blind, parallel-group, multicenter trial in MS patients with a history of active disease during IFN-beta treatment. Patients were randomized to either cyclophosphamide 800 mg/m2 plus methylprednisolone 1 g IV (CY/MP) or methylprednisolone (MP) once monthly for 6 months then followed for an additional 18 months. All patients received IFN-beta1a for the 24-month study period. The primary endpoint was mean change from baseline in the number of gadolinium-enhancing (Gd+) lesions. Secondary endpoints included the percentage of patients with Gd+ lesions, change in T2 lesion burden, change in brain parenchymal fraction (BPF), time to treatment failure, and cumulative probability of relapse. Safety was assessed by the incidence of adverse events and the results of blood and urine testing. A higher number of patients completed the study in the pulse cyclophosphamide group because approximately half as many of these patients became treatment failures (26% vs. 52%, p = 0.03). During the infusion phase, the mean number of Gd+ lesions declined 70-80% from baseline in the CY group vs. a small increase in MP (p = 0.02 and 0.04 at 3 and 6 months). We conclude that pulse cyclophosphamide appears to be well tolerated in combination with IFN-beta1a. Pulse cyclophosphamide decreases the number of Gd+ lesions in patients with active disease on IFN-beta compared to pulse methylprednisolone alone. Six doses of pulse cyclophosphamide in combination with IFN-beta1a both prevent and delay clinical disease activity in patients with previously active disease on IFN-beta alone. Pulse cyclophosphamide is a therapeutic option as rescue therapy for patients thought to be interferon non-responders. | lld:pubmed |
| pubmed-article:15261565 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15261565 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15261565 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15261565 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:15261565 | pubmed:issn | 0022-510X | lld:pubmed |
| pubmed-article:15261565 | pubmed:author | pubmed-author:SmithDerekD | lld:pubmed |
| pubmed-article:15261565 | pubmed:copyrightInfo | Copyright 2004 Elsevier B.V. | lld:pubmed |
| pubmed-article:15261565 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15261565 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:15261565 | pubmed:volume | 223 | lld:pubmed |
| pubmed-article:15261565 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15261565 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15261565 | pubmed:pagination | 73-9 | lld:pubmed |
| pubmed-article:15261565 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
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| pubmed-article:15261565 | pubmed:meshHeading | pubmed-meshheading:15261565... | lld:pubmed |
| pubmed-article:15261565 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15261565 | pubmed:articleTitle | Preliminary analysis of a trial of pulse cyclophosphamide in IFN-beta-resistant active MS. | lld:pubmed |
| pubmed-article:15261565 | pubmed:affiliation | Department of Neurology, Harvard Medical School, BIDMC KS 413, 330 Brookline Ave, Boston, MA 02215, USA. drsmith@bidmc.harvard.edu | lld:pubmed |
| pubmed-article:15261565 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15261565 | pubmed:publicationType | Clinical Trial | lld:pubmed |
| pubmed-article:15261565 | pubmed:publicationType | Randomized Controlled Trial | lld:pubmed |
| pubmed-article:15261565 | pubmed:publicationType | Multicenter Study | lld:pubmed |
