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231223s2009 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2009.04.007
|2 doi
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|a pubmed24n1324.xml
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|a (DE-627)NLM188536248
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|a (NLM)19443276
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Herold, Kevan C
|e verfasserin
|4 aut
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| 245 |
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|a Treatment of patients with new onset Type 1 diabetes with a single course of anti-CD3 mAb Teplizumab preserves insulin production for up to 5 years
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|c 2009
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 17.09.2009
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|a Date Revised 12.03.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Anti-CD3 mAbs may prolong beta cell function up to 2 years in patients with new onset Type 1 diabetes (T1DM). A randomized open label trial of anti-CD3 mAb, Teplizumab, in T1DM was stopped after 10 subjects because of increased adverse events than in a previous trial related with higher dosing of drug. Teplizumab caused transient reduction in circulating T cells, but the recovered cells were not new thymic emigrants because T cell receptor excision circles were not increased. There was a trend for reduced loss of C-peptide over 2 years with drug treatment (p=0.1), and insulin use was lower (p<0.001). In 4 drug-treated subjects followed up to 60 months, C-peptide responses were maintained. We conclude that increased doses of Teplizumab are associated with greater adverse events without improved efficacy. The drug may marginate rather than deplete T cells. C-peptide levels may remain detectable up to 5 years after treatment
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|a Journal Article
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|a Randomized Controlled Trial
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Antibodies, Monoclonal, Humanized
|2 NLM
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|a C-Peptide
|2 NLM
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|a CD3 Complex
|2 NLM
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|a Hypoglycemic Agents
|2 NLM
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|a Insulin
|2 NLM
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| 650 |
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|a Muromonab-CD3
|2 NLM
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| 650 |
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|a teplizumab
|2 NLM
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| 650 |
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|a S4M959U2IJ
|2 NLM
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| 700 |
1 |
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|a Gitelman, Stephen
|e verfasserin
|4 aut
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|a Greenbaum, Carla
|e verfasserin
|4 aut
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|a Puck, Jennifer
|e verfasserin
|4 aut
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|a Hagopian, William
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gottlieb, Peter
|e verfasserin
|4 aut
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| 700 |
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|a Sayre, Peter
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Bianchine, Peter
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wong, Emelita
|e verfasserin
|4 aut
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1 |
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|a Seyfert-Margolis, Vicki
|e verfasserin
|4 aut
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| 700 |
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|a Bourcier, Kasia
|e verfasserin
|4 aut
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| 700 |
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|a Bluestone, Jeffrey A
|e verfasserin
|4 aut
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| 700 |
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|a Immune Tolerance Network ITN007AI Study Group
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 132(2009), 2 vom: 26. Aug., Seite 166-73
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:132
|g year:2009
|g number:2
|g day:26
|g month:08
|g pages:166-73
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2009.04.007
|3 Volltext
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