Graves’ disease after treatment with Alemtuzumab for multiple sclerosis
Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Tsourdi, Elena [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Anmerkung: |
© Hellenic Endocrine Society 2015 |
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| Übergeordnetes Werk: |
Enthalten in: Hormones - [Cham] : Springer International Publishing, 2002, 14(2015), 1 vom: 01. Jan., Seite 148-153 |
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| Übergeordnetes Werk: |
volume:14 ; year:2015 ; number:1 ; day:01 ; month:01 ; pages:148-153 |
| Links: |
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| DOI / URN: |
10.14310/horm.2002.1501 |
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SPR038407205 |
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| 520 | |a Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. | ||
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| 700 | 1 | |a Ziemssen, Tjalf |4 aut | |
| 700 | 1 | |a Hofbauer, Lorenz C. |4 aut | |
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10.14310/horm.2002.1501 doi (DE-627)SPR038407205 (SPR)horm.2002.1501-e DE-627 ger DE-627 rakwb eng Tsourdi, Elena verfasserin aut Graves’ disease after treatment with Alemtuzumab for multiple sclerosis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hellenic Endocrine Society 2015 Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. Gruber, Matthias aut Rauner, Martina aut Blankenburg, Judith aut Ziemssen, Tjalf aut Hofbauer, Lorenz C. aut Enthalten in Hormones [Cham] : Springer International Publishing, 2002 14(2015), 1 vom: 01. Jan., Seite 148-153 (DE-627)640092357 (DE-600)2581819-3 2520-8721 nnns volume:14 year:2015 number:1 day:01 month:01 pages:148-153 https://dx.doi.org/10.14310/horm.2002.1501 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 14 2015 1 01 01 148-153 |
| spelling |
10.14310/horm.2002.1501 doi (DE-627)SPR038407205 (SPR)horm.2002.1501-e DE-627 ger DE-627 rakwb eng Tsourdi, Elena verfasserin aut Graves’ disease after treatment with Alemtuzumab for multiple sclerosis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hellenic Endocrine Society 2015 Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. Gruber, Matthias aut Rauner, Martina aut Blankenburg, Judith aut Ziemssen, Tjalf aut Hofbauer, Lorenz C. aut Enthalten in Hormones [Cham] : Springer International Publishing, 2002 14(2015), 1 vom: 01. Jan., Seite 148-153 (DE-627)640092357 (DE-600)2581819-3 2520-8721 nnns volume:14 year:2015 number:1 day:01 month:01 pages:148-153 https://dx.doi.org/10.14310/horm.2002.1501 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 14 2015 1 01 01 148-153 |
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10.14310/horm.2002.1501 doi (DE-627)SPR038407205 (SPR)horm.2002.1501-e DE-627 ger DE-627 rakwb eng Tsourdi, Elena verfasserin aut Graves’ disease after treatment with Alemtuzumab for multiple sclerosis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hellenic Endocrine Society 2015 Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. Gruber, Matthias aut Rauner, Martina aut Blankenburg, Judith aut Ziemssen, Tjalf aut Hofbauer, Lorenz C. aut Enthalten in Hormones [Cham] : Springer International Publishing, 2002 14(2015), 1 vom: 01. Jan., Seite 148-153 (DE-627)640092357 (DE-600)2581819-3 2520-8721 nnns volume:14 year:2015 number:1 day:01 month:01 pages:148-153 https://dx.doi.org/10.14310/horm.2002.1501 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 14 2015 1 01 01 148-153 |
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10.14310/horm.2002.1501 doi (DE-627)SPR038407205 (SPR)horm.2002.1501-e DE-627 ger DE-627 rakwb eng Tsourdi, Elena verfasserin aut Graves’ disease after treatment with Alemtuzumab for multiple sclerosis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hellenic Endocrine Society 2015 Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. Gruber, Matthias aut Rauner, Martina aut Blankenburg, Judith aut Ziemssen, Tjalf aut Hofbauer, Lorenz C. aut Enthalten in Hormones [Cham] : Springer International Publishing, 2002 14(2015), 1 vom: 01. Jan., Seite 148-153 (DE-627)640092357 (DE-600)2581819-3 2520-8721 nnns volume:14 year:2015 number:1 day:01 month:01 pages:148-153 https://dx.doi.org/10.14310/horm.2002.1501 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 14 2015 1 01 01 148-153 |
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10.14310/horm.2002.1501 doi (DE-627)SPR038407205 (SPR)horm.2002.1501-e DE-627 ger DE-627 rakwb eng Tsourdi, Elena verfasserin aut Graves’ disease after treatment with Alemtuzumab for multiple sclerosis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hellenic Endocrine Society 2015 Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. Gruber, Matthias aut Rauner, Martina aut Blankenburg, Judith aut Ziemssen, Tjalf aut Hofbauer, Lorenz C. aut Enthalten in Hormones [Cham] : Springer International Publishing, 2002 14(2015), 1 vom: 01. Jan., Seite 148-153 (DE-627)640092357 (DE-600)2581819-3 2520-8721 nnns volume:14 year:2015 number:1 day:01 month:01 pages:148-153 https://dx.doi.org/10.14310/horm.2002.1501 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 14 2015 1 01 01 148-153 |
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Tsourdi, Elena @@aut@@ Gruber, Matthias @@aut@@ Rauner, Martina @@aut@@ Blankenburg, Judith @@aut@@ Ziemssen, Tjalf @@aut@@ Hofbauer, Lorenz C. @@aut@@ |
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Tsourdi, Elena Graves’ disease after treatment with Alemtuzumab for multiple sclerosis |
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graves’ disease after treatment with alemtuzumab for multiple sclerosis |
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Graves’ disease after treatment with Alemtuzumab for multiple sclerosis |
| abstract |
Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. © Hellenic Endocrine Society 2015 |
| abstractGer |
Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. © Hellenic Endocrine Society 2015 |
| abstract_unstemmed |
Abstract CONTEXT: Alemtuzumab, a humanized monoclonal antibody against CD52, is effective in the treatment of early relapsing-remitting multiple sclerosis (MS). Common adverse effects include an acute-phase reaction, infections and autoimmune diseases, including thyroid disorders. SETTING: Patients from two phase 3 trials (CARE MS 1 and 2, n=15) were studied in a clinical research center. PATIENTS: Five out of fifteen patients developed severe Graves’ disease after a mean of 32 months following the first alemtuzumab treatment. MAIN OUTCOME MEASURES: Thyroid function tests and thyroid antibodies were assessed. In addition, endocrine tests and measurement of antibodies indicative of autoimmunity were performed. RESULTS: Of the five patients developing Graves’ disease, four patients were initially treated with antithyroid drugs, whereas the fifth patient had mild and self-limiting hyperthyroidism. Of the four patients treated with antithyroid drugs, one is currently under medical treatment in a dose-reducing regimen, whereas three patients underwent near-total thyroidectomy 2, 12 and 16 months later. Two patients developed endocrine ophthalmopathy. Pituitary, adrenal and gonadal hormones were normal in all patients. While four out of five patients were positive for several other autoantibodies, none developed other autoimmune diseases. CONCLUSION: Since autoimmune thyroid disease is common after alemtuzumab treatment for MS, pretreatment screening and careful follow-up may allow for early diagnosis and treatment. © Hellenic Endocrine Society 2015 |
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Graves’ disease after treatment with Alemtuzumab for multiple sclerosis |
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https://dx.doi.org/10.14310/horm.2002.1501 |
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Gruber, Matthias Rauner, Martina Blankenburg, Judith Ziemssen, Tjalf Hofbauer, Lorenz C. |
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Gruber, Matthias Rauner, Martina Blankenburg, Judith Ziemssen, Tjalf Hofbauer, Lorenz C. |
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10.14310/horm.2002.1501 |
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2024-07-03T17:55:25.095Z |
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| score |
7.399479 |