Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature
Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gentileschi, Stefano [verfasserIn] Rigante, Donato [verfasserIn] Vitale, Antonio [verfasserIn] Sota, Jurgen [verfasserIn] Frediani, Bruno [verfasserIn] Galeazzi, Mauro [verfasserIn] Cantarini, Luca [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Clinical rheumatology - London : Springer, 1982, 36(2017), 7 vom: 23. Mai, Seite 1687-1690 |
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| Übergeordnetes Werk: |
volume:36 ; year:2017 ; number:7 ; day:23 ; month:05 ; pages:1687-1690 |
| Links: |
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| DOI / URN: |
10.1007/s10067-017-3688-4 |
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| Katalog-ID: |
SPR008526591 |
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| 100 | 1 | |a Gentileschi, Stefano |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
| 264 | 1 | |c 2017 | |
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| 520 | |a Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. | ||
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| 650 | 4 | |a TRAPS |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Treatment |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Rigante, Donato |e verfasserin |4 aut | |
| 700 | 1 | |a Vitale, Antonio |e verfasserin |4 aut | |
| 700 | 1 | |a Sota, Jurgen |e verfasserin |4 aut | |
| 700 | 1 | |a Frediani, Bruno |e verfasserin |4 aut | |
| 700 | 1 | |a Galeazzi, Mauro |e verfasserin |4 aut | |
| 700 | 1 | |a Cantarini, Luca |e verfasserin |4 aut | |
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10.1007/s10067-017-3688-4 doi (DE-627)SPR008526591 (SPR)s10067-017-3688-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl 44.83 bkl Gentileschi, Stefano verfasserin aut Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Rigante, Donato verfasserin aut Vitale, Antonio verfasserin aut Sota, Jurgen verfasserin aut Frediani, Bruno verfasserin aut Galeazzi, Mauro verfasserin aut Cantarini, Luca verfasserin aut Enthalten in Clinical rheumatology London : Springer, 1982 36(2017), 7 vom: 23. Mai, Seite 1687-1690 (DE-627)27159909X (DE-600)1480901-1 1434-9949 nnns volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 https://dx.doi.org/10.1007/s10067-017-3688-4 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_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_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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_4393 GBV_ILN_4700 44.00 ASE 44.83 ASE AR 36 2017 7 23 05 1687-1690 |
| spelling |
10.1007/s10067-017-3688-4 doi (DE-627)SPR008526591 (SPR)s10067-017-3688-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl 44.83 bkl Gentileschi, Stefano verfasserin aut Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Rigante, Donato verfasserin aut Vitale, Antonio verfasserin aut Sota, Jurgen verfasserin aut Frediani, Bruno verfasserin aut Galeazzi, Mauro verfasserin aut Cantarini, Luca verfasserin aut Enthalten in Clinical rheumatology London : Springer, 1982 36(2017), 7 vom: 23. Mai, Seite 1687-1690 (DE-627)27159909X (DE-600)1480901-1 1434-9949 nnns volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 https://dx.doi.org/10.1007/s10067-017-3688-4 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_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_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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_4393 GBV_ILN_4700 44.00 ASE 44.83 ASE AR 36 2017 7 23 05 1687-1690 |
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10.1007/s10067-017-3688-4 doi (DE-627)SPR008526591 (SPR)s10067-017-3688-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl 44.83 bkl Gentileschi, Stefano verfasserin aut Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Rigante, Donato verfasserin aut Vitale, Antonio verfasserin aut Sota, Jurgen verfasserin aut Frediani, Bruno verfasserin aut Galeazzi, Mauro verfasserin aut Cantarini, Luca verfasserin aut Enthalten in Clinical rheumatology London : Springer, 1982 36(2017), 7 vom: 23. Mai, Seite 1687-1690 (DE-627)27159909X (DE-600)1480901-1 1434-9949 nnns volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 https://dx.doi.org/10.1007/s10067-017-3688-4 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_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_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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_4393 GBV_ILN_4700 44.00 ASE 44.83 ASE AR 36 2017 7 23 05 1687-1690 |
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10.1007/s10067-017-3688-4 doi (DE-627)SPR008526591 (SPR)s10067-017-3688-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl 44.83 bkl Gentileschi, Stefano verfasserin aut Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Rigante, Donato verfasserin aut Vitale, Antonio verfasserin aut Sota, Jurgen verfasserin aut Frediani, Bruno verfasserin aut Galeazzi, Mauro verfasserin aut Cantarini, Luca verfasserin aut Enthalten in Clinical rheumatology London : Springer, 1982 36(2017), 7 vom: 23. Mai, Seite 1687-1690 (DE-627)27159909X (DE-600)1480901-1 1434-9949 nnns volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 https://dx.doi.org/10.1007/s10067-017-3688-4 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_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_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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_4393 GBV_ILN_4700 44.00 ASE 44.83 ASE AR 36 2017 7 23 05 1687-1690 |
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10.1007/s10067-017-3688-4 doi (DE-627)SPR008526591 (SPR)s10067-017-3688-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl 44.83 bkl Gentileschi, Stefano verfasserin aut Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Rigante, Donato verfasserin aut Vitale, Antonio verfasserin aut Sota, Jurgen verfasserin aut Frediani, Bruno verfasserin aut Galeazzi, Mauro verfasserin aut Cantarini, Luca verfasserin aut Enthalten in Clinical rheumatology London : Springer, 1982 36(2017), 7 vom: 23. Mai, Seite 1687-1690 (DE-627)27159909X (DE-600)1480901-1 1434-9949 nnns volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 https://dx.doi.org/10.1007/s10067-017-3688-4 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_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_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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_4393 GBV_ILN_4700 44.00 ASE 44.83 ASE AR 36 2017 7 23 05 1687-1690 |
| language |
English |
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Enthalten in Clinical rheumatology 36(2017), 7 vom: 23. Mai, Seite 1687-1690 volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 |
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Enthalten in Clinical rheumatology 36(2017), 7 vom: 23. Mai, Seite 1687-1690 volume:36 year:2017 number:7 day:23 month:05 pages:1687-1690 |
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findex.gbv.de |
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Anakinra Autoinflammatory diseases gene TRAPS Treatment |
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| container_title |
Clinical rheumatology |
| authorswithroles_txt_mv |
Gentileschi, Stefano @@aut@@ Rigante, Donato @@aut@@ Vitale, Antonio @@aut@@ Sota, Jurgen @@aut@@ Frediani, Bruno @@aut@@ Galeazzi, Mauro @@aut@@ Cantarini, Luca @@aut@@ |
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2017-05-23T00:00:00Z |
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3610 |
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englisch |
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Gentileschi, Stefano |
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Gentileschi, Stefano ddc 610 bkl 44.00 bkl 44.83 misc Anakinra misc Autoinflammatory diseases misc gene misc TRAPS misc Treatment Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
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610 ASE 44.00 bkl 44.83 bkl Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature Anakinra (dpeaa)DE-He213 Autoinflammatory diseases (dpeaa)DE-He213 gene (dpeaa)DE-He213 TRAPS (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 |
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Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
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Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
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Gentileschi, Stefano Rigante, Donato Vitale, Antonio Sota, Jurgen Frediani, Bruno Galeazzi, Mauro Cantarini, Luca |
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efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (traps) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
| title_auth |
Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
| abstract |
Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. |
| abstractGer |
Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. |
| abstract_unstemmed |
Abstract Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), caused by mutations in the TNFRSF1A gene, is the most frequent autosomal dominant autonflammatory disease displaying a relevant risk of reactive AA amyloidosis, if left untreated. Our report deals with one adult with TRAPS complicated by amyloidosis-related renal failure, treated with the recombinant human interleukin-1 receptor antagonist anakinra at a higher than conventional dosage. This treatment did not present any adverse event and led remarkably to the disappearance of all TRAPS-related manifestations and prompt decrease of laboratory abnormalities, including proteinuria. A review of the medical literature has been also considered to evaluate efficacy and safety of interleukin-1 inhibition in patients with TRAPS. |
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Efficacy and safety of anakinra in tumor necrosis factor receptor-associated periodic syndrome (TRAPS) complicated by severe renal failure: a report after long-term follow-up and review of the literature |
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| score |
7.4006968 |