A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism
Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated marke...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nishiyama, Atsuko [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Anmerkung: |
© Japanese Society of Hematology 2022 |
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| Übergeordnetes Werk: |
Enthalten in: International journal of hematology - Tokyo [u.a.] : Springer, 1995, 116(2022), 2 vom: 13. Apr., Seite 276-287 |
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| Übergeordnetes Werk: |
volume:116 ; year:2022 ; number:2 ; day:13 ; month:04 ; pages:276-287 |
| Links: |
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| DOI / URN: |
10.1007/s12185-022-03339-3 |
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| Katalog-ID: |
SPR047683686 |
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| 100 | 1 | |a Nishiyama, Atsuko |e verfasserin |4 aut | |
| 245 | 1 | 2 | |a A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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| 520 | |a Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. | ||
| 650 | 4 | |a Fibrinolysis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Plasminemia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Fibrin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Streptokinase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Streptococcal infection |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Ogiwara, Kenichi |0 (orcid)0000-0002-3046-6915 |4 aut | |
| 700 | 1 | |a Nakajima, Yuto |4 aut | |
| 700 | 1 | |a Furukawa, Shoko |4 aut | |
| 700 | 1 | |a Matsumoto, Tomoko |4 aut | |
| 700 | 1 | |a Takeda, Hiroki |4 aut | |
| 700 | 1 | |a Nogami, Keiji |4 aut | |
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10.1007/s12185-022-03339-3 doi (DE-627)SPR047683686 (SPR)s12185-022-03339-3-e DE-627 ger DE-627 rakwb eng Nishiyama, Atsuko verfasserin aut A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Japanese Society of Hematology 2022 Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 Ogiwara, Kenichi (orcid)0000-0002-3046-6915 aut Nakajima, Yuto aut Furukawa, Shoko aut Matsumoto, Tomoko aut Takeda, Hiroki aut Nogami, Keiji aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 116(2022), 2 vom: 13. Apr., Seite 276-287 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:116 year:2022 number:2 day:13 month:04 pages:276-287 https://dx.doi.org/10.1007/s12185-022-03339-3 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_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_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_2056 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_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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 116 2022 2 13 04 276-287 |
| spelling |
10.1007/s12185-022-03339-3 doi (DE-627)SPR047683686 (SPR)s12185-022-03339-3-e DE-627 ger DE-627 rakwb eng Nishiyama, Atsuko verfasserin aut A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Japanese Society of Hematology 2022 Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 Ogiwara, Kenichi (orcid)0000-0002-3046-6915 aut Nakajima, Yuto aut Furukawa, Shoko aut Matsumoto, Tomoko aut Takeda, Hiroki aut Nogami, Keiji aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 116(2022), 2 vom: 13. Apr., Seite 276-287 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:116 year:2022 number:2 day:13 month:04 pages:276-287 https://dx.doi.org/10.1007/s12185-022-03339-3 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_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_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_2056 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_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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 116 2022 2 13 04 276-287 |
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10.1007/s12185-022-03339-3 doi (DE-627)SPR047683686 (SPR)s12185-022-03339-3-e DE-627 ger DE-627 rakwb eng Nishiyama, Atsuko verfasserin aut A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Japanese Society of Hematology 2022 Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 Ogiwara, Kenichi (orcid)0000-0002-3046-6915 aut Nakajima, Yuto aut Furukawa, Shoko aut Matsumoto, Tomoko aut Takeda, Hiroki aut Nogami, Keiji aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 116(2022), 2 vom: 13. Apr., Seite 276-287 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:116 year:2022 number:2 day:13 month:04 pages:276-287 https://dx.doi.org/10.1007/s12185-022-03339-3 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_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_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_2056 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_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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 116 2022 2 13 04 276-287 |
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10.1007/s12185-022-03339-3 doi (DE-627)SPR047683686 (SPR)s12185-022-03339-3-e DE-627 ger DE-627 rakwb eng Nishiyama, Atsuko verfasserin aut A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Japanese Society of Hematology 2022 Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 Ogiwara, Kenichi (orcid)0000-0002-3046-6915 aut Nakajima, Yuto aut Furukawa, Shoko aut Matsumoto, Tomoko aut Takeda, Hiroki aut Nogami, Keiji aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 116(2022), 2 vom: 13. Apr., Seite 276-287 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:116 year:2022 number:2 day:13 month:04 pages:276-287 https://dx.doi.org/10.1007/s12185-022-03339-3 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_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_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_2056 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_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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 116 2022 2 13 04 276-287 |
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10.1007/s12185-022-03339-3 doi (DE-627)SPR047683686 (SPR)s12185-022-03339-3-e DE-627 ger DE-627 rakwb eng Nishiyama, Atsuko verfasserin aut A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Japanese Society of Hematology 2022 Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 Ogiwara, Kenichi (orcid)0000-0002-3046-6915 aut Nakajima, Yuto aut Furukawa, Shoko aut Matsumoto, Tomoko aut Takeda, Hiroki aut Nogami, Keiji aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 116(2022), 2 vom: 13. Apr., Seite 276-287 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:116 year:2022 number:2 day:13 month:04 pages:276-287 https://dx.doi.org/10.1007/s12185-022-03339-3 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_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_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_2056 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_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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 116 2022 2 13 04 276-287 |
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Enthalten in International journal of hematology 116(2022), 2 vom: 13. Apr., Seite 276-287 volume:116 year:2022 number:2 day:13 month:04 pages:276-287 |
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Enthalten in International journal of hematology 116(2022), 2 vom: 13. Apr., Seite 276-287 volume:116 year:2022 number:2 day:13 month:04 pages:276-287 |
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Fibrinolysis Plasminemia Fibrin Streptokinase Streptococcal infection |
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International journal of hematology |
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Nishiyama, Atsuko @@aut@@ Ogiwara, Kenichi @@aut@@ Nakajima, Yuto @@aut@@ Furukawa, Shoko @@aut@@ Matsumoto, Tomoko @@aut@@ Takeda, Hiroki @@aut@@ Nogami, Keiji @@aut@@ |
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Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. 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Nishiyama, Atsuko |
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Nishiyama, Atsuko misc Fibrinolysis misc Plasminemia misc Fibrin misc Streptokinase misc Streptococcal infection A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism Fibrinolysis (dpeaa)DE-He213 Plasminemia (dpeaa)DE-He213 Fibrin (dpeaa)DE-He213 Streptokinase (dpeaa)DE-He213 Streptococcal infection (dpeaa)DE-He213 |
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misc Fibrinolysis misc Plasminemia misc Fibrin misc Streptokinase misc Streptococcal infection |
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A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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Nishiyama, Atsuko |
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Nishiyama, Atsuko Ogiwara, Kenichi Nakajima, Yuto Furukawa, Shoko Matsumoto, Tomoko Takeda, Hiroki Nogami, Keiji |
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case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
| abstract |
Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. © Japanese Society of Hematology 2022 |
| abstractGer |
Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. © Japanese Society of Hematology 2022 |
| abstract_unstemmed |
Abstract An 8-year-old Japanese boy with no underlying disease presented with severe intramuscular hematoma of the hip, and was admitted for a disseminated intravascular coagulation-like state with fibrinolytic dominance. Laboratory examinations revealed severe hyper-fibrinolysis with elevated markers, markedly shortened euglobulin clot lysis time, mildly decreased prothrombin, and severely decreased fibrinogen and factor XIII. Natural fibrin precipitates rapidly appeared in citrate-treated, ethylene-diamine-tetra-acetic-treated, and heparin-treated samples, but not in argatroban-treated samples, indicating that the mechanism of thrombin and fibrin formation was $ Ca^{2+} $-independent. The precipitates were physically similar to thrombin-triggered plasma fibrin. A global coagulation assay revealed that thrombin generation potentials were normal throughout the clinical course, whereas plasmin generation was already detected before initiation of fibrin formation in the acute phase. This phenomenon disappeared with time. Changes in coagulation abnormalities and nature of fibrinolysis paralleled those seen in specific markers for streptococcal infections. Streptokinase was possibly involved in this disease, as SDS–polyacrylamide gel electrophoresis revealed that plasmin derived from streptokinase-plasminogen complex proteolyzed the prothrombin to approximately 35-kDa α-thrombin consisting of the A–B single chain, which was identified by $ NH_{2} $-terminal sequence analysis. The involvement of streptokinase–plasminogen–prothrombin caused by streptococcal infection may be one mechanism that produces marked hyper-fibrinolysis associated with natural fibrin precipitates. © Japanese Society of Hematology 2022 |
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| title_short |
A case of a young boy with hyper-fibrinolysis associated with natural fibrin precipitates suspected to have occurred through a novel coagulation and fibrinolysis mechanism |
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https://dx.doi.org/10.1007/s12185-022-03339-3 |
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Ogiwara, Kenichi Nakajima, Yuto Furukawa, Shoko Matsumoto, Tomoko Takeda, Hiroki Nogami, Keiji |
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Ogiwara, Kenichi Nakajima, Yuto Furukawa, Shoko Matsumoto, Tomoko Takeda, Hiroki Nogami, Keiji |
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10.1007/s12185-022-03339-3 |
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| score |
7.4008226 |