Eculizumab for Severe Thrombotic Microangiopathy Secondary to Surgical Invasive Stress and Bleeding
Atypical hemolytic uremic syndrome (aHUS) is an extremely rare condition caused by an excessive activation of the complement pathway based on genetic or acquired dysfunctions in complement regulation, leading to thrombotic microangiopathy (TMA). A complement-amplifying condition (CAC) can trigger aHUS occurrence along with complement abnormality. We herein report a case of severe TMA after laparoscopic myomectomy in a healthy woman. This case was eventually diagnosed as complement-mediated TMA secondary to surgical invasive stress as a CAC, with no definitive diagnosis of aHUS despite a genetic test. The patient fully recovered after several eculizumab administrations.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:59 |
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| Enthalten in: |
Internal medicine (Tokyo, Japan) - 59(2020), 1 vom: 01., Seite 93-99 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Fujita, Yoko [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 23.03.2020 Date Revised 23.03.2020 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.2169/internalmedicine.3315-19 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM305024590 |
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| 500 | |a Date Completed 23.03.2020 | ||
| 500 | |a Date Revised 23.03.2020 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Atypical hemolytic uremic syndrome (aHUS) is an extremely rare condition caused by an excessive activation of the complement pathway based on genetic or acquired dysfunctions in complement regulation, leading to thrombotic microangiopathy (TMA). A complement-amplifying condition (CAC) can trigger aHUS occurrence along with complement abnormality. We herein report a case of severe TMA after laparoscopic myomectomy in a healthy woman. This case was eventually diagnosed as complement-mediated TMA secondary to surgical invasive stress as a CAC, with no definitive diagnosis of aHUS despite a genetic test. The patient fully recovered after several eculizumab administrations | ||
| 650 | 4 | |a Case Reports | |
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a TMA | |
| 650 | 4 | |a aHUS | |
| 650 | 4 | |a atypical hemolytic uremic syndrome | |
| 650 | 4 | |a complement amplifying condition | |
| 650 | 4 | |a eculizumab | |
| 650 | 4 | |a thrombotic microangiopathy | |
| 650 | 7 | |a Antibodies, Monoclonal, Humanized |2 NLM | |
| 650 | 7 | |a Complement Inactivating Agents |2 NLM | |
| 650 | 7 | |a eculizumab |2 NLM | |
| 650 | 7 | |a A3ULP0F556 |2 NLM | |
| 700 | 1 | |a Terashita, Maho |e verfasserin |4 aut | |
| 700 | 1 | |a Yazawa, Masahiko |e verfasserin |4 aut | |
| 700 | 1 | |a Yamasaki, Yukitaka |e verfasserin |4 aut | |
| 700 | 1 | |a Imamura, Tomonori |e verfasserin |4 aut | |
| 700 | 1 | |a Kibayashi, Junichiro |e verfasserin |4 aut | |
| 700 | 1 | |a Sawai, Toshihiro |e verfasserin |4 aut | |
| 700 | 1 | |a Hidaka, Yoshihiko |e verfasserin |4 aut | |
| 700 | 1 | |a Ohtani, Katsuki |e verfasserin |4 aut | |
| 700 | 1 | |a Inoue, Norimitsu |e verfasserin |4 aut | |
| 700 | 1 | |a Shibagaki, Yugo |e verfasserin |4 aut | |
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