自身免疫性肝炎患者接受泼尼松龙和硫唑嘌呤治疗后失代偿期肝硬化肝纤维化的组织学改善情况

Q4 Medicine Kurume Medical Journal Pub Date : 2024-11-27 DOI:10.2739/kurumemedj.MS7112007
Hiroyuki Suzuki, Keisuke Amano, Kanji Yamaguchi, Tomoya Sano, Teruko Arinaga-Hino, Jun Akiba, Atsushi Takahashi, Hiromasa Ohira, Atsushi Tanaka, Yoshito Itoh, Takumi Kawaguchi
{"title":"自身免疫性肝炎患者接受泼尼松龙和硫唑嘌呤治疗后失代偿期肝硬化肝纤维化的组织学改善情况","authors":"Hiroyuki Suzuki, Keisuke Amano, Kanji Yamaguchi, Tomoya Sano, Teruko Arinaga-Hino, Jun Akiba, Atsushi Takahashi, Hiromasa Ohira, Atsushi Tanaka, Yoshito Itoh, Takumi Kawaguchi","doi":"10.2739/kurumemedj.MS7112007","DOIUrl":null,"url":null,"abstract":"<p><p>The treatment of the underlying cause of liver disease may potentially reverse hepatic fibrosis. However, it remains uncertain whether improvement in fibrosis can be observed in decompensated liver cirrhosis (LC). Here, we present a case of autoimmune hepatitis (AIH)-related LC in which histological improvement of fibrosis was achieved despite the presence of decompensated LC. A Japanese female in her 20s was initially identified as having liver function impairments during her employment medical checkup. Following a laparoscopic liver biopsy, she was diagnosed with AIH-related decompensated LC (F4 and A3) with a Child-Pugh score of 10. The patient initially received treatment with prednisolone at a daily dose of 40 mg, followed by 20 mg/day of prednisolone plus 25 mg/day of azathioprine (subsequent increase of azathioprine to 100 mg/day). With this treatment, the abnormal serum marker levels returned to normal, thereby enabling the patient to avoid liver transplantation eight months after the initiation of treatment. Moreover, marked improvement was observed in non-invasive tests for hepatic fibrosis, including the FIB-4 index and FibroIndex, as well as liver stiffness evaluated by FibroScan®. Eleven months after diagnosis, the patient developed a cholestatic liver injury and was diagnosed with drug-induced cholestatic liver disease (azathioprine overcapacity as the causative agent). By percutaneous liver biopsy at this point, hepatic fibrosis (F2-3) was markedly improved compared with that at the diagnosis. Along with the improvement of hepatic fibrosis, notable improvements were also observed in patient-reported outcomes such as the SF-36® score and chronic liver disease questionnaire. In this report, we first described a case of AIH that showed a histological improvement of hepatic fibrosis even in decompensated LC by treatment with prednisolone and azathioprine.</p>","PeriodicalId":39559,"journal":{"name":"Kurume Medical Journal","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Histological Improvement of Hepatic Fibrosis of Decompensated Liver Cirrhosis after Prednisolone and Azathioprine Treatment in a Patient with Autoimmune Hepatitis.\",\"authors\":\"Hiroyuki Suzuki, Keisuke Amano, Kanji Yamaguchi, Tomoya Sano, Teruko Arinaga-Hino, Jun Akiba, Atsushi Takahashi, Hiromasa Ohira, Atsushi Tanaka, Yoshito Itoh, Takumi Kawaguchi\",\"doi\":\"10.2739/kurumemedj.MS7112007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The treatment of the underlying cause of liver disease may potentially reverse hepatic fibrosis. However, it remains uncertain whether improvement in fibrosis can be observed in decompensated liver cirrhosis (LC). Here, we present a case of autoimmune hepatitis (AIH)-related LC in which histological improvement of fibrosis was achieved despite the presence of decompensated LC. A Japanese female in her 20s was initially identified as having liver function impairments during her employment medical checkup. Following a laparoscopic liver biopsy, she was diagnosed with AIH-related decompensated LC (F4 and A3) with a Child-Pugh score of 10. The patient initially received treatment with prednisolone at a daily dose of 40 mg, followed by 20 mg/day of prednisolone plus 25 mg/day of azathioprine (subsequent increase of azathioprine to 100 mg/day). With this treatment, the abnormal serum marker levels returned to normal, thereby enabling the patient to avoid liver transplantation eight months after the initiation of treatment. Moreover, marked improvement was observed in non-invasive tests for hepatic fibrosis, including the FIB-4 index and FibroIndex, as well as liver stiffness evaluated by FibroScan®. Eleven months after diagnosis, the patient developed a cholestatic liver injury and was diagnosed with drug-induced cholestatic liver disease (azathioprine overcapacity as the causative agent). By percutaneous liver biopsy at this point, hepatic fibrosis (F2-3) was markedly improved compared with that at the diagnosis. Along with the improvement of hepatic fibrosis, notable improvements were also observed in patient-reported outcomes such as the SF-36® score and chronic liver disease questionnaire. In this report, we first described a case of AIH that showed a histological improvement of hepatic fibrosis even in decompensated LC by treatment with prednisolone and azathioprine.</p>\",\"PeriodicalId\":39559,\"journal\":{\"name\":\"Kurume Medical Journal\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-11-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kurume Medical Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2739/kurumemedj.MS7112007\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kurume Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2739/kurumemedj.MS7112007","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

摘要

治疗肝病的根本原因有可能逆转肝纤维化。然而,在失代偿期肝硬化(LC)中能否观察到肝纤维化的改善仍不确定。在这里,我们介绍了一例与自身免疫性肝炎(AIH)相关的肝硬化病例,在该病例中,尽管存在失代偿性肝硬化,但肝纤维化在组织学上得到了改善。一名 20 多岁的日本女性在就业体检中被初步确定为肝功能受损。腹腔镜肝活检后,她被诊断为 AIH 相关失代偿性 LC(F4 和 A3),Child-Pugh 评分为 10 分。患者最初接受了每天 40 毫克剂量的泼尼松龙治疗,随后又接受了每天 20 毫克泼尼松龙加每天 25 毫克硫唑嘌呤的治疗(随后硫唑嘌呤的剂量增加到每天 100 毫克)。通过这种治疗,异常的血清标志物水平恢复了正常,从而使患者在开始治疗 8 个月后避免了肝移植。此外,肝纤维化的非侵入性检测(包括 FIB-4 指数和 FibroIndex 指数)以及 FibroScan® 评估的肝脏硬度也有明显改善。确诊11个月后,患者出现胆汁淤积性肝损伤,被诊断为药物性胆汁淤积性肝病(硫唑嘌呤过量是致病因素)。通过此时的经皮肝活检,肝纤维化(F2-3)与诊断时相比明显改善。在肝纤维化改善的同时,患者报告的结果也有显著改善,如 SF-36® 评分和慢性肝病问卷调查。在本报告中,我们首次描述了一例 AIH 病例,通过使用泼尼松龙和硫唑嘌呤治疗,即使是失代偿期 LC 患者的肝纤维化在组织学上也得到了改善。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Histological Improvement of Hepatic Fibrosis of Decompensated Liver Cirrhosis after Prednisolone and Azathioprine Treatment in a Patient with Autoimmune Hepatitis.

The treatment of the underlying cause of liver disease may potentially reverse hepatic fibrosis. However, it remains uncertain whether improvement in fibrosis can be observed in decompensated liver cirrhosis (LC). Here, we present a case of autoimmune hepatitis (AIH)-related LC in which histological improvement of fibrosis was achieved despite the presence of decompensated LC. A Japanese female in her 20s was initially identified as having liver function impairments during her employment medical checkup. Following a laparoscopic liver biopsy, she was diagnosed with AIH-related decompensated LC (F4 and A3) with a Child-Pugh score of 10. The patient initially received treatment with prednisolone at a daily dose of 40 mg, followed by 20 mg/day of prednisolone plus 25 mg/day of azathioprine (subsequent increase of azathioprine to 100 mg/day). With this treatment, the abnormal serum marker levels returned to normal, thereby enabling the patient to avoid liver transplantation eight months after the initiation of treatment. Moreover, marked improvement was observed in non-invasive tests for hepatic fibrosis, including the FIB-4 index and FibroIndex, as well as liver stiffness evaluated by FibroScan®. Eleven months after diagnosis, the patient developed a cholestatic liver injury and was diagnosed with drug-induced cholestatic liver disease (azathioprine overcapacity as the causative agent). By percutaneous liver biopsy at this point, hepatic fibrosis (F2-3) was markedly improved compared with that at the diagnosis. Along with the improvement of hepatic fibrosis, notable improvements were also observed in patient-reported outcomes such as the SF-36® score and chronic liver disease questionnaire. In this report, we first described a case of AIH that showed a histological improvement of hepatic fibrosis even in decompensated LC by treatment with prednisolone and azathioprine.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Kurume Medical Journal
Kurume Medical Journal Medicine-Medicine (all)
CiteScore
0.20
自引率
0.00%
发文量
33
期刊最新文献
A Case of Sarcoid Reaction in Subcarinal Lymph Node in A Postoperative Breast Cancer Diagnosed by Thoracoscopic Biopsy. Comminuted Transverse Femoral Shaft Fractures Are at Risk for Nonunion. High Expression of NDRG1 is a Poor Prognostic Factor in Patients with Endometrial Endometrioid Carcinoma with Long-Term Observation. Histological Improvement of Hepatic Fibrosis of Decompensated Liver Cirrhosis after Prednisolone and Azathioprine Treatment in a Patient with Autoimmune Hepatitis. Surgical Treatment of Simultaneous Common Femoral and Profunda Femoris Artery Aneurysms.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1