• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

亚临床型艾迪生病:转氨酶值持续异常的一个原因。

Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values.

作者信息

Boulton R, Hamilton M I, Dhillon A P, Kinloch J D, Burroughs A K

机构信息

University Department of Medicine, Royal Free Hospital, London, England.

出版信息

Gastroenterology. 1995 Oct;109(4):1324-7. doi: 10.1016/0016-5085(95)90595-2.

DOI:10.1016/0016-5085(95)90595-2
PMID:7557102
Abstract

A common reason for referring patients to hepatologists is persistently abnormal serum transaminase levels with vague constitutional symptoms. In the United Kingdom, these abnormalities are most often caused by a fatty liver either related to obesity or alcohol abuse; they are less commonly caused by chronic liver disease, particularly chronic viral hepatitis, autoimmune hepatitis, or chronic biliary disease. Endocrine disease is rarely a cause of these abnormalities, although hypothyroidism and hyperthyroidism are well-recognized causes. Addison's disease has been only reported once in the literature by R. G. Olsson as a cause of increased transaminase levels associated with constitutional symptoms; it is not mentioned in textbooks on hepatology. Three patients with Addison's disease are reported here, all of whom had increased serum transaminase levels for more than 6 months before the recognition of the hypoadrenalism with resolution to normal after steroid replacement. Hepatologists should consider subclinical Addison's disease as a cause of persistently increased transaminase levels with constitutional symptoms in the absence of evidence for fatty liver as well as viral and autoimmune markers.

摘要

将患者转诊给肝病专家的一个常见原因是血清转氨酶水平持续异常并伴有模糊的全身症状。在英国,这些异常情况最常见的原因是与肥胖或酒精滥用相关的脂肪肝;较少见的原因是慢性肝病,尤其是慢性病毒性肝炎、自身免疫性肝炎或慢性胆道疾病。内分泌疾病很少是这些异常的原因,尽管甲状腺功能减退和甲状腺功能亢进是公认的病因。文献中仅由R.G.奥尔森报道过1例艾迪生病作为伴有全身症状的转氨酶水平升高的病因;肝病学教科书中未提及。本文报道了3例艾迪生病患者,他们在肾上腺功能减退被识别之前,血清转氨酶水平升高均超过6个月,在接受类固醇替代治疗后恢复正常。在没有脂肪肝以及病毒和自身免疫标志物证据的情况下,肝病专家应考虑亚临床艾迪生病是伴有全身症状的转氨酶水平持续升高的一个原因。

相似文献

1
Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values.亚临床型艾迪生病:转氨酶值持续异常的一个原因。
Gastroenterology. 1995 Oct;109(4):1324-7. doi: 10.1016/0016-5085(95)90595-2.
2
Liver involvement in Addison's disease.艾迪生病中的肝脏受累情况。
Am J Gastroenterol. 1990 Apr;85(4):435-8.
3
Should we consider Addison's disease in the differential diagnosis of persistent hypertransaminasemia? A case report.在持续性高转氨酶血症的鉴别诊断中,我们是否应考虑艾迪生病?一例病例报告。
Acta Gastroenterol Belg. 2011 Mar;74(1):95-6.
4
Addison's disease: a rare cause of hypertransaminasaemia.艾迪生病:高转氨酶血症的罕见病因。
Dig Dis Sci. 2008 Dec;53(12):3269-71. doi: 10.1007/s10620-008-0297-8. Epub 2008 May 9.
5
[Addison's disease and hepatic biochemical disorders. Retrospective analysis].[艾迪生病与肝脏生化紊乱。回顾性分析]
Rev Clin Esp. 1998 Jul;198(7):488.
6
[Addison's disease as a rare cause of chronically elevated liver enzymes].
Z Gastroenterol. 2006 Feb;44(2):179-83. doi: 10.1055/s-2005-858976.
7
Addison's disease and hypertransaminasemia.艾迪生病与高转氨酶血症。
Expert Rev Endocrinol Metab. 2009 May;4(3):251-261. doi: 10.1586/eem.09.6.
8
Hypertransaminasaemia and Addison's disease.高转氨酶血症与艾迪生病
Eur J Gastroenterol Hepatol. 1998 Oct;10(10):891-2. doi: 10.1097/00042737-199810000-00014.
9
Autoantibodies to cytochrome P450 enzymes P450scc, P450c17, and P450c21 in autoimmune polyglandular disease types I and II and in isolated Addison's disease.自身免疫性多内分泌腺病Ⅰ型和Ⅱ型以及孤立性艾迪生病中细胞色素P450酶P450scc、P450c17和P450c21的自身抗体
J Clin Endocrinol Metab. 1994 Feb;78(2):323-8. doi: 10.1210/jcem.78.2.8106620.
10
Unexplained hypertransaminasaemia: clue to diagnosis of Addison's disease.不明原因的高转氨酶血症:艾迪生病诊断的线索
Eur J Gastroenterol Hepatol. 2002 Nov;14(11):1285-6. doi: 10.1097/00042737-200211000-00022.

引用本文的文献

1
Mild liver injury following withdrawal of long-term prednisone therapy: A case report.长期泼尼松治疗停药后发生的轻度肝损伤:一例报告。
World J Gastroenterol. 2025 Jan 28;31(4):102135. doi: 10.3748/wjg.v31.i4.102135.
2
Adrenal insufficiency as a cause of hypertransaminasemia and hyperferritinemia: case report and review of the literature.肾上腺功能不全作为高转氨酶血症和高铁蛋白血症的病因:病例报告及文献综述
Porto Biomed J. 2024 Oct 25;9(5):269. doi: 10.1097/j.pbj.0000000000000269. eCollection 2024 Sep-Oct.
3
A reproducible extended ex-vivo normothermic machine liver perfusion protocol utilising improved nutrition and targeted vascular flows.
一种可重复的体外常温机器肝脏灌注方案,采用改良营养和靶向血流。
Commun Med (Lond). 2024 Oct 24;4(1):214. doi: 10.1038/s43856-024-00636-2.
4
The Selective Progesterone Receptor Modulator Ulipristal Acetate Inhibits the Activity of the Glucocorticoid Receptor.选择性孕激素受体调节剂醋酸乌利司他抑制糖皮质激素受体的活性。
J Clin Endocrinol Metab. 2020 Mar 1;105(3):716-34. doi: 10.1210/clinem/dgz139.
5
Atypical Presentation of Adrenocortical Insufficiency with Anorexia and Jaundice.肾上腺皮质功能不全伴厌食和黄疸的非典型表现。
Am J Case Rep. 2018 Jun 18;19:705-709. doi: 10.12659/AJCR.909190.
6
Bilateral adrenal hemorrhage in polycythemia vera.真性红细胞增多症中的双侧肾上腺出血。
J Community Hosp Intern Med Perspect. 2016 Sep 7;6(4):32416. doi: 10.3402/jchimp.v6.32416. eCollection 2016.
7
Peri-portal lymphedema in association with an acute adrenal insufficiency: case report.门静脉周围淋巴水肿合并急性肾上腺功能不全:病例报告
J Med Case Rep. 2014 Mar 24;8:98. doi: 10.1186/1752-1947-8-98.
8
An Unusual Presentation of Addison's Disease-A Case Report.艾迪生病的一种不寻常表现——病例报告
Clin Pediatr Endocrinol. 2011 Jul;20(3):57-60. doi: 10.1297/cpe.20.57. Epub 2011 Oct 7.
9
Adrenal insufficiency as a cause of acute liver failure: a case report.肾上腺功能不全作为急性肝衰竭的病因:一例报告
Case Rep Endocrinol. 2013;2013:487189. doi: 10.1155/2013/487189. Epub 2013 Feb 25.
10
Endocrine and liver interaction: the role of endocrine pathways in NASH.内分泌与肝脏的相互作用:内分泌途径在非酒精性脂肪性肝炎中的作用
Nat Rev Gastroenterol Hepatol. 2009 Apr;6(4):236-47. doi: 10.1038/nrgastro.2009.33.