Adrenal Insufficiency Due to Adrenal Insult Following Acute Pancreatitis in a Child.

JCEM case reports Pub Date : 2025-02-10 eCollection Date: 2025-03-01 DOI:10.1210/jcemcr/luaf025
Sabitha Sasidharan Pillai, Renee Robilliard, Meghan E Fredette, Lisa Swartz Topor, Lynn Della Grotta, Monica Serrano-Gonzalez
{"title":"Adrenal Insufficiency Due to Adrenal Insult Following Acute Pancreatitis in a Child.","authors":"Sabitha Sasidharan Pillai, Renee Robilliard, Meghan E Fredette, Lisa Swartz Topor, Lynn Della Grotta, Monica Serrano-Gonzalez","doi":"10.1210/jcemcr/luaf025","DOIUrl":null,"url":null,"abstract":"<p><p>We report an 8-year-old girl who developed primary adrenal insufficiency (AI) in the setting of severe acute pancreatitis. Symmetrically thickened centrally hypoenhancing adrenal glands were incidentally noted on computed tomography (CT) of the abdomen obtained for evaluation for pancreatitis. Laboratory studies included a low morning cortisol level (1.5 µg/dL [41.4 nmol/L], reference range, 5.5-20 µg/dL [151.7-551.7 nmol/L]) on day of hospitalization (DOH) 5. Cortisol did not rise following administration of 250 µg of cosyntropin. She had elevated adrenocorticotropin (ACTH), low aldosterone and dehydroepiandrosterone sulfate levels, normal very long-chain fatty acid levels, and negative 21-hydroxylase autoantibody. Follow-up CT of the abdomen on DOH 9 demonstrated bilateral adrenal gland enlargement with central hypoenhancement and slightly shaggy appearance at the margins. A diagnosis of AI due to adrenal gland injury in the setting of acute pancreatitis was made. The adrenal injury was attributed to ischemic injury, as there were no findings to suggest substantial hemorrhage. Hydrocortisone and fludrocortisone therapies were initiated. Magnetic resonance imaging of the abdomen obtained 8 months later showed diminutive adrenal glands with a marked decrease in size compared to the initial CT scan finding. She has continued to require replacement doses of hydrocortisone and fludrocortisone.</p>","PeriodicalId":73540,"journal":{"name":"JCEM case reports","volume":"3 3","pages":"luaf025"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11809432/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JCEM case reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1210/jcemcr/luaf025","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

We report an 8-year-old girl who developed primary adrenal insufficiency (AI) in the setting of severe acute pancreatitis. Symmetrically thickened centrally hypoenhancing adrenal glands were incidentally noted on computed tomography (CT) of the abdomen obtained for evaluation for pancreatitis. Laboratory studies included a low morning cortisol level (1.5 µg/dL [41.4 nmol/L], reference range, 5.5-20 µg/dL [151.7-551.7 nmol/L]) on day of hospitalization (DOH) 5. Cortisol did not rise following administration of 250 µg of cosyntropin. She had elevated adrenocorticotropin (ACTH), low aldosterone and dehydroepiandrosterone sulfate levels, normal very long-chain fatty acid levels, and negative 21-hydroxylase autoantibody. Follow-up CT of the abdomen on DOH 9 demonstrated bilateral adrenal gland enlargement with central hypoenhancement and slightly shaggy appearance at the margins. A diagnosis of AI due to adrenal gland injury in the setting of acute pancreatitis was made. The adrenal injury was attributed to ischemic injury, as there were no findings to suggest substantial hemorrhage. Hydrocortisone and fludrocortisone therapies were initiated. Magnetic resonance imaging of the abdomen obtained 8 months later showed diminutive adrenal glands with a marked decrease in size compared to the initial CT scan finding. She has continued to require replacement doses of hydrocortisone and fludrocortisone.

Abstract Image

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
儿童急性胰腺炎后肾上腺损伤所致肾上腺功能不全。
我们报告一个8岁的女孩谁发展原发性肾上腺功能不全(AI)在设置严重急性胰腺炎。在评估胰腺炎的腹部计算机断层扫描(CT)上偶然发现对称增厚的中央低增强肾上腺。实验室研究包括住院当天早晨皮质醇水平较低(1.5µg/dL [41.4 nmol/L],参考范围为5.5-20µg/dL [151.7-551.7 nmol/L]) 5。皮质醇在给予250µg共syntropin后没有升高。促肾上腺皮质激素(ACTH)升高,醛固酮和硫酸脱氢表雄酮水平低,甚长链脂肪酸水平正常,21-羟化酶自身抗体阴性。后续腹部CT DOH 9示双侧肾上腺肿大,中央增强低,边缘略粗。诊断急性胰腺炎合并肾上腺损伤所致急性胰腺炎。肾上腺损伤归因于缺血性损伤,因为没有发现提示大量出血。开始氢化可的松和氟化可的松治疗。8个月后腹部磁共振成像显示,与最初的CT扫描结果相比,肾上腺体积明显减小。她继续需要替代剂量的氢化可的松和氟化可的松。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Moderate weight loss decreases lipedema-affected body fat mass in a woman who is lean with lipedema. Hypoglycemia secondary to type B insulin resistance syndrome. Gluteal hemangioma mimicking a neuroendocrine tumor: pitfalls in neuroendocrine tumor diagnostic testing. Successful Management of Ectopic Adrenocorticotropin-Secreting Thymic Carcinoid With Mitotane: A New Look at an Old Drug. Unilateral Graves disease with Takayasu arteritis.
×
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:604180095
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