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.