Korean J Obes 2013; 22(4): 254-258
Published online December 31, 2013
Copyright © Korean Society for the Study of Obesity.
Seung Ah Park, Dong min Jung, Soon young Kim, Nan Young Choi, Tae-jun Kim, Yong kyun Kim, Seong kyun Na, Chul Sik Kim, Seong Jin Lee, Sung-Hee Ihm, Jun Goo Kang*
Department of Internal Medicine, College of Medicine, Hallym University
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
ACTH-independent Cushing syndrome, which is mainly caused by a unilateral adrenal adenoma or adrenal carcinoma, account for 15~20% of Cushing’s syndrome. Cushing’s syndrome caused by bilateral adrenal masses is rare, including bilateral adrenal adenomas or carcinomas (AIMAH and PPNAD). Adrenal adenoma is commonly treated by Laparoscopic total adrenalectomy. However, bilateral total adrenalectomy causes acute adrenal insufficiency (Addisonian crisis), requiring lifelong steroid replacement. We present a young female patient with bilateral adrenocortical adenoma causing Cushing’s syndrome who was completely cured by successful laparoscopic total & partial adrenalectomy.
Primarily we decided to remove the right adrenal gland to preserve the residual function of the left adrenal gland. However, after right total adrenalectomy, the patient manifested symptoms of subclinical Cushing syndrome including hypertension, truncal obesity, diabetes, low HDL
cholesterol, and elevated triglycerides. Subsequently the patient underwent partial left adrenal mass excision, preserving the normal portion of the adrenal gland. The patient thereafter achieved biochemical resolution and significant improvement of hypertension, obesity, and
diabetes without the need of any medication.
Keywords: Cushing’s syndrome, Bilateral adrenal adenoma, Obesity, Diabetes
Online ISSN : 2508-7576Print ISSN : 2508-6235
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