Category: Adrenal Disorders

Monitor: 33


Saturday, Apr 27
10:30 AM – 11:00 AM

Objective :

The diagnosis of Cushing’s syndrome is often missed, given its variable presentation. We describe a case of Cushing’s syndrome presenting with macromastia, which was initially attributed to a pituitary adenoma. 

Methods : NA

Results : NA

Discussion :

A 44-year-old female presented with progressive breast enlargement (36 B to 38 DDD) and milky nipple discharge over 6 months. She had a weight gain of 20 lbs despite a calorie restricted diet and a physically demanding job. She also reported mood changes, constant fatigue and worsening back pain due to the breast enlargement. On physical exam, she had central obesity with macromastia and bruising around the brassiere strap area. She did not have pathological striae, hirsutism or proximal muscle weakness.

Earlier blood work at primary care physician’s office revealed an elevated prolactin level of 40.3 ng/mL. A brain MRI revealed a 4 x 5.6 mm cystic lesion in the pituitary. Cabergoline was started and the patient was referred to an endocrinologist. Lab workup revealed non-suppressible overnight low dose dexamethasone suppression test, elevated urinary free cortisol (90ug/24hr), suppressed ACTH (3.2pg/mL), low DHEA Sulfate (11.2pg/mL) and normal estradiol level (71.1pg/mL). CT imaging showed a 2.8 cm right adrenal mass. Cabergoline was stopped as the elevated prolactin level was attributed to tight-fitting bra and the cystic lesion on MRI was likely an incidentaloma. The adrenal mass was resected and pathology revealed hypercellular adrenal cortical tissue consistent with adrenocortical adenoma. One month after surgery, the patient lost 4 lbs of weight and was feeling better with marked improvement in mood, facial plethora, back pain and excessive bruising. Repeat labs were normal, including suppressible cortisol following low dose dexamethasone, early morning cortisol level (12.3mcg/dL), prolactin (17.4pg/mL) and ACTH (33.1pg/mL).

Our patient presented with macromastia and galactorrhea in addition to subtle manifestations of Cushing’s syndrome (mood changes and bruising). However, the findings of macromastia with galactorrhea swayed the provider towards hyperprolactinemia, which delayed the diagnosis of Cushing’s syndrome. There is a single case report of PBMAH with macromastia secondary to elevated estrogen levels1. To the best of our knowledge, this is the first reported case of a unilateral adrenal adenoma presenting as macromastia. Given the normal estradiol level and absent estradiol staining of the adrenal mass, we believe that the macromastia is a component of her central obesity. 

Conclusion :

Cushing’s is a challenging diagnosis given its non-specific and variable clinical presentation.



Jhansi L. Maradana

Resident, Internal Medicine
St Vincent Hospital, Massachusetts

Name: Jhansi Lakshmi Maradana
Current Position: Resident, Internal Medicine, St Vincent Hospital, Worcester, MA.
Professional preparation:
Guntur Medical College, Guntur, India. M.B.B.S., 2016.
Professional Memberships:
1. American College of Physicians.
2. American Association of Clinical Endocrinologists.
3. Massachusetts Medical Society.
Poster presentation on “ Euglycemic Diabetic Ketoacidosis secondary to Empagliflozin”, at ACP 2018, Massachusetts Chapter.
Areas of interest:
Management of type 1 diabetes mellitus.

Ibragim Al-Seykal

Resident, Internal Medicine
St Vincent Hospital, Worcester, MA
Worcester, Massachusetts

Dr. Ibragim Al-Seykal is currently an Internal Medicine resident at St. Vincent Hospital, Worcester, MA. Prior to that, he studied medicine in Moscow, Russia at I.M. Sechenov First Moscow Medical University. He is a member of American College of Physicians and Massachusetts Medical Society. His oral presentations include a poster presentation on "Non-Access Site Bleeding Risk Related to Bivalirudin Versus Heparin Guided Therapy in Trans-Radial Coronary Intervention" at ACP 2018, Massachusetts Chapter.

Trivedi Nitin

Division Director, Endocrinology
Saint Vincent Hospital
Shrewsbury, Massachusetts

Dr. Nitin Trivedi is an Associate Professor of Medicine at the University of Massachusetts Medical School and one of the Associate Program Directors in the Internal Medicine Residency Program at Saint Vincent Hospital in Worcester, MA. He is board certified in Internal Medicine and Endocrinology. He is a fellow of American College of Physicians and American Association of Clinical Endocrinologists. He has served as the President of the New England Chapter of American Association of Clinical Endocrinologists. He has received the Gilbert E. Levinson Award for the best resident voted by the faculty members and the John J Mckeever Medical Educator Award from the Department of Medicine at Saint Vincent Hospital. His research interests include management of diabetes in hospitalized patients and insulin pump use in type 2 diabetes.
Dr. Trivedi earned his medical degrees from MGM Medical College in Indore, India and completed his Internal Medicine Residency at Saint Vincent Hospital and Endocrinology Fellow at Brown Medical School. He has worked as a Research Fellow in the section of Islet Transplantation and Cell Biology at Joslin Diabetes Center, Harvard Medical School in Boston. He was an Assistant Professor at Brown Medical School from 2004 -2005.
He has authored several publications and abstracts.

Selected Bibliography:
1. Suzuki K, Bonner-Weir, Trivedi N, Yoon KH, Lock JH, Colton CK, Weir GC: Survival and function of macroencapsulated syngeneric islets transplanted into Streptozotocin diabetic mice. Transplantation 1998;66:21-28.
2. Trivedi N, Mithal A, Sharma AK, Mishra SK, Trivedi B, Daughaday WH. Nonislet tumor induced
hypoglycemia with acromegaloid facial and acral swelling. Clinical Endocrinology (Oxf.)
3. Trivedi N, Suzuki K, Bonner-Weir S, Hollister-Lock J, Weir GC: Islet number in an immunobarrier required to cure diabetes in mice. Transplantation Proceedings 1997;29-21-2143.
4. Trivedi N, Steil GM, Colton CK, Bonner Weir S, Weir GC: Improved vascularization on planar diffusion devices following continuous infusion of vascular endothelial growth factor. Cell Transplantation 1999;8:673-689.
5. Steil GM, Trivedi N, Jonas JC, Hasenkemp WM, Sharma A, Bonner Weir, Weir GC. Enhanced beta-cell function with normal islet gene expression following Adaptation of B-cell mass to substrate oversupply. Am J Physiology 2001;280:E788-E796.
6. Trivedi N, Keegan M, Steil GM, Hollister-Lock J, Hasenkemp WM, Colton CK, Bonner-Weir S, Weir GC. Islets in alginate macrobeads reverse diabetes despite minimal acute insulin secretory responses. Transplantation 2001;27:203-211.
7. Omer A, Duvivier-Kaul, Trivedi N, Wilmot K, Bonner-Weir S, Weir GC. Survival and maturation of microencapsulated porcine neonatal pancreatic cell clusters transplanted into immunocompetent diabetic mice. Diabetes 2003;52(1):69-75
8. Xu G, Kaneto H, Laybutt DR, Duvivier VF, Trivedi N, Suzuma K, Kiong GL, Weir GC, Bonner-Weir S. Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: Possible contribution to impaired incretin effect in diabetes. Diabetes 2007;56(6):1551-8.

9. Vyas A, Fillipon N. Lynn, Vyas P, Vijayakrishnan R, Trivedi N. Successful treatment of thyroid storm in a patient with methimazole-induced toxicity. Endocrine Practice 2010;16673-675.
10. Chhabra L, Liti B, Kuraganti G, Kaul S, Trivedi N. Challenges in the management of Type 2 Diabetes Mellitus and Cardiovascular Risk Factors in Obese Subjects: What is the Evidence and What are the Myths? Int J Endocrinol Endocrinology 2013; Article ID 856793: 10 pages.
11. Alang N, Trivedi N. Secure email communication between patients and physicians is associated with better glycemic control. R I Med J (2013). 2014 Jan 3;97(1):15.
12. Sahni P, Trivedi A, Omer AO, Trivedi N. Adrenal incidentaloma: Are they getting work up appropriately? J Community Hospital Perspective 2016;6(5):32913. Doi:10.3402/jchimp.v6.32913.