Diagnosis of Cushing’s Disease Post Bariatric Surgery

Obesity is a major risk factor for the development of metabolic comorbidities and is the leading cause of preventable death. Despite recent advances in pharmacotherapy, bariatric surgery (BS) remains the most effective treatment for obesity, leading to weight loss and improvement of metabolic comorbidities. The preoperative evaluation for BS does not recommend for the routine screening of secondary causes for weight gain such as hypercortisolism, unless clinically indicated. The diagnosis of Cushing syndrome can be challenging and many BS patients do not see an endocrinologist preoperatively. Studies have shown that mortality is increased in CS, but effective therapy improves long-term survival. We present a case of a patient with inadequate weight loss or resolution of metabolic comorbidities after BS with undiagnosed Cushing's disease (CD). After effective treatment for CD patient’s metabolic comorbidities improved drastically.

Case Description:

A 31-year-old female with a history of resistant hypertension requiring five antihypertensive medications, severe obesity, binge eating disorder and pre-diabetes was referred to our endocrine clinic due to recurrent episodes of hypoglycemia. After a thorough evaluation it was determined to be due to post gastric sleeve non-dietary compliance as she was consuming high glycemic index meals, leading to post-prandial hypoglycemia episodes. The evaluation also identified signs suggestive of hypercortisolemia.

Six months after BS she started regaining the weight she initially lost. Additionally, she reported mood disturbances and easy bruising. On physical exam she had a round face, abdominal striae, and bilateral lower extremity swelling. A 1 mg dexamethasone suppression test showed failure to suppress a 8 am cortisol level (9.90 ug/dL). Further evaluation of the hypothalamic pituitary adrenal axis demonstrated an inappropriately elevated ACTH level (65 pg/mL), with an elevated 8 am cortisol level (32.60 ug/dL) and a elevated DHEA-SO4 level (577.5 ug/dL), concerning for an ACTH dependent CD. A 24-hour urine cortisol was also elevated (368 mcg/24h). Additionally, two consecutive elevated late-night salivary cortisol levels were obtained (306 ug/dL and 170 ug/dL respectively). A subsequent pituitary MRI confirmed a 8 mm hypoenhancing lesion in the inferior left aspect of the adenohypophysis.

The patient underwent transsphenoidal hypophysectomy with pathology revealing a corticotroph adenoma that stained positive for ACTH, further confirming our diagnosis of CD. At follow up, she reported decrease in facial fullness, resolution of lower extremity edema and successfully discontinued all antihypertensive medications.

Discussion:

This case highlights the importance of evaluating patients for hypercortisolism prior to undergoing bariatric surgery to help improve patient outcomes post-surgery. The patient above did not have the expected results regarding resolution of her metabolic comorbidities post BS due to her undiagnosed CD. The diagnosis and early treatment of hypercortisolism can achieve greater health benefits than BS alone.