Why “Adrenal Hypercortisolism” Is the Right Name—and Why “MACS” and “Cushing Syndrome” Need to Take a Backseat

A 47-year-old woman presented to my clinic from California last month with a 2.4 cm left adrenal adenoma. Her local endocrinologist had diagnosed Mild Autonomous Cortisol Secretion (MACS) and recommended observation only. In the preceding 18 months, she had developed hypertension requiring two medications, new-onset type 2 diabetes, and two spontaneous rib fractures from minor coughing. Bone-density scanning revealed osteopenia with a T-score of –1.8 at the spine. I diagnosed adrenal hypercortisolism and performed a Mini Back Scope Adrenalectomy (MBSA) in 17 minutes. Twelve weeks later, she is off all antihypertensive drugs, her fasting glucose is 88 mg/dL without medication, her bone pain has resolved, and she has resumed teaching third grade full-time.

This case is not unusual. I see variations of it several times each week. In fact, I perform almost 300 adrenal operations on patients with adrenal hypercortisolism every year. The difference between cure and chronic illness often comes down to the name we give the condition. Words matter.

The Fundamental Flaws in “MACS”

Mild Autonomous Cortisol Secretion was introduced to describe adrenal tumors that suppress incompletely after dexamethasone but do not produce the florid phenotype of classic Cushing syndrome. The word “mild” is the central problem. Longitudinal cohort studies demonstrate that 20–30 % of patients labeled MACS progress to cardiovascular and other risks similar to overt Cushing syndrome within five years. Even among those who do not progress, excess cardiovascular events and fractures occur at twice the expected rate. Mild is a misnomer; the process is early-stage, treatable disease.

Equally problematic, MACS fails to specify the anatomic source and is vague. Patients and many doctors are confused. Where is this autonomous cortisol secretion coming from? The pituitary (Cushing disease), ectopic ACTH tumors, or the adrenal gland itself? Without anatomic precision, clinicians waste time and resources ordering pituitary MRI, inferior petrosal sinus sampling, or CRH stimulation tests when a simple ACTH measurement and adrenal-protocol CT would suffice.

The Historical Baggage of “Cushing”

Harvey Cushing described severe hypercortisolism driven by pituitary adenomas in 1932. The eponym Cushing Syndrome became synonymous with moon facies, dorsal fat pad, wide purple striae, and profound proximal myopathy. In reality, fewer than 5% of patients with adrenal cortisol excess ever develop that textbook appearance. In my personal series of close to 3,000 adrenal operations, the classic phenotype was present in only 6.4% of cases with adrenal hypercortisolism.

The vast majority present with insidious metabolic injury:

• Resistant hypertension despite multiple agents
• Impaired glucose tolerance progressing to overt diabetes
• Premature bone loss
• Central adiposity with sparing of the extremities
• Thinning skin, easy bruising, and poor wound healing

Labeling these patients “subclinical Cushing” implies the disease is not yet clinically relevant. The damage is already measurable, progressive, and reversible with adrenalectomy. The term “subclinical” delays intervention and misleads patients.

The Precision and Neutrality of “Adrenal Hypercortisolism”

Adrenal hypercortisolism is anatomically specific, hormonally explicit, and severity-neutral:

• Adrenal identifies the gland of origin.
• Hyper denotes excess production.
• Cortisolism names the offending hormone.

The construction mirrors established endocrine terminology:

• Primary hyperaldosteronism (Conn syndrome)
• Primary hyperparathyroidism
• Primary hypogonadism

No historical baggage. No implied severity. No diagnostic ambiguity.

Streamlined Diagnostic Pathway

The evaluation is efficient and reproducible:

1. Adrenal mass ≥1 cm on thin-slice CT or MRI with adrenal protocol
2. Morning serum cortisol >1.8 μg/dL after 1 mg dexamethasone at 11 p.m. the prior night
3. Plasma ACTH <5 pg/mL (suppressed, confirming ACTH-independent production)

When all three criteria are met, the diagnosis is adrenal hypercortisolism. No further localization is required. MBSA cures >99 % of patients. Blood pressure normalizes or improves in 70–80 %, diabetes resolves or improves in 60–70 %, and bone mineral density increases

Grading Severity of Adrenal Hypercortisolism: Implications for Surgery and Post-Operative Care

Unlike MACS, which forces every case into a single “mild” bucket, adrenal hypercortisolism can be graded using objective biochemical and clinical criteria. This grading directly informs surgical selection and post-operative management, and whether patients may need postoperative glucocorticoid replacement.

A Call to Update Practice and Guidelines

I urge endocrinologists, radiologists, and primary care physicians to retire MACS and subclinical Cushing syndrome from clinical vocabulary, imaging reports, and society guidelines. Replace them with adrenal hypercortisolism. Accurate nomenclature drives better treatment, prevents irreversible complications, and aligns with the precision we demand in every other endocrine disorder.

Patients deserve clarity and action. If you or a loved one carry the label MACS or subclinical Cushing, contact us at the Carling Adrenal Center.

Dr. Tobias Carling, of the Carling Adrenal Center, is one of the world's leading experts in adrenal gland surgery. Dr. Carling performs more adrenal operations than any other surgeon in America. Dr. Carling left Yale University in 2020 to open the Carling Adrenal Center in Tampa, Florida.

To discuss the details of your case with Dr. Carling and become his patient, fill out the new patient form and he will be in touch with you shortly.

Additional Resources: 

• Learn more about the Carling Adrenal Center
• Learn more about Dr. Tobias Carling
• Learn more about our sister surgeons at the Norman Parathyroid Center, and Clayman Thyroid Center.
• Learn more about the Hospital for Endocrine Surgery