The Incorrect Statement is D
Statement D is INCORRECT: Treatment of Cushing's syndrome does NOT involve chronic administration of corticosteroids—in fact, the opposite is true. The goal of treatment is to normalize or reduce cortisol levels, not to administer more corticosteroids 1.
Why Statement D is Wrong
The fundamental treatment principle for Cushing's syndrome is to eliminate excess cortisol exposure, not perpetuate it. According to the 2015 Endocrine Society Clinical Practice Guidelines, treatment goals explicitly recommend "normalizing cortisol levels or action at its receptors to eliminate the signs and symptoms of CS" 1. The primary approach is surgical resection of the causative lesion (pituitary adenoma, adrenal tumor, or ectopic ACTH-secreting tumor), with second-line options including medical therapy to block cortisol synthesis, bilateral adrenalectomy, or radiation therapy 1.
The only scenario where glucocorticoids are administered is after successful treatment when patients develop adrenal insufficiency following tumor removal or bilateral adrenalectomy—but this is replacement therapy for deficiency, not treatment of the syndrome itself.
Why the Other Statements are Correct
Statement A: Central Obesity and Moon Face
These are hallmark clinical features of Cushing's syndrome. Central adiposity with thin extremities, round facies (moon face), dorsocervical fat pads (buffalo hump), and supraclavicular fat accumulation are classic physical findings 2, 3. The "moon face" results from fat deposition in the cheeks and is so characteristic that it's used as a phenotypic marker even in animal models 3.
Statement B: Osteoporosis and Hypertension
Both are well-established complications that significantly contribute to morbidity and mortality. Hypertension has multifactorial pathogenesis in Cushing's syndrome and increases risk for myocardial infarction, cardiac failure, and stroke—the most common causes of death 4. Osteoporosis leads to skeletal fragility and vertebral fractures, representing a major musculoskeletal complication 2, 4.
Statement C: Laboratory Findings
Hyperglycemia, leukocytosis, and hypokalemia are all documented laboratory abnormalities. Hyperglycemia results from cortisol-induced insulin resistance 5, 4. Hypokalemia is particularly prominent in ectopic ACTH secretion, often presenting with hypokalemic metabolic alkalosis 2, 6. While not mentioned in every case, leukocytosis can occur due to glucocorticoid effects on white blood cell distribution and immune function 4.
Statement E: Alcohol in Differential Diagnosis
Alcohol abuse must be considered as it causes "pseudo-Cushing's syndrome"—a state that mimics true Cushing's syndrome biochemically and clinically 7. Alcoholism can cause insufficient suppression on low-dose dexamethasone testing and increased 24-hour urinary free cortisol, making differentiation from true Cushing's syndrome challenging. The key distinguishing feature is that biochemical abnormalities normalize after alcohol cessation 7.
Clinical Pitfall to Avoid
The most critical error would be administering corticosteroids to a patient with suspected or confirmed Cushing's syndrome, as this would worsen hypercortisolism and its life-threatening complications including infections, thromboembolism, cardiovascular events, and metabolic derangements 4.