A 48-year-old man presents to the endocrinology clinic with progressive coarsening of facial features, jaw enlargement, and ring tightening over the past 8 years. A lateral skull X-ray is obtained. The structure marked **A** in the diagram shows enlargement to 13 mm in depth. Serum IGF-1 is elevated at 2.5× the upper limit of normal for his age. Growth hormone fails to suppress below 1 ng/mL after a 75 g oral glucose tolerance test. Which of the following best explains the radiological finding at **A** and the biochemical abnormality?
A. Adrenocorticotropic hormone-secreting pituitary adenoma causing cortisol excess and protein catabolism
B. Prolactin-secreting pituitary adenoma causing galactorrhea and secondary hypogonadism
C. Thyroid hormone excess from primary hyperthyroidism causing increased metabolic rate and bone remodeling
D. Pituitary somatotroph adenoma causing growth hormone hypersecretion and hepatic IGF-1 overproduction
Explanation
Why option 1 is right
The enlarged sella turcica (marked A, >11 mm depth on skull X-ray) in the context of elevated IGF-1, clinical acromegaly (coarse facies, prognathism, ring tightening), and failure of GH suppression after OGTT is pathognomonic for a pituitary somatotroph adenoma. This adenoma hypersecrets growth hormone, which stimulates hepatic insulin-like growth factor-1 (IGF-1) production—IGF-1 is the primary mediator of the somatic and metabolic effects of acromegaly. The sella turcica enlargement reflects the mass effect of the adenoma on the pituitary fossa. This is the classic presentation of acromegaly, which accounts for >95% of GH excess in adults (Endocrine Society Acromegaly Guidelines 2024).
Why each distractor is wrong
Option 2 (Thyroid hormone excess): Primary hyperthyroidism causes tachycardia, weight loss, and tremor, not the characteristic coarse facies, prognathism, or macroglossia of acromegaly. Thyroid hormone does not enlarge the sella turcica. TSH-secreting adenomas are exceedingly rare and would present with secondary hyperthyroidism, not the clinical picture described.
Option 3 (ACTH-secreting adenoma): Cushing syndrome from an ACTH-secreting adenoma causes central obesity, proximal weakness, striae, and hypertension—not the progressive jaw enlargement, ring tightening, or coarse facial features of acromegaly. While Cushing syndrome can enlarge the sella turcica, the biochemical profile (elevated IGF-1, failure of GH suppression) is incompatible with ACTH excess.
Option 4 (Prolactin-secreting adenoma): Prolactinomas cause galactorrhea, amenorrhea, and hypogonadism but do not produce the characteristic acromegalic features (prognathism, coarse facies, ring tightening) or elevated IGF-1. Although prolactinomas are the most common pituitary adenoma, they do not explain this clinical and biochemical presentation.
High-YieldNEET PG
Enlarged sella turcica (>11 mm depth) on skull X-ray + elevated IGF-1 + failure of GH suppression after OGTT = acromegaly from somatotroph adenoma; IGF-1 is the key mediator of somatic effects.
Endocrine Society Acromegaly Guidelines 2024
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