A 70-year-old woman was referred for a pituitary lesion incidentally discovered during the evaluation of headaches. A noncontrast computed tomography scan of the head revealed a prominent pituitary gland, measuring 11 mm × 10 mm in maximum orthogonal dimension, and focal calcification in the anterior sella (Fig. 1). Magnetic resonance imaging scan of the brain revealed a plump pituitary gland with upward tenting, measuring 10 mm × 9 mm × 8 mm, and a focal area of reduced enhancement in the left sella (Fig. 2). There was a complete loss of signal within the anterior sella, correlating with the calcification observed on computed tomography of the head. The infundibulum was deviated to the right and there was no extension into the cavernous sinuses. A review of the patient’s medical records revealed that the intrasellar calcification had been identified on imaging 10 years earlier. The calcification had remained stable in size and morphology. The patient denied head trauma, brain injury, stroke, or seizure. She denied a history of tuberculosis or other granulomatous diseases. She denied changes in hand or shoe size, skin or weight changes, or vision changes. A pituitary panel was unremarkable.
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What is the diagnosis?
Answer
Pituitary stone. A pituitary stone is a dense calcification in the pituitary gland. It is a rare but well-recognized radiographic entity that arises de novo or secondary to pathologic intrasellar lesions. Schwartz and Ellis described a pituitary calculus in their 1951 text on the skull and brain radiography. However, the term pituitary “stone” was coined by Glasser and Earll reference the original text by Schwartz and Ellis from 1951 in their 1968 JAMA letter. The differential diagnosis of a calcified lesion in the sella turcica includes craniopharyngioma, meningioma, aneurysm, Rathke cleft cyst, and pituitary adenoma; very rarely, it represents a de novo pituitary stone. The pathogenesis is incompletely understood, although it is attributed to local effects of pituitary tumors, inflammation, hemorrhage, amyloid deposits, or infection. Calcification may result from progressive tumor enlargement with central ischemic effects and osteoid metaplasia or by degenerative changes following pituitary apoplexy. Calcification may arise secondary to tumor compression and increased sellar pressure. Finally, prolactin, growth hormone, and vascular endothelial growth factor may promote calcification through autocrine and paracrine effects. The mechanism of the de novo pituitary stone is unknown. The patient had no neurologic or endocrine deficits, and the pituitary lesion had remained stable in size over a decade. Thus, she was managed conservatively with imaging surveillance.
Disclosure
The authors have no multiplicity of interest to disclose.
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