Pituitary calcification masquerading as pituitary apoplexy.

Pituitary calcification occurs commonly in lactotroph or somatotroph adenoma but rare in chomophobe or gonadotroph adenoma. On imaging, it can mimic hemorrhage, hence may masquerade pituitary apoplexy if patient present with neurological manifestations. We present a case of pituitary calcification which mimicked pituitary apoplexy.

INTRODUCTION

The most common cause of sellar calcification is craniopharyngioma but it can be seen very rarely in pituitary adenomas and Rathke's cleft cysts.[1] Incidence of calcification in pituitary adenoma on imaging varies from 0.8 to 8.0%, but usually it is <2%.[123] However, higher incidence has been reported on histological examination.[14] Pituitary calcification has been reported most commonly in prolactinoma, somatotroph adenoma, thyrotroph adenoma and rarely in gonadotroph and corticotroph adenoma.[56] Here we report a case of pituitary calcification, which was earlier thought to have pituitary apoplexy because of findings on imaging. However, on follow up he had normal pituitary functions and findings on imaging remain unchanged and were suggestive of pituitary calcification.

CASE REPORT

A 32-year-old male reported for review after three years of an episode of headache, vomiting, and confusional state when he was posted to high altitude area, when his computerized tomography (CT) scan of the sella showed a mildly enlarged sella with hyperdensity within the adenohypophysis [Figure 1a] and magnetic resonance imaging (MRI) revealed focal hyperintensity within the pituitary on T1 weighted imaging [Figure 1b] which appeared hypointense on T2 weighted scans [Figure 1c]. He was diagnosed as a case of pituitary apoplexy by treating physician. He had low basal cortisol and visual perimetry was normal. He was given steroid replacement, and no surgical intervention was done. He recovered completely and was under follow-up. Presently, he was asymptomatic and not on any medication. He has normal libido and his youngest child is six-year-old. There was no history of tuberculosis or granulomatous disease in the past. His vital parameters were normal and had no clinical evidence of hypopituitarism. His visual perimetry was normal. He has normal hematological and biochemical parameters. His hormonal evaluation showed normal thyroid (FT4-1.5 ng/dl, TSH - 1.72 mIU/L), adrenal (basal cortisol - 10.6 μg/dL, stimulated cortisol-29.12 μg/dL), gonadal (LH - 6.78 IU/L, FSH - 7.97 IU/L, testosterone - 4.08 ng/ml) and prolactin levels (9.97 ng/ml). MRI and CT done for the sella revealed unchanged findings compared to the previous imaging done in 2009 [Figure 2a-c]. He was diagnosed as a case of non-functioning pituitary adenoma with pituitary calcification. In view of normal visual perimetry and pituitary function with no progression of lesion for three years, any surgical intervention was deferred.

Figure 1

(a) CT scan showing hyperdense lesion in sella; (b) T1 weighted hyperintensity and (c) T2 weighted hypointensity in the sellar region in MRI in 2009

Figure 2

(a) CT scan showing hyperdense lesion in sella; (b) T1 weighted hyperintensity and (c) T2 weighted hypointensity in the sellar region in MRI in 2012

DISCUSSION

Calcification in pituitary has been reported from mid 19th century.[78] Surprisingly most of reports of pituitary calcifications are from Japan and few from other countries in Asia including India.[9] Though calcifications in pituitary adenomas are rare on imaging, a higher incidence of microscopically proven calcified adenomas has been recently reported.[1234] Our case had initially presented with headache, vomiting and altered sensorium. NCCT and MRI pituitary showed hyper-dense lesion and T1 weighted focal hyper-intensity within the pituitary respectively, suggestive of hemorrhage. Hormonal evaluation revealed evidence of secondary adrenal insufficiency, hence was diagnosed as a case of pituitary apoplexy. He recovered without any surgical intervention. On present review, he had normal pituitary function with similar finding on imaging. This has lead to re-evaluation of the case. Pituitary calcification with normal pituitary function has been reported by Glasser et al. and they proposed that these are probably benign in nature.[10] Horiuchi et al.,[6] reported a case of male prolactinoma with pituitary calcification who also had features of hypopituitarism. They speculated that calcification was due to massive degeneration secondary to asymptomatic pituitary apoplexy. A similar view was expressed by Tamaki et al.,[11] to explain pituitary stone in a case of acromegaly. In present case, sella is enlarged; hence there is high probability of pituitary adenoma which is hormonally inactive. However, normal pituitary function makes pituitary apoplexy in the past unlikely but possibility cannot be rules out. He had normal libido and had a child about 6-year old, which also indicate unlikelihood of long standing prolactinoma or hypopituitarism in the past. We speculate that adenoma might have undergone degenerative changes and calcification in our case. Calcification on chomophobe adenoma has been reported by others also.[1213]

T1 weighted hyperintensity of the sellar region at MRI is a common finding due to vasopressin storage in the posteriorly located neurohypophysis. It is also seen normally in newborns and pregnant or lactating women due to hyperactive hormone secretion in the anteriorpituitary. Pathologically, T1 weighted hyperintensity can be caused by blood as in hemorrhagic pituitary adenoma, pituitary apoplexy or by the presence of a high concentration of protein in Rathke's cleft cyst, craniopharyngioma, or mucocele, by presence of fat in lipoma, dermoid cyst, and lipomatous meningioma, and due to calcificationas in craniopharyngioma, and sometimes due to presence of paramagnetic substance like manganese or melanin.[1415] In our case presence of calcification on CT scan ruled out presence of blood, protein and fat.

Histologically, calcifications in pituitary adenomas can be divided into three types. Firstly, calcifications in the intratumoral hematoma; secondly, calcifications in the degenerative adenoma tissue; and finally, scattered psammoma bodies between the adenoma cells. The last type of calcification is characteristic of calcified prolactinomas. Other types of calcification were thought to be the result from degenerative or hemorrhagic change of the adenoma.[14] In our case surgical intervention was deferred in view of asymptomatic, non-progressive nature of lesion, hence histopathology of the lesion is not available.