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CASE REPORT
Year : 2020  |  Volume : 17  |  Issue : 1  |  Page : 19-21

Vanishing pituitary macroprolactinoma and secondary hypothyroidism due to pituitary apoplexy


1 Department of Endocrinology, Center for Endocrinology Diabetes Arthritis and Rheumatism (CEDAR) Superspeciality Clinics, New Delhi, India
2 Department of Rheumatology and Immunology, Center for Endocrinology Diabetes Arthritis and Rheumatism (CEDAR) Superspeciality Clinics, New Delhi, India
3 Department of Endocrinology, CEDAR Superspeciality Clinics, Bengaluru, Karnataka, India
4 Department of Endocrinology, CEDAR Superspeciality Clinics, Zirakpur, Punjab, India

Correspondence Address:
Dr. Deep Dutta
Department of Endocrinology, Center for Endocrinology Diabetes Arthritis and Rheumatism Superspeciality Clinics, 33 Netaji Subhash, Pocket-1, Phase-2, Sector 13, Dwarka, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/trp.trp_11_20

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Macroprolactinomas usually need long-term cabergoline therapy, often lifelong, as complete resolution of these tumors is rare. We present a vanishing pituitary macroprolactinoma which evolved into a complete empty sella following 2 years of cabergoline therapy. A 17-year-old girl with primary amenorrhea, chronic headache, and galactorrhea for 2 months was diagnosed to have pituitary macroprolactinoma (20 mm × 17 mm × 16 mm; prolactin 451 ng/ml). T2-weighted imaging revealed fluid level in adenoma suggestive of bleed in the tumor suggestive of pituitary apoplexy. Cabergoline was initiated at 0.5 mg/week and was uptitrated to 3 mg/week over 6 months to ensure prolactin was suppressed. Magnetic resonance imaging pituitary after 2 years of cabergoline therapy revealed empty sella with pituitary stalk traced till the floor of sella turcica, without any evidence of adenoma. Hormone evaluation revealed low total T4 levels (5.1 mcg/dl); low thyroid-stimulating hormone (0.9 mIU/L); normal morning cortisol (18.1 mcg/dl); and normal prolactin (4 ng/ml), leading to the diagnosis of secondary hypothyroidism. Cabergoline dose was tapered gradually. Levothyroxine replacement was started at 50 mcg/day. Pituitary apoplexy and associated infarction 2 years back lead to ischemic necrosis in adenoma, leading to its spontaneous resolution in our patient. The adenoma had damaged adjacent normal pituitary cells due to limited space in sella, resulting in empty sella. Pituitary apoplexy is nature's way of curing pituitary adenoma. Complete disappearance of adenoma and the resulting empty sella syndrome are the novelty of this report.


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