Abstract
Introduction: Diabetes insipidus (DI) rarely occurs in pituitary tumors although some patients may develop DI following pituitary tumor resection. However DI is known to occur in patients with tumors metastatic to the pituitary or in infiltrative disorders of the pituitary gland. We are reporting a patient with a 2 cm pituitary macroadenoma whose DI was unmasked by glucocorticoid therapy. Case Presentation: A 61-year-old male with a history of non-functioning pituitary macroadenoma, incidentally discovered on imaging in 2015 and stable at 1.6cm for 4 years, was referred to endocrinology for interval enlargement of his macroadenoma. He had presented to primary care due to new headache during extreme physical exertion, but otherwise denied any symptoms such as vision loss, fatigue, decreased libido, weight loss, or urinary frequency. Repeat MRI indicated growth to 2.1cm in the suprasellar component, no cavernous sinus involvement, and abutting the optic chiasm. Laboratory results revealed new onset central hypothyroidism (FT4 0.21 ng/dL (ref 0.78-2.19) with triiodothyronine 68 ng/dL (ref 80-200) and TSH 1.61 mIU/L (ref 0.47-4.68), central hypogonadism (Testosterone Free 1.3 pg/mL (ref 6.6-18.1)) and concern for adrenal insufficiency with a cortisol of 4.4 mcg/dL. He was empirically started on hydrocortisone replacement until an ACTH stimulation test could be completed, and after 3 days instructed to begin low dose levothyroxine replacement. At close followup, patient revealed that he developed new hourly nocturia causing significant distress. An overnight water deprivation test yielded a serum sodium 152 mmol/L with a urine osmolality 191 mOsm/kg, both rapidly improving with intravenous desmopressin. Copeptin was 4.6 pmol/L. Discussion Diabetes insipidus occurring in pituitary tumors including macroadenomas is extremely rare. Secretion of AVP occurs in the hypothalamic osmoreceptors, supraoptic or paraventricular nuclei, and the superior portion of the supraopticohypophyseal tract. AVP deficiency is most commonly due to damage to these areas either through neurosurgery or trauma, and more rarely tumors or infiltrative disease. However, glucocorticoid and thyroid replacement each may precipitate the development of diabetes insipidus. Well described in literature, glucocorticoid deficiency and hypothyroidism each independently impairs free water excretion. Low cortisol stimulates release of antidiuretic hormone, but this secretion is then inhibited by exogenous steroid replacement. Cortisol interferes with AVP signaling through unclear mechanisms either at the V2 receptor or post-receptor level, decreasing translocation of type 2 aquaporins and therefore reducing free water reabsorption. It is important to recognize that CDI can be unmasked after glucocorticoid or thyroid hormone replacement.
Pituitary Macroadenoma: A Case of Balanced Deficiencies
