Abstract
INTRODUCTION: Central diabetes insipidus (DI) develops when production or release of antidiuretic hormone is disrupted. A large number of cases are idiopathic with the vast majority of all remaining adult cases a result of primary or secondary hypothalmic tumor, infiltrative disease, neurosurgery, or trauma. Pituitary adenoma is not typically a cause of central diabetes insipidus. We present a case of previously undiagnosed pituitary macroadenoma resulting in central diabetes insipidus that presented critically after months of polyuria and nocturia that had previously been attributed to benign prostatic hyperplasia. CASE PRESENTATION: A 67-year-old man with a history of hypertension and taking no medications initially presented to the Hilo Medical Center with headache, nausea, nocturia, and polyuria. He had had symptoms for a year and presented to the ED after acute worsening. He was hypotensive and tachycardic with an initial sodium of 145. He quickly became hemodynamically unstable, unresponsive to fluid resuscitation, and was admitted to the ICU, briefly requiring vasopressors for blood pressure support. He was noted to have large volume output of dilute urine and elevated serum sodium. An MRI demonstrated a concentric sellar mass, with lymphocytic hypophysitis as a resultant working diagnosis. He was transferred to TAMC for Neurosurgical evaluation and further management. He was started on corticosteroids but after no improvement a follow up MRI showed a 2.0 × 1.3 × 2.5 cm lobulated, heterogeneously enhancing mass seen centered within the sella with T2 hyperintensity concerning for necrosis. After stabilization the patient underwent a transspenoidal excision of the mass. Pathology was consistent with nonsecreting pituitary adenoma. He responded appropriately to treatment with PO and nasal desmopressin. DISCUSSION: Central diabetes insipidus is frequently seen with tumors that involve the hypothalamus such as craniopharyngiomas. It is also frequently seen in metastatic spread of lung or breast cancer to the posterior pituitary or hypothalamus. However, tumors originating from the anterior pituitary very rarely cause DI. This led to a working diagnosis of lymphocytic hypophysitis in this patient but a lack of response to therapy with corticosteroids led to excision and final diagnosis of adenoma. There is also an interesting cultural twist to this case. The patient was working as a construction worker on the Big Island of Hawai‘i and noted that there was significant social pressure to avoid drinking water while at work. Several coworkers were in this patient's age range and had similar symptoms of frequent urination and nocturia and had been diagnosed with BPH. They managed their symptoms with decreased PO water intake at work and the patient felt pressure to do the same. As a result the patient had developed a significant ability to ignore his thirst response and this contributed to his not seeking medical care for his persistent symptoms before becoming very ill. The patient required coaching prior to discharge in order to adequately respond to his thirst response to achieve stable serum sodium levels with scheduled PO and intranasal desmopressin.