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These analyses support the hypothesis that hyponatremia is a risk factor for osteoporosis and fracture. Additional studies are required to evaluate whether correction of hyponatremia will improve patient outcomes.

There is a clinical impression that when tumors invade the cavernous sinus, compression of the internal carotid artery is rare with pituitary adenomas and more common with other types of lesions but there are no actual data to support this impression. To confirm the impression that the finding of internal carotid artery compression by tumors invading the cavernous sinus is inconsistent with a diagnosis of a pituitary adenoma, we performed a retrospective analysis of MRI scans performed between 2000 and July 2009. An initial search of the radiology database was performed using the terms "invasive mass cavernous MRI" and subsequent refinement narrowed the evaluation to 141 patients with cavernous sinus invasion by sellar/parasellar tumors for whom there were clinical/pathological data to determine tumor type. 83 of the 141 patients with cavernous sinus invasion had carotid artery encasement; 58 were pituitary adenomas and 25 were other types of lesions. Eight of these 83 scans revealed compression of the internal carotid lumen, with only one being a pituitary adenoma and seven being other types of lesions. Therefore, only 1/58 (1.7%) of pituitary adenomas and 7/25 (28%) of non-pituitary adenoma lesions that encased the internal carotid artery caused compression of the artery (P = 0.0007). A mass lesion that invades the cavernous sinus and encases the internal carotid artery is very unlikely, therefore, to be a pituitary adenoma if it compresses the lumen of the internal carotid artery.

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Introduction: Ectopic adrenocorticotrophic hormone (ACTH) producing Pancreatic Neuroendocrine Tumor (p-NET) are extremely rare with incidence of 1.2% and confer a poor prognosis (5-year survival <20%). Case Report: 31-year old female with diabetes mellitus type 2 (DM-2) and hypertension (HTN) was found to be severely hypokalemic on routine labs and was sent to the Emergency Department for potassium replacement. Vitals; BP:139/87 mmHg, HR:108 bpm, RR:18, T:37°C and saturating 98% on ambient air. Examination revealed cushingoid features; hyperpigmented face, bilateral upper extremity pigmented papules, proximal muscle weakness, acanthosis nigricans, violaceous abdominal striae, truncal obesity, ecchymoses, bilateral lower extremity edema, memory impairment and anxiety. Initial labs; BG: 289 mg/dL, HbA1c: 9.5%, K: 2 mmol/L (N 3.5-5.2), WBC: 12.5 k/μL (N 4-10.8), Cortisol >150 mcg/dL (N 5-23), TSH: 0.325 μIU/mL (N 0.45-4.5), and FT4: 0.69 ng/dL (N 0.82-1.77). Diagnosis of Cushing’s syndrome was made based on elevated cortisol level and confirmed with elevated 24-hour urinary free cortisol: 13,294 μg (N<45), midnight salivary cortisol >15 ug/dL (N 0.09-1.5) and 1 mg dexamethasone suppression test (Cortisol >150 mcg/dL, ACTH: 621 pg/ml). Additional labs showed Chromogranin A: 717 ng/mL (N 0-160). She was started on prophylactic Enoxaparin & Trimethoprim/Sulfamethoxazole and treated with Spironolactone, Basal/Bolus insulin, and Ketoconazole for hypercortisolemia. Pituitary MRI was negative for pituitary adenoma. Abdominal/Pelvic CT scan demonstrated a solid 5 cm pancreatic head mass with innumerable haptic metastases consistent with metastatic p-NET which was confirmed on PET-CT Ga68 Dotatate scan. Liver biopsy was positive for a well differentiated p-NET with ki-67 <5% and negative ACTH staining. Hospital course was complicated by fluctuating cortisol levels with intermittent psychotic manifestations despite up-titration of Ketoconazole, addition of Octreotide as well as anti-psychotics. She later developed transaminitis on maximum dose of Ketoconazole and thus underwent laparoscopic total adrenalectomy for treatment of her hypercortisolemia. Post-operatively, she was started on Hydrocortisone & Fludrocortisone and Spironolactone was discontinued. She was transitioned to monthly Lanreotide and treated with Capecitabine and Temozolomide with adequate therapeutic response and subsequent down trending of her Chromogranin A: 188 ng/mL and ACTH: 228 pg/ml levels. Currently, she is doing well with significant improvement of her DM-2, HTN, psychiatric symptoms and overall clinical status. Conclusions: Symptoms of ectopic Cushing’s syndrome may be delayed, however given the rare and aggressive nature of ACTH producing p-NET, timely diagnosis, prophylaxis and individualized treatment approach is crucial in achieving favorable prognosis.