METASTASIS-INDUCED ACUTE PANCREATITIS. S. Chebrolu 1 , A. Naidu 1 , F. Zar 1 ; 1 St. Francis Hospital, Evanston, IL LEARNING OBJECTIVES: 1) Recognize that metastatic tumors to pancreas may rarely induce acute pancreatitis referred to as Metastasis-Induced Acute Pancreatitis (MIAP). 2) Diagnose and manage MIAP. CASE INFORMATION: A 37-year-old woman presented with a one-day history of epigastric pain radiating to the back associated with nausea and decreased appetite. One and half years ago, she had a missed abortion followed by a Placental Site Trophoblastic Tumor (PSST) which was treated with total abdominal hysterectomy and chemotherapy with methotrexate. Her beta-HCG was less than 2 IU/l six months prior to this presentation. She had no history of alcoholism. On examination, she was found to have epigastric tenderness. Laboratory investigations revealed amylase 309 IU/l, lipase 154 IU/l, lactate dehydrogenase 544 IU/l, calcium 8.5mg/dl, glucose 221mg/dl and hemoglobin 13.6g/dl. She was diagnosed as acute pancreatitis and treated medically. Her pain persisted and she had CT scan of the abdomen that showed a swollen and enlarged pancreas with multiple rounded lesions of variable sizes. There was also a lobulated 3x4cm mass behind the sigmoid colon with a surgical clip adjacent to it associated with retroperitoneal and inguinal lymphadenopathy. Beta-HCG was found to be 2320.6 IU. ERCP was unremarkable. Exploratory laparotomy with bilateral salpingoopherectemy and tumor dissection was done showing histologic evidence of recurrent PSTT. A diagnosis of MIAP secondary to metastatic PSST was made and chemotherapy with etoposide, methotrexate and adriamycin was started with resolution of her symptoms. DISCUSSION: MIAP refers to non-pancreatic tumors metastasizing to the pancreas and resulting in acute pancreatitis. It is a very rare cause of acute pancreatitis and only 42 such cases have been reported in the literature. Most of them were associated with bronchogenic carcinoma and lymphoma. Mechanisms implicated in the causation of MIAP include mechanical ductal obstruction and rupture with direct parenchymal tumor invasion or ischemia secondary to vascular occlusion and encasement of pancreatic vessels. The clinical and laboratory presentation is similar to the other causes of pancreatitis and MIAP remains a diagnosis of exclusion. An accurate history, supportive clinical evidence and radiological findings of pancreatic and peri-pancreatic metastatic lesions in the presence of a known primary tumor aid in the diagnosis. MIAP is managed conservatively with nasogastric tube suction, intravenous fluids and analgesics and this approach is helpful in most cases. If it persists, systemic chemotherapy for the metastatic tumor or palliative abdominal radiation may help. Overall, MIAP portends a bad prognosis and many patients succumb to the metastatic tumor sooner or later. PSST, a rare form of Gestational Trophoblastic Disease, has never previously been reported as a cause of MIAP and this is the first such instance. year old female Stanford graduate student presented with three days of fever and headache with associated nausea, neck stiffness, and photophobia. Past medical history significant for migraine headache and menstrual irregularity which responded well to oral contraceptives. Current medication includes three days of leuprolide injections for commercial egg donation. On exam, patient was febrile to 39.6 degrees Celsius with otherwise normal and stable vital signs. Patient was slightly lethargic and had slight photophobia and mild posterior neck tenderness on palpation, but otherwise completely normal exam. Ophthalmologic and neurologic exams were completely normal. Labs were normal except for Sodium 126 and Potassium 3.3. Lumbar puncture revealed opening pressure of 13cm. CSF studies revealed Glucose 44, Protein 51, WBC 27, RBC 510, and negative microscopic evaluation. Bacterial, viral and fungal cultures were eventually all negative. Empiric antibiotics of ceftriaxone, vancomycin and acyclovir were started. Patient continued to have headache, nausea, and fever with no clinical improvement or worsening except for Sodium continue to drop to 115 over next three days. On hospital day three, patient developed seizure and head MRI revealed 2.3cm Â 1.8cm sellar mass with hemorrhage and compression on optic chiasm. Surgical decompression of mass was complicated by right ACA/MCA territory infarct secondary to vasospasm and great sodium fluctuation due to SIADH and adrenal insufficiency. Patient eventully was discharged on thyroxine, cortisone, and DDAVP. She has made incredible recovery and will be resuming her PhD studies. DISCUSSION: The risk of pituitary apoplexy with use of leuprolide has been described in the literature but not well screened. Detailed clinical history, exam, and laboratory investigation might identify patients at higher risk of pituitary apoplexy for selective imaging evaluation. In this patient, the history of menstral irregularity controlled by oral contraceptives, the hyponatremia and loss of body temperature control could have been the starting point of investigation for pituitary adenoma and apoplexy. With increasing number of patients receiving elective leuprolide for fertility purpose, the medical community should be aware of potential risk in order to assess and advise patients accordingly. CASE INFORMATION: A 63-year-old male with a history of diabetes mellitus, hypertension, heavy alcohol consumption, and a T6 vertebral fracture was admitted to hospital with a one year history of progressive lower extremity proximal muscle weakness. Concurrent with his worsening weakness, the patient noticed increasing central obesity and easy bruising. Physical examination revealed a classic cushingoid appearance. The neurological examination demonstrated symmetric polyneuropathy as well as lower extremity proximal muscle weakness and wasting. A T6 sensory level was present. The reflexes were 1+ and the plantar responses were flexor bilaterally. Laboratory investigations confirmed Cushing's syndrome and suggested a pituitary source of hypercortisolism. An MRI of the spine showed multiple vertebral fractures and epidural lipomatosis in the posterior epidural space, from T2 to T8, compressing the spinal cord maximally at T6. Given the fragility of this patient's spine and the ongoing investigations to determine the cause of hypercortisolism, the patient did not undergo emergent epidural fat debulking. A pituitary microadenoma was diagnosed and resected by a transphenoidal approach. Although repeat imaging was not performed to document regression of the spinal lipomatosis, there was clinical and laboratory evidence of resolution of the hypercortisolemia. The post-operative course was complicated by pulmonary emboli and recurrent sepsis; the patient suffered a fatal cardiac arrest 96 days after surgery. DISCUSSION: Epidural lipomatosis has been described in steroid use and obesity, and more rarely in association with endogenous hypercortisolism such as Cushing's disease. This case emphasizes the difficulty in suspecting epidural lipomatosis in a patient with Cushing's syndrome in the setting of other neurologic processes. The diagnosis of epidural lipomatosis needs to be systematically considered in any patient with Cushing's syndrome who presents with back pain, lower extremity weakness, radiculopathy, or subtle signs of myelopathy. MRI of the spine is the diagnostic test of choice. Treatment modality (surgical debulking of epidural fat versus correction of the hypercortisolic state or weight loss) should be individualized based on the severity of neurological signs, the potential reversibility of the causative factor, and the estimated operative morbidity.