SPACE OCCUPYING LIVER LESIONS WITH FAMILIAR OCCUPANTS. F. Francois 1 , L. Yatskar 2 ; 1 New York University, Brooklyn, NY; 2 New York University, New York, NY LEARNING OBJECTIVES: 1. Develop a high index of suspicion for tuberculosis in refugees and immigrants 2. Recognize immunocompromised hosts as being at risk for extrapulmonary tuberculosis 3. Assess space occupying hepatic lesions in the setting of possible tuberculosis CASE INFORMATION: A 35 year old Tibetan male with the Acquired Immune Deficiency Syndrome (AIDS), CD4 = 32/mm 3 and viral load = 102,000 copies/ml, presented complaining of fever, chills, abdominal pain, diarrhea, and malaise of increasing severity over five days. Six years prior to this clinic visit the patient was treated with Isoniazid for 4 months after a positive purified protein derivative skin test. Two years prior to the visit he was diagnosed with AIDS and completed treatment for multiple episodes of infectious diarrhea. Two weeks prior to this current evaluation he began to experience abdominal discomfort associated with loose non bloody stools. A course of Metronidazole did not improve his symptoms. He had never been on antiretroviral therapy, and on examination was noted to be a thin febrile male in no acute distress with bitemporal wasting, oral thrush, nonicteric sclerae, moderate right upper quadrant tenderness to deep palpation, and hyperactive bowel sounds. The patient was admitted to the hospital for evaluation, at which time laboratory analysis was notable for a white blood count of 5.8, an hematocrit of 26.6, and an INR of 1.59. An abdominal CT revealed low attenuated lesions in the liver, the largest measuring 6cm in diameter, with a smaller lesion in the porta hepatis extending into the head of the pancreas. Percutaneous drainage of one of the lesions revealed acid fast organisms subsequently identified as Mycobacterium Tuberculosis (MTB) which was pan sensitive. A bronchoscopy did confirm concurrent pulmonary TB. There was radiographic evidence of resolution of the hepatic lesions over several months after initiating treatment with Isoniazid, Rifampin, Pyrazinamide, and Ethambutol. DISCUSSION: One in three individuals worldwide is infected with MTB. In the U.S., 40% of cases occur among foreign born persons. Tuberculosis most commonly presents as pulmonary or lymph node disease, but can also affect other organs. Immunosuppressive therapy, malignancy, and AIDS are known risk factors for disseminated complications with the organism. Extrapulmonary disease is seen in 60% of AIDS patients with lung disease, and of those patients, 7.5% have tuberculosis of the liver. Hepatic tubercular involvement is most commonly described as granulomatous, but can also be seen as discrete space occupying lesions such as tuberculomas, and abscesses. Patients typically present with fever, night sweats, abdominal discomfort, weight loss, and hepatomegaly. Diagnosis is made by aspirating a lesion, and treatment is based on drug sensitivities. her abdominal wall, breasts, thighs, and calves. The lesions were associated with central necrosis and peripheral mottling. She was alert, oriented, afebrile, and without leukocytosis. She had a calcium-phosphorus product of 75 and a parathyroid hormone level of 438. Despite aggressive wound care and antibiotics, her condition worsened precipitously over 72 hours. Her skin lesions became necrotic, ulcerative, and suppurative. She became febrile, hypotensive, and stuporous. Despite broadened antibiotics and aggressive fluid resuscitation, she became unresponsive, pulseless, apneic, and died. DISCUSSION: Calcific Uremic Arteriolopathy (CUA) is characterized by calcification of subcutaneous arterioles and infarction of skin and subcutaneous adipose tissue. It occurs in a minority of chronic renal failure patients. In CUA, calcification of the media of arteriolar vessels leads to regional ischemia and then infarction of skin and subcutaneous tissue, especially in areas of high adipose content. Skin necrosis and ulceration develop and patients usually die as a result of ischemic or infectious complications. While the true pathogenesis of CUA is unknown, several factors have been associated with a higher incidence. A high calcium-phosphorus product and secondary hyperparathyroidism are often associated with a increased incidence of CUA. Other features such as female gender, white race, obesity, recent significant weight loss, insulinrequiring diabetes mellitus, and use of calcium carbonate as a phosphorus binder have been reported as predisposing factors. It is likely that modification of these factors in our patient, such as management of high calcium-phosphorus product with non-calcium containing phosphorus binders, reduction of calcium content in dialysate fluid, and gradual weight loss may have prevented this deadly outcome.