MITOCHONDRIAL TOXICITY AND HIV THERAPY. S. Burridge 1 , L. Coberly 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #75159) LEARNING OBJECTIVES: Recognize the clinical presentation of mitochondrial toxicity secondary to nucleoside reverse transcriptase inhibitors. CASE INFORMATION: A 43-year-old white male with AIDS presented with altered mental status, nausea, vomiting, right upper quadrant pain and myalgias. Medications included didanosine, efavirenz, lopinavir/ritonavir and stavudine. His temperature was 101.28F, HR 120, BP 135/85 and RR of 26. Physical examination was significant for bitemporal wasting, oral thrush, dry oral mucosa, ketotic breath, pain to palpation in the right upper quadrant and a liver span of 20cm. There were no identified sources of infection. Laboratory examination was significant for sodium 126mmol/L, potassium 5.1mmol/L, chloride 88mmol/L, and bicarbonate 13mmol/L. Lactate was markedly elevated at 9.9mmol/L. Transaminases were 111 IU/L and 128 IU/L, alkaline phosphatase was 209 IU/L and total bilirubin was 4.10 mg/ dL. Triglycerides were greater than 1,000 mg/dL. Abdominal CT revealed hepatomegaly with fatty infiltrate. Medication toxicity was suspected and HAART therapy was discontinued. Riboflavin supplementation was initiated. IMPLICATIONS/DISCUSSION: Mitochondrial toxicity is a rare syndrome that has been reported in patients treated with nucleoside reverse transcriptase inhibitors, particularly zalcitabine, didanosine, and stavudine. The diagnosis is clinical. Patients present with nausea/ vomiting, abdominal pain, weight loss, malaise, fatigue, dyspnea and sometimes fever. Laboratory evaluation reveals lactic acidosis, hypertriglyceridemia and elevated liver enzymes. Imaging studies demonstrate hepatomegaly with fatty infiltration. The mechanism of mitochondrial injury is postulated to be inhibition of the mitochondrial gamma polymerase, the enzyme that directs the replication of mitochondrial DNA. The mitochondria are unable to replicate, the citric acid cycle is blocked and lactate production increases. Fatty acid oxidation is inhibited leading to accumulation of lipid droplets. Treatment involves the administration of mitochondrial supportive therapy such as riboflavin, thiamine, ubiquinone and acetyl-carnitine in addition to the cessation of antiretroviral therapy. Unrecognized, this syndrome carries a 60% mortality attributed to worsening acidosis with resulting cardiovascular collapse or progressive hepatic failure. (Tracking ID #76589) LEARNING OBJECTIVES: To recognize the dilemma posed by an inconclusive MRI in cases of intracerebral mucormycosis and to emphasize the need for brain biopsy. CASE INFORMATION: A 42 year-old male with HIV presented with a five-day history of headache, fever, left sided weakness and multiple falls. Physical exam showed a left sided, central, facial nerve palsy, weakness and left sided hyperreflexia. The patient's CD4 count was 56. Cryptococcus, toxopolasmosis, tuberculous meningitis, atypical infectious agents and lymphoma were considered in the working differential diagnosis. CT scanning and CSF analysis were negative. MRI revealed a mass in the right basal ganglia with associated edema and a midline shift. An MRI guided brain biopsy showed mucormycosis. In spite of amphotericin B therapy he expired ten days later. IMPLICATIONS/DISCUSSION: Mucormycosis in an immunocompromised host with HIV has rarely been described in the literature. Notably, in such cases neither CT nor MRI scanning is sufficient to make the diagnosis. In these instances, surgical exploration is mandatory and can provide crucial diagnostic information.