There have been 5 reported cases in the English literature of PTU-associated ANCA-positive syndrome with the development of diffuse alveolar hemorrhage. All patients had a preceding influenza-like prodrome, and all improved with discontinuation of PTU. Two were treated with corticosteroids and cyclophosphamide, and one with steroids alone. The mechanism of PTUinduced ANCA-positive vasculitis is unknown. It has been proposed that activated neutrophils in the presence of hydrogen peroxide release myeloperoxidase (MPO) which converts PTU into cytotoxic products. Alternatively, in the presence of MPO, PTU is converted to PTU-sulfonate which is immunogenic for T cells. CASE INFORMATION: CASE: A 23-year-old G8P1 female with diet controlled gestational diabetes presented at 33 weeks gestation with dyspnea and productive cough. She was febrile, tachypneic and tachycardic. Her chest film revealed bilateral perihilar infiltrates and left lower lobe airspace disease. She was empirically treated for a community-acquired pneumonia. Initial laboratory results showed a HCO3 of 9, an anion gap of 20, and a glucose of 94. Urinalysis showed greater than 80 ketones and no glucose. Arterial blood gas was 7.32/18/68. Subsequent investigation revealed a lactic acid level of 0.6 and large serum ketones. Shortly after admission, the patient exhibited worsening respiratory distress and polydipsia. Repeat labs showed a HCO3 of 5, an anion gap of 24, a glucose of 113, and an ABG of 7.16/17/68. The patient was started on D5 1/2 NS and a continuous insulin infusion. Continued therapy led to resolution of the anion gap acidosis and clearance of serum ketones. DISCUSSION: Pregnancy is a state of relative insulin resistance marked by enhanced lipolysis and ketogenesis. Under certain circumstances, this hormonal milieu may lead to DKA. DKA can present differently in the pregnant patient, making the diagnosis difficult. The mechanism responsible for insulin resistance in pregnancy involves human placental lactogen, progesterone, cortisol, and prolactin, all of which impair glucose uptake by insulin sensitive cells. The cause of DKA with euglycemia is not well understood, but may result from constant fetal removal of glucose, the expanded blood volume of pregnancy, or the rapid clearance of glucose due to increased glomerular filtration. As seen in our patient, DKA in pregnancy may not present classically. As such, high clinical suspicion of DKA is required in ill gestational diabetics to prevent adverse maternal and fetal outcomes. LEARNING OBJECTIVES: 1). Review the newly described association of osteoporosis and HIV disease 2). Identify the secondary causes of osteoporosis in AIDS patients. CASE INFORMATION: A 39 year old man with AIDS presented to the emergency department with the acute onset of back pain over his thoracic spine. He denied trauma or radicular symptoms. His past medical history included Kaposi's Sarcoma of the lower legs and esophagus, CMV esophagitis, and adrenal insufficiency. He had received multiple antiretroviral regimens over the past 10 years. His current combination therapy included abacavir, lamivudine, and nelfinavir. His exam revealed marked tenderness over the thoracic spine from T4 to T10. His WBC was 3.1, hematocrit was 31%, electrolytes, renal and liver function tests were normal. A recent CD4 count was 10 cells/ul with a viral load of 85,000 RNA copies/ml. Spine radiographs revealed multiple new vertebral fractures at T5, T6 and T9 confirmed by MRI. Bone biopsy at T6, however, revealed normal cellularity without infiltrate, granuloma or obvious infection. A subsequent lumbar DEXA bone mineral density demonstrated a T score of -2.9, consistent with severe osteoporosis. Laboratory evaluation of secondary causes of osteoporosis demonstrated hypogonadism with a free testosterone of 0.8pg/ml (NL 47-244) and a total testosterone of 7ng/dl (NL 400-1080). The patient was managed with opioid analgesics, calcitonin, and calcium with vitamin D supplimentation. DISCUSSION: Metabolic bone disease may represent an important complication of HIV antiretroviral therapy. A few published reports have noted a prevalence of osteopenia or osteoporosis as high as 50% in some groups of HIV patients. This case, however, illustrates the multifactorial nature of osteoporosis and the importance of identifying all of the potential secondary causes. Since AIDS patients have a higher rate of GI malabsorptive syndromes, poor PO intake, immobility, and hypogonadism they are already at a substantial risk for osteoporosis regardless of the potential risk from antiretroviral therapies. As AIDS patients continue to live longer, the cumulative consequences of these risks may lead to a substantial rise in complications from osteoporosis. It is important for clinicians caring for HIV patients to be cognizant of this risk. Recognize accessory spleen as a rare cause of a pancreatic mass 3. Identify strategies to differentiate accessory spleen from a pancreatic hypervascular tumor CASE INFORMATION: A 41 year old female with a past medical history of uric acid nephrolithiasis presented to the Emergency Department complaining of right flank pain and blood in her urine. Her only medication was allopurinol 300 mg daily. Physical exam revealed right flank tenderness to palpation. A spiral CT of the abdomen revealed two renal calculi in the right and one in the left kidney. In addition, a mass was seen in the tail of the pancreas. A CT scan of the abdomen with contrast confirmed a 4.1 Â 4.8 cm hyperenhancing, hypervascular, well defined mass within the tail of the pancreas consistent with an islet cell tumor. Upon further questioning, the patient denied symptoms of peptic ulcer disease (gastrinoma), hypoglycemia (insulinoma), diarrhea and renal failure (VIPoma), hyperglycemia (glucagonoma), or diabetes, steatorrhea and cholelithiasis (somatostatinoma). A presumptive diagnosis of a nonfunctioning islet cell tumor was considered and the patient was referred to a surgeon. A distal pancreatectomy was performed and pathology revealed an intrapancreatic accessory spleen. DISCUSSION: Accessory spleen has been recognized as a rare cause of an intrapancreatic mass. It is seldomly detected clinically due to its lack of symptoms. Due to the rise in abdominal imaging procedures performed, though, the detection of accessory splenic tissue in the pancreas can be expected to increase. Its importance lies in the fact that it can mimic a pancreatic hypervascular tumor. Strategies to differentiate an accessory spleen from a pancreatic hypervascular tumor include angiographic demonstration of splenic blood supply, similar enhancement of the accessory spleen and the spleen on CT or MRI, radionuclide testing or biopsy. In this case, the possibility of an accessory spleen should have been considered and potentially could have avoided unnecessary surgery. (1) to recognize that thyrotoxicosis can potentiate warfarin's anticoagulant effects; (2) to manage warfarin therapy in thyrotoxic patients. CASE INFORMATION: A 59 yo woman with hypertension noted new-onset palpitations and "shakiness" at a routine clinic visit. She had no prior history of cardiac or thyroid disease and denied dizziness, loss of consciousness, chest pain, use of new medications, dietary supplements, drugs or alcohol. Current medications included benazepril and aspirin. Physical examination revealed a thin, anxious woman with a HR of 128 and BP of 100/60. She had a prominent, smooth, non-tender thyroid gland. Cardiopulmonary exam was notable for an irregularly irregular tachycardia, a normal S1 and S2 without gallops, and a II/VI short, systolic ejection murmur at the apex. An ECG showed rapid atrial fibrillation, prompting transfer to the emergency department, where work-up revealed a normal PT/INR, creatinine, and hepatic function. After cardiopulmonary stabilization, she was discharged on metoprolol and warfarin 2.5 mg/d. Subsequent TSH < 0.03 mIU/L, free T4 > 71 pmol/L, total T3 of 667 ng/dL, elevated anti-TSH receptors, and abnormal thyroid uptake scan confirmed Graves' disease. The patient's palpitations resolved, but anti-coagulation proved challenging, with INR' s above 4 on average warfarin doses of < 1.0 mg/d (Table I) . She exhibited exquisite warfarin sensitivity until her free T4 levels normalized three weeks after starting methimazole. DISCUSSION: Warfarin exhibits many drug-drug interactions, including an increased effect with l-thyroxin administion. Warfarin potentiation by endogenous thyroid hormone is a less appreciated phenomenon documented in case reports dating to 1972. As this patient's initial INR illustrates, thyrotoxicosis alone does not prolong bleeding times. Rather, thyroxin enhances the metabolic clearance of vitamin K-dependent clotting factors II, VII, IX, and X, resulting in relative hypoprothrombinemia and warfarin potentiation. As in this case, potentiation closely parallels free T4 levels and can occur after one dose. Thus, in thyrotoxic patients, appropriate initial warfarin doses may range from 1.0 mg QOD and require upward titration as hyperthyroidism improves. Awareness of such patients' potential enhanced warfarin sensitivity and judicious anti-coagulation may minimize hospital stays and prevent bleeding complications. A 17-year-old male presented to the emergency room with a history of myalgias for two weeks. Two weeks prior to admission he underwent a dental extraction that required general anesthesia with succinylcholine. He developed symptoms of myalgias four hours after procedure that persisted until readmission. While in the emergency room, he described severe muscle pain in the upper and lower extremities. Enzyme analysis revealed a creatine kinase of 22, 000, and he was admitted for rhabdomyolysis. The patient was treated with IV fluids and rest. His urinalysis was negative for myoglobinuria after hydration. He subsequently underwent a muscle biopsy that revealed a generalized myopathy. After hydration, pain control and initial rest, he gradually improved over the ensuing weeks. DISCUSSION: Growth hormone excess in childhood results in an uncommon condition of giantism. Gigantism causes inappropriate growth of both bones and muscles that results in a large individual. With the continued muscle growth, gigantism can cause an underlying myopathy. Succinylcholine provides muscle relaxation during anesthesia; however, it can cause rhabdomyolysis. This normally occurs in patients with an underlying muscle disorder. Succinylcholine may damage muscle in patients with muscular dystrophy or other primary muscle disorders. This is the first case of succinylcholine-induced rhabdomyolysis in a patient with primary myopathy from gigantism. While unusual, rhabdomyolysis from succinylcholine must be considered in all patients with potential myopathy. Treatment involves IV fluids and supportive care. Sugar water test was negative. Occult mediastianl lymphadenopathy was not found with contrasted chest CT. Bone marrow biopsy showed normocellularity with blasts of less than 5%, myeloid with left shift and one lymphoid aggregate, with adequate numbers of megakaryocytes. The iron was absent. CD59 and CD55 cell markers were normal. Comprehensive studies for lymphoma/leukemia were normal. Autoimmune pancytopenia was confirmed. He was treated with platelet pheresis transfusion initially, which hemolyzed shortly. He responded to IVIG and solumedrol with normalized WBC and platelet count. He was discharged home on prednisone taper. One month follow up showed normal WBC and platelet, but with persistent iron deficient anemia. Pt remained asymptomatic. DISCUSSION: There are three general causes of pancytopenia: splenic sequestion, insufficient production, and excessive destruction. In our case, drug-induced autoimmune processes were suspected after thorough work-up. Treatment for autoimmune hemolytic processes includes steroid, IVIG. If not effective, splenectomy may be an option. Immunosuppressive drugs such as azothioprine and cyclophosphamide, have been used with satisfactory results. Recently, we have had two patients present with autoimmune hematologic disorders within one to two weeks after using Levofloxacin. This association has not been reported previously in the literature. Submission of these cases may assist primary care providers recognize this adverse effect of Levofloxacin.