Siddique et al. Journal of Medical Case Reports 2011, 5:269 http://www.jmedicalcasereports.com/content/5/1/269 positive (bright), CD45-positive (dim to moderate) and CD20-negative, and cytoplasmic IgM was not expressed. Dim to moderate positivity of CD13 was identified. CD33 was negative. Cytogenetic studies showed an addi- tional copy of chromosomes X and 8 in 7 of 20 mitotic cells. BCR/ABL rearrangement was not found. Cere- brospinal fluid cytology and flow cytometry did not reveal any evidence of leptomeningeal involvement (Fig- ures 2 and 3). We planned to initiate a hyper-CVAD protocol (hyperfractionated cyclophosphamide/vincristine/doxor- ubicin/dexamethasone) as an induction therapy. As the patient’s serum bilirubin level had elevated up to a very high level of 13 mg/dL by that time, it was decided to administer corticosteroids prior to chemotherapy. Pre- dnisone 100 mg every 12 hours was administered for five days before hyper-CVAD therapy was initiated. Day four chemotherapy had to be omitted because of the patient’s bilirubin level of 11 mg/dL. By day 11, his bilir- ubin had dropped to 4 mg/dL, and vincristine was admi- nistered with a 50% dose reduction. The day four doxorubicin that had been omitted was also adminis- tered with a 50% dose reduction on day 11. As central nervous system prophylaxis, intra-thecal methotrexate was administered on the same day. His bilirubin level continued to fall gradually. It had completely normalized by the time cycle 2 of hyper-CVAD therapy was begun. The patient tolerated the chemotherapy fairly well, except that he required intermittent packed red blood cells and platelet transfusions to support his cell counts and granulocyte colony-stimulating factor and prophy- lactic intravenous antibiotics for neutropenia. He was discharged after the recovery of his cell counts with Figure 2 Ultrasound-guided core biopsy of the liver showing small to medium-sized lymphoblasts infiltrating the hepatic parenchyma. Page 3 of 4 Figure 3 Bone marrow biopsy showing lymphoblastic infiltration. instructions to follow up with the hematology/oncology department as an out-patient. Discussion Liver involvement by hematologic malignancies is not infrequent, though it is rarely the initial presentation. Histopathological examinations of the liver specimens in an autopsy series revealed that 44% of untreated patients with leukemias and lymphomas and 26% of the speci- mens from patients who received chemotherapy either alone or in combination with radiotherapy had evidence of neoplastic involvement [1]. Several patterns of hepatic involvement in hematologic malignancies have been described in the literature. It var- ies from an asymptomatic hepatic lesion or hepatomegaly to liver failure. Four cases of fulminant hepatic failure were reported by Zafrani et al. [2]. These patients had moderate to severe infiltration of the liver parenchyma by leukemic cells with or without accompanying hepatic necrosis. Rarely, obstructive jaundice is the initial presen- tation. Lee et al. [3] described a case of AML with granu- locytic sarcoma obstructing the biliary tract. Granulocytic sarcoma represents masses of granulocytic cells. The presence of myeloperoxidase in these myeloid cells gives these masses a greenish coloration and there- fore they were historically termed as chloromas [4]. Obstructive jaundice is a very rare presentation of ALLs. Some cases of T-cell ALL [5] and B-cell ALL [6,7] have been reported to have presented in associa- tion with jaundice. Only a few of these cases had no evidence of biliary obstruction on imaging. The patho- physiology of jaundice in these cases of ALL was leu- kemic infiltration of hepatic sinusoids. This is similar to the pathophysiology of jaundice in our case and is in contrast to how AML has been reported to cause