Case Presentation:
An 18 year old male with no past medical history presented with one month history of nausea and vomiting, 10 pound weight loss, and abdominal pain. Vital signs were normal and physical exam only remarkable for mild tenderness to palpation in the right upper quadrant. Admission labs were notable for leukocytosis (WBC 14) with lymphocyte predominance (51% lymphs, 33% atypical). His creatinine was 2.0 with normal urinalysis and FeNa suggesting intrinsic acute kidney injury (AKI). Liver function tests were as follows: total bilirubin 1.6, AST 263, ALT 893, ALP 192. Further history revealed that our patient had recently joined the marines and started boot camp, for which he was lifting weights and taking creatine supplements. CPK was normal. Viral studies for EBV, CMV, HBV, HCV and HSV were negative. His liver function improved and he was discharged home. He returned one week later for continued symptoms, with total bilirubin of 2.6 and ALT of 869. Liver biopsy was performed and revealed modest hepatocyte apoptosis and scattered portal and lobular inflammatory cells (primarily lymphocytes), consistent with drug-induced or viral hepatitis. Given his elevated creatinine unresponsive to intravenous fluids, a kidney biopsy was performed, which revealed normal histology. He then developed an extensive left lower extremity deep vein thrombosis (DVT). Given unprovoked DVT with weight loss and peripheral lymphocytosis, the possibility of tumor lysis was considered. Uric acid was 12, LDH 290, phosphorous 5, potassium 4.3. His peripheral blood was sent for flow cytometry, which revealed 10% lymphoblasts. Bone marrow biopsy revealed 78% blasts with markers consistent with B-cell acute lymphoblastic leukemia (ALL). CT chest, abdomen, and pelvis were negative for lymphadenopathy or masses. He was transferred to the malignant Hematology service and started on induction chemotherapy (CALGB induction protocol with imatinib and asparaginase).
Discussion:
This case demonstrates an extremely remarkable systemic presentation of ALL in a young adult patient. ALL is one of the few cancers that impact the entire lifespan, with peak incidence between 2-5 years of age, and decreased incidence in adult patients. Although survival approaches 90% for children with ALL, adolescents and younger adults have a much poorer prognosis.
The most common presenting symptoms of ALL are fever, night sweats, fatigue, bone pain, lymphadenopathy and bleeding. Our patient’s presentation was atypical as he presented with nausea, vomiting, and right upper quadrant abdominal pain with hepatitis and AKI. Although uncommon, hepatocellular injury at the time of ALL diagnosis can be secondary to viral illnesses or tumor infiltration of the liver. Etiologies for acute renal failure at the time of leukemia diagnosis include leukemic infiltration of the kidney, spontaneous tumor lysis syndrome, and acute tubular necrosis. The appearance of an unprovoked DVT was a major clue for diagnosis of ALL in our patient.
Conclusions:
In summary, acute lymphoblastic leukemia should be considered in a young adult with multiple systemic involvement including hepatitis, acute kidney injury and hypercoagulability. It is important for hospitalists to consider malignancy in patients with systemic end organ damage and weight loss, even in the absence of classical symptoms.