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HEPATIC TRANSAMINASEMIA AT PRESENTATION OF ACUTE LYMPHOBLASTIC LEUKEMIA OF CHILDHOOD: IMPACT ON INDUCTION THERAPY AND OUTCOME

I Segal-Suchar¹, R Rassekh², M Bond², R Schreiber¹
¹The Divisions of Gastroenterology; ²Hematology-Oncology, Department of Pediatrics, British Columbia Children's Hospital, Vancouver, British Columbia

INTRODUCTION: Acute lymphoblastic leukemia (ALL) is the most common malignancy in childhood. While hepatic complications associated with the treatment of ALL are widely recognized, few reports have described the nature and extent of liver involvement in ALL patients at the time of initial diagnosis.
PURPOSE: To characterize the spectrum of liver function abnormalities in children who present with ALL and examine its impact on treatment and outcome.
PATIENTS AND METHODS: The Oncology Database at BC Children's Hospital was searched for new cases of ALL between 2001 and 2006. Levels of AST, ALT, GGT, bilirubin, INR, viral serology, imaging studies, induction therapy and outcome were recorded.
RESULTS: Over the 5 yrs, 147 patients were diagnosed with ALL: 56% male, 67% Caucasian. Abnormal transaminases were identified in 50/147 (34%) of the patients. Of 41 patients with abnormal AST levels: 39%, 22% and 39% had AST values <1.5x, 1.5-2x, and >2x normal respectively. Of 29 patients with abnormal ALT levels: 24%, 24% and 52% had ALT values <1.5x, 1.5-2x and >2x normal, respectively. 31% of patients with abnormal ALT levels had normal AST levels; 51% with abnormal AST had normal ALT. There were 7 patients (5%) who had elevated conjugated bilirubin (>17 umol/L) and all of them had abnormal transaminases. Two of these patients underwent liver biopsy: one demonstrated interface hepatitis and blast infiltration; the other showed giant cell hepatitis. None of the patients had fulminant liver failure. All patients with only transaminase elevation received standard therapy. Of the four patients with conjugated bilirubin >32 umol/L, three had high risk ALL and received steroids alone for 4-7 days; the fourth patient received steroids with 50% reduction of DNM and no vincristine. There was no delay in initiation of consolidation therapy in the patients, implying no untoward events with the induction protocol. All patients had a rapid and marked diminution in their liver enzymes and bilirubin.
CONCLUSION: Abnormalities in hepatic transaminases are common at the time of presentation of ALL. Conjugated hyperbilirubinemia is unusual. Patients with isolated elevation in liver transaminases had rapid resolution with standard induction therapy. Most patients presenting with conjugated hyperbilirubinemia received an altered protocol, yet all had marked response to steroid induction therapy. Whether there is a need to delay or modify the dose of other induction chemotherapeutic agents in this setting is questionable and requires further study.

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