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Late Effects of Treatment for Childhood Cancer (PDQ®): Treatment - Health Professional Information [NCI] - Late Effects of the Digestive System

Table 5. Digestive Tract Late Effects continued...

Viral hepatitis B and C may complicate the treatment course of childhood cancer and result in chronic hepatic dysfunction. Hepatitis B tends to have a more aggressive acute clinical course and a lower rate of chronic infection. Hepatitis C is characterized by a mild acute infection and a high rate of chronic infection. The incidence of transfusion-related hepatitis C in childhood cancer survivors has ranged from 5% to 50% depending on the geographic location of the reporting center.[45,46,47,48,49,50,51] Chronic hepatitis predisposes cirrhosis, end-stage liver disease, and hepatocellular carcinoma. Concurrent infection with both viruses accelerates the progression of liver disease. Since the majority of patients received some type of blood product during childhood cancer treatment and many are unaware of their transfusion history, screening based on date of diagnosis/treatment is recommended unless there is absolute certainty that the patient did not receive any blood or blood products.[52] Therefore, all children who received blood transfusions before 1972 should be screened for hepatitis B and before 1993 should be screened for hepatitis C virus and referred for discussion of treatment options.

Less commonly reported hepatobiliary complications include cholelithiasis, focal nodular hyperplasia, nodular regenerative hyperplasia, and microvesicular fatty change. In limited studies, an increased risk of cholelithiasis has been linked to ileal conduit, parenteral nutrition, abdominal surgery, abdominal radiation, and HSCT.[53,54] Gallbladder disease was the most frequent late-onset liver condition reported among participants in the CCSS and they had a twofold excess risk compared with sibling controls (RR = 2.0; 95% CI, 2.0–40.0).[29] Lesions made up of regenerating liver called focal nodular hyperplasia have been incidentally noted after chemotherapy or HSCT.[55,56] These lesions are thought to be iatrogenic manifestations of vascular damage and have been associated with VOD, high-dose alkylating agents (e.g., busulfan and melphalan), and liver radiation therapy. The prevalence of this finding is unknown, noted at less than 1% in some papers;[56] however, this is likely an underestimate. In one study of patients who were followed by magnetic resonance imaging (MRI) after transplant to assess liver iron stores, the cumulative incidence was 35% at 150 months posttransplant.[55] The lesions can mimic metastatic or subsequent tumors, but MRI imaging is generally diagnostic, and unless the lesions grow or patients have worrisome symptoms, biopsy or resection is generally not necessary.

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