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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

Predisposing TherapyGastrointestinal EffectsHealth Screening/Interventions
GVHD = graft-versus-host disease; KUB = kidneys, ureter, bladder (plain abdominal radiograph).
Radiation impacting esophagus; hematopoietic cell transplantation with any history of chronic GVHDEsophageal strictureHistory: dysphagia, heart burn
Esophageal dilation, antireflux surgery
Radiation impacting bowelChronic enterocolitis; fistula; stricturesHistory: nausea, vomiting, abdominal pain, diarrhea
Serum protein and albumin levels yearly in patients with chronic diarrhea or fistula
Surgical and/or gastroenterology consultation for symptomatic patients
Radiation impacting bowel; laparotomyBowel obstructionHistory: abdominal pain, distention, vomiting, constipation
Exam: tenderness, abdominal guarding, distension (acute episode)
Obtain KUB in patients with clinical symptoms of obstruction
Surgical consultation in patients unresponsive to medical management
Pelvic surgery; cystectomyFecal incontinenceHistory: chronic constipation, fecal soiling
Rectal exam

Hepatobiliary

Hepatic complications resulting from childhood cancer therapy are uncommon and observed primarily as acute treatment toxicities.[30] Dutch investigators observed hepatobiliary dysfunction in 8.7% of 1,362 long-term survivors (12.4 years median follow-up since diagnosis) evaluated by alanine aminotransferase (ALT) for hepatocellular injury and gamma-glutamyltransferase (GGT) for biliary tract injury. Cases with a history of viral hepatitis and a history of veno-occlusive disease were excluded. Predictors for elevated ALT and GGT by multivariable analysis included treatment with radiation therapy involving the liver, higher body mass index, higher alcohol intake, and longer follow-up time; older age at diagnosis was only significantly associated with elevated GGT levels.[31]

Recipients of HSCT are the exception to this rule because these individuals frequently experience chronic liver dysfunction related to microvascular, immunologic, infectious, metabolic, and toxic etiologies. Chemotherapeutic agents with established hepatotoxic potential include antimetabolite agents like 6-mercaptopurine, 6-thioguanine, methotrexate, and rarely, dactinomycin. Veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS) and cholestatic disease have been observed after thiopurine administration, especially 6-thioguanine. Progressive fibrosis and portal hypertension has been reported in a subset of children who developed VOD/SOS after treatment with 6-thioguanine.[32,33,34] Acute, dose-related, reversible VOD/SOS has been observed in children treated with dactinomycin for pediatric solid tumors.[35,36] In the transplant setting, VOD/SOS has also been observed after conditioning regimens that have included cyclophosphamide/TBI, busulfan/cyclophosphamide and carmustine/cyclophosphamide/etoposide.[37] Because high-dose cyclophosphamide is common to all of these regimens, toxic cyclophosphamide metabolites resulting from the agent's variable metabolism have been speculated as a causative factor.

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