Eradication of Cryptosporidium in a child undergoing maintenance chemotherapy for leukemia using high dose azithromycin therapy.
Russell TS. Lynch J. Ottolini MG.
Department of Pediatric Infectious Diseases, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.
PURPOSE: To describe a case of severe diarrhea caused by Cryptosporidium in a patient undergoing maintenance chemotherapy. Important aspects of disease caused by Cryptosporidium, including diagnosis and treatment, are also reviewed. METHODS AND RESULTS: A 4-year-old boy with acute lymphoblastic anemia in remission had a prolonged course of diarrhea and wasting. C. parvum was identified in the gastrointestinal tract by biopsy and in the stool using modified acid fast staining. Improvement in the stool consistency was noted after 3 days of therapy with azithromycin, and, after 14 days of therapy, Cryptosporidium oocysts could no longer be identified in the stool. CONCLUSIONS: C. parvum should be considered in all immunocompromised patients with severe or prolonged diarrhea, especially if there is no blood or leukocytes in the stool. Because Cryptosporidium is not always tested for in a routine ova and parasite examination, the lab should be notified if it is in the differential diagnosis. Azithromycin therapy may prove beneficial in the treatment of intestinal Cryptosporidium in immunocompromised individuals.
Hepatocellular carcinoma in children associated with Gardner syndrome or familial adenomatous polyposis.
Gruner BA. DeNapoli TS. Andrews W. Tomlinson G. Bowman L. Weitman SD.
Department of Pediatrics, University of Texas Health Science Center, San Antonio 78284-7810, USA.
PURPOSE: Gardner syndrome, a variant of familial adenomatous polyposis, is characterized by colonic polyps that undergo malignant change and benign and malignant extracolonic lesions. Tumors frequently associated with Gardner syndrome include carcinoma of the ampulla of Vater, papillary carcinoma of the thyroid, and, in children, hepatoblastoma. The childhood malignancies often precede the appearance of other manifestations by several years. PATIENTS AND METHODS: Two patients are described. Gardner syndrome was diagnosed in a 15-year-old girl with fibrolamellar hepatocellular carcinoma after desmoid tumors and colonic polyposis developed. Classic hepatocellular carcinoma was also diagnosed in a 9 1/2-year-old boy with familial adenomatous polyposis. RESULTS: In patient 1, the diagnosis of fibrolamellar hepatocellular carcinoma preceded the diagnosis of Gardner syndrome by almost 2 years. The diagnosis was confirmed by identifying a germline mutation of the adenomatous polyposis coli (APC) gene. This is the first patient reported with fibrolamellar hepatocellular carcinoma associated with Gardner syndrome. Patient 2 had a strong family history of familial adenomatous polyposis but no manifestations of Gardner syndrome. He was not tested for the APC mutation. The current literature and previously reported cases of hepatocellular carcinoma in patients with Gardner syndrome or familial adenomatous polyposis are reviewed. CONCLUSIONS: Because hepatocellular carcinoma is uncommon in the pediatric and adolescent population, it is important to consider the possibility of Gardner syndrome or familial adenomatous polyposis in these patients.