American Journal of Pediatric Hematology/Oncology

None &NA;

The American journal of pediatric hematology/oncology

ERRATUM

勘误

Professor of Oncology and Pediatrics, University of Calgary, Director, Children's Cancer Program, Alberta Children's Hospital and Tom Baker Cancer Centre Professor of Pediatrics, University of Toronto, Chief, Division of Haematology/Oncology, Hospital for Sick Children

Max J. Coppes

Victor S. Blanchette

Tribute to Dr. Maureen Andrew

致敬莫琳·安德鲁博士

William S. Ferguson

J Pediatr Hematol Oncol

Exploring End-of-Life Care for Children With Cancer

探索儿童癌症临终关怀

Schnog, J. B. M.D.; van der Dijs, F. P. L. Ph.D.; Fokkema, M. R. Ph.D.; Muskiet, F. D. M.D.; Muskiet, F. A. J. Ph.D. Author Information

J. B. Schnog

F. P. L. van der Dijs

M. R. Fokkema

F. D. Muskiet

F. A. J. Muskiet

Folate Status Assessment and Folic Acid Supplements in Sickle Cell Disease

叶酸状态评估与镰状细胞病中的叶酸补充

This report encourages clinicians to consider a diagnosis of Carney's triad in patients with multifocal gastric stromal sarcoma, extraadrenal paraganglioma (predominantly mediastinal), or pulmonary chondroma. The authors conducted a retrospective 20-year survey at the Hospital for Sick Children and identified two children with Carney's triad. One child, presenting atypically with papilledema and fundal hemorrhages from malignant hypertension and benign intracranial hypertension from chronic iron-deficiency anemia, is the second patient ever to date be described with the complete Carney's triad of neoplasms at diagnosis. Another child presented more typically with gastric stromal sarcoma and pulmonary chondroma without paraganglioma. Carney's triad is a rare differential diagnosis for “idiopathic” hypertension or iron-deficiency anemia from chronic gastrointestinal bleeding. If missed, patients with Carney's triad may have the debilitating physical and mental consequences of chronic iron deficiency and may die of untreated prolonged hypertension and metastatic leiomyosarcoma.

Kathia Valverde

Melanie Henderson

Charles R. Smith

Susan Tallett

Helen S. L. Chan

Typical and Atypical Carney's Triad Presenting With Malignant Hypertension and Papilledema

典型和不典型卡尼三联征表现为恶性高血压和视乳头水肿

Division of Pediatric Hematology/Oncology/Blood and Marrow Transplantation Department of Pediatrics University of Minnesota School of Medicine Minneapolis U.S.A.

Nina Kadan-Lottick

Joseph P. Neglia

Pediatric Acute Lymphoblastic Leukemia: Redefining Outcomes

儿童急性淋巴细胞白血病：重新定义预后

To determine the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of cisplatin after a 72-hour continuous infusion of topotecan.Thirty-six children younger than age 22 years (range 3-21) with recurrent solid tumors were treated with cisplatin 45 to 75 mg/m2 infused over the course of 6 hours, followed by a 72-hour continuous infusion of topotecan 0.75 or 1 mg/m2 per day, followed by granulocyte colony stimulating factor (G-CSF), either immediately after treatment or when neutropenia developed. Patients were stratified by the presence of bone marrow tumor involvement and previous radiation to the bone marrow.The DLT was neutropenia (absolute neutrophil count <500/microL for >7 days). The MTD was cisplatin 60 mg/m2 and topotecan 1 mg/m2 per day followed by G-CSF starting 24 hours after chemotherapy for patients without marrow involvement or previous radiation to the bone marrow. An acceptable MTD was not found for patients with previous radiation to the bone marrow or bone marrow involvement or without the use of G-CSF starting 24 hours after chemotherapy was completed. Topotecan clearance and steady-state levels were determined. Limited evidence for antitumor activity with this combination was found in rhabdomyosarcoma.The recommended dose for phase II trials is cisplatin 60 mg/m2 followed by a 72-hour infusion of topotecan 1 mg/m2 per day with G-CSF starting 24 hours after the completion of topotecan.

Robert J. Wells

Joel M. Reid

Matthew M. Ames

Wen Lieu Mares

Mark D. Krailo

Nita L. Seibel

Revonda Mosher

Gregory H. Reaman

Susan R. Wiersma

Phase I Trial of Cisplatin and Topotecan in Children With Recurrent Solid Tumors: Children's Cancer Group Study 0942

复发性实体瘤儿童顺铂和拓扑替康的I期临床试验：儿童癌症组研究0942

Robert J. Arceci

Comments From the Editor-in-Chief

主编寄语

The authors describe a child with an unusual presentation of mesenteric inflammatory pseudotumor in association with leukemoid reaction. An 11-year-old-boy admitted with short stature was found to have an abdominal mass localized in the right lower quadrant. The leukocyte count was 92,000/mm3 with neutrophilic leukemoid reaction. Abdominal ultrasonography and computed tomography revealed a massive calcified mass in the pelvis. Total resection of the mass was performed and the pathologic diagnosis of inflammatory pseudotumor of the mesentery was made. Leukemoid reaction dramatically resolved within a few days after surgical resection. Physicians should be aware of the association of inflammatory pseudotumor, leukemoid reaction, and massive calcification.

Tezer Kutluk

Suna Emir

Ibrahim Karnak

Melda Gağlar

Münevver Büyükpamukçu

Mesenteric Inflammatory Pseudotumor: Unusual Presentation With Leukemoid Reaction and Massive Calcified Mass

肠系膜炎性假瘤：伴有类白血病反应和巨大钙化肿块的不典型表现

To study hepatic lesions in living children with sickle cell disease. Although such lesions are well known, the possibility of chronic persistent damage to the parenchyma resulting from the disease itself or iron overload is controversial.Sixteen children with sickle cell disease aged 15 months to 18 years were prospectively investigated out of 741 patients younger than 20 years registered at Hemominas Foundation, Brazil. Inclusion criteria for biopsy were as follows: five had positive anti-hepatitis C virus (HCV) antibody, two had positive hepatitis B virus (HBV) surface antigen and persistently increased levels of aminotransferases, and nine underwent biopsy during abdominal surgery.Children with B or C hepatitis were significantly older than the others and also had increased levels of both alanine and aspartate aminotransferases. Lobular architecture was preserved in all nonviral cases; mild to moderate sinusoidal dilatation was present in eight, hepatocellular regenerative activity in six, and focal necrosis and corresponding mild inflammatory infiltrate in three. No fibrosis or bile duct damage was observed. Mild to severe hemosiderosis was present in all children except one. The degree of iron overload was clearly associated with the number of previous blood transfusions. All five children with HCV had chronic hepatitis. One of the children with HBV had incomplete and the other had definite cirrhosis.These data indicate that chronic hepatic lesions in children with sickle cell disease may be caused by viral damage. Patients without evidence for viral etiology had reversible vascular lesions. Follow-up studies would be necessary to confirm this hypothesis but are precluded for ethical reasons. Hemosiderosis was not associated with fibrosis in any nonviral cases, but a larger number of patients would be necessary to establish valid conclusions.

Ana Lúcia Teixeira

Marcos Borato Viana

Mariza Leitão Valadares Roquete

Nivaldo Hartung Toppa

Sickle Cell Disease: A Clinical and Histopathologic Study of the Liver in Living Children

镰状细胞病：活体儿童肝脏的临床和组织病理学研究

Publication Information	Publisher: Raven Press，Publishing cycle: ，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2000，Proportion of original research papers: ，Self Citation Rate:， Gold OA Rate:

American Journal of Pediatric Hematology/Oncology

Journal Citation Format

A journal article with 1 author

A journal article with 2 authors

A journal article with 3 authors

A journal article with 5 or more authors

Books Citation Format

Thesis Citation Format

Web sites Citation Format

Patent Citation Format

Staying up late manually editing references? ivySCI automatically matches journals and helps you generate references with a single click.

Share Submission Experience