1
TI: Age-associated changes in the symptomatology of Guillain-Barre syndrome in children.
AU: Sakakihara-Y; Kamoshita-S
SO: Dev-Med-Child-Neurol. 1991 Jul; 33(7): 611-6
AB: The medical records were reviewed of 83 children with Guillain-Barre syndrome, with reference to the age-associated changes found in the initial symptoms, the intervals between the preceding illness and the onset of disease, and the patterns of affected cranial nerves. A close correlation was observed between cranial nerve involvement and respiratory complications. The findings suggest the involvement of nervous system maturation in the clinical manifestations of Guillain-Barre syndrome in children.
2
TI: Chromosome abnormalities and prognosis in childhood acute leukemia.
AU: Hayashi-Y; Hanada-R; Yamamoto-K
SO: Acta-Paediatr-Jpn. 1991 Aug; 33(4): 497-506
AB: We report here on the leukemic cell karyotypes of 134 children with acute nonlymphocytic leukemia (ANLL) examined at Saitama Children's Medical Center (SCMC), and of 88 children with acute lymphoblastic leukemia (ALL) referred to SCMC. The patients were mainly treated according to the protocol of the Tokyo Children's Cancer Study Group. Of 106 ANLL cases with adequate banding, 18% were normal, 34% had miscellaneous clonal abnormalities, and 48% were classified into known cytogenetic subgroups: t(8;21) (n = 21), 11q23 abnormalities (n = 14), -7/del(7q) (n = 6), inv (16)/del(16) (n = 5), and t(15;17) (n = 5). According to the FAB classification, M7 (21.7%) were more frequent than in previous reports because this study included a number of Down's Syndrome patients with M7 morphology. The present study confirmed the well-known association of t(15;17) with M3, t(8;21) with M2, 11q23 abnormalities with M4 and M5, and inv (16)/del(16) with M4. Patients with t(8;21) or inv (16)/del(16q) ANLL fared no better overall than the entire group. Of 51 ALL cases with adequate banding, 13.7% were normal, and 86.3% were classified into abnormal subgroups: translocation (n = 14), hyperdiploidy (greater than 50) (n = 13), and miscellaneous abnormalities (n = 17). Cases with hyperdiploidy (greater than 50) were restricted to a common phenotype and fared better overall than the entire group. Patients with translocation were found in all phenotypes, and had a poor prognosis. We concluded that childhood acute leukemia could be subgrouped according to karyotypic patterns, and that patients with translocations had a poor prognosis in ALL as well as ANLL.
3
TI: [Clinical features of childhood Ph1 positive acute leukemia]
AU: Hayashi-Y; Nakazawa-S
SO: Rinsho-Ketsueki. 1991 Apr; 32(4): 338-44
AB: Clinical, immunologic, cytogenetic and molecular studies were performed on 9 patients with childhood Ph1 positive acute leukemia. FAB-L1 was found in 2 patients, L2 in 5 patients, and M1 and M2 in each patient. Six patients were older than 10 years old, and white blood cell count of 5 patients was more than 10(5)/microliters. All but one patient have died within 18 months. Immunologic analysis revealed that leukemic cells from all patients expressed lymphoid antigens CD10 and CD19, and myeloid antigen, CD13, was expressed on leukemic cells from 3 patients initially, and from 6 patients after short term in vitro culture without stimulation. bcr rearrangements were not observed in 3 patients tested. RNA analysis showed that 5 patients expressed P190bcr-abl pattern and one patient expressed P210bcr-abl pattern using polymerase chain reaction study. We conclude that Ph1 positive acute leukemia had a poor prognosis and differentiate into both myeloid and lymphoid lineages as well as chronic myelogenous leukemia (CML), and that this disease could not be possibly distinguished from CML by use of the molecular studies.
　
　　　　　　　　　　　　　　　　　　　　　　　　　

Edited by Toshio Hishi