Cytotoxic and genotoxic monitoring of sickle cell anaemia patients treated with hydroxyurea

被引:18
作者
Khayat, AS
Antunes, LM
Guimaraes, AC
Bahia, MO
Lemos, JAR
Cabral, IR
Lima, PDL
Amorim, MIM
Cardoso, PCS
Smith, MAC
Santos, RA
Burbano, RR
机构
[1] Fed Univ Para, Ctr Ciencias Biol, Dept Biol, Lab Citogenet Humana, BR-66075900 Belem, Para, Brazil
[2] Fac med Triangulo Mineiro, Dept Ciencias Biol, Uberaba, MG, Brazil
[3] Ctr Hemoterapia & Hematol Estado Para, Belem, Para, Brazil
[4] Univ Amazonia, Belem, Para, Brazil
[5] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Genet, Sao Paulo, Brazil
[6] Univ Fed Sao Paulo, Escola Paulista Med, Disciplina Genet, Dept Morfol, Sao Paulo, Brazil
关键词
hydroxyurea; sickle cell anaemia; foetal haemoglobin; genotoxic monitoring;
D O I
10.1007/s10238-006-0091-x
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Very satisfactory results have been obtained with the treatment of sickle cell anaemia with hydroxyurea (HU), an antineoplastic drug. This is because it significantly increases the levels of foetal haemoglobin. Nevertheless, inadequate dosages or prolonged treatment with this pharmaceutical can provoke cytotoxicity or genotoxicity, increasing the risk of neoplasia. We monitored patients under treatment with HU for possible mutagenic effects, through cytogenetic tests (mitotic index and chromosome aberrations) for one year. Checking at two-month intervals, the cytotoxic effect was not evident. There was no evidence of genotoxicity under the conditions of our experiment. However individuals treated with HU should be constantly monitored, as an absence of genotoxicity could be transitory; the mitotic index should also be observed, as an indicator of cytotoxicity.
引用
收藏
页码:33 / 37
页数:5
相关论文
共 25 条
  • [1] THE MUTAGENICITY OF 5-AZACYTIDINE AND OTHER INHIBITORS OF REPLICATIVE DNA-SYNTHESIS IN THE L5178Y MOUSE LYMPHOMA CELL
    AMACHER, DE
    TURNER, GN
    [J]. MUTATION RESEARCH, 1987, 176 (01): : 123 - 131
  • [2] Ayres M, 2000, BioEstat 2.0: Aplicacoes estatisticas nas areas das ciencias biologicas e medicas
  • [3] HYDROXYUREA AS TREATMENT FOR SICKLE-CELL-ANEMIA
    CHARACHE, S
    [J]. HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA, 1991, 5 (03) : 571 - 583
  • [4] CHOY BK, 1988, CANCER RES, V48, P2029
  • [5] GENE FOR M1-SUBUNIT OF RIBONUCLEOTIDE REDUCTASE IS AMPLIFIED IN HYDROXYUREA-RESISTANT HAMSTER-CELLS
    COCKING, JM
    TONIN, PN
    STOKOE, NM
    WENSING, EJ
    LEWIS, WH
    SRINIVASAN, PR
    [J]. SOMATIC CELL AND MOLECULAR GENETICS, 1987, 13 (03) : 221 - 233
  • [6] de Lima Patricia Danielle Lima, 2003, Genet Mol Res, V2, P328
  • [7] de Montalembert M, 1999, PATHOL BIOL, V47, P55
  • [8] Three-year follow-up of hydroxyurea treatment in severely ill children with sickle cell disease
    deMontalembert, M
    Belloy, M
    Bernaudin, F
    Gouraud, F
    Capdeville, R
    Mardini, R
    Philippe, N
    Jais, JP
    Bardakdjian, J
    Ducrocq, R
    MaierRedelsperger, M
    Elion, J
    Labie, D
    Girot, R
    [J]. JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY, 1997, 19 (04) : 313 - 318
  • [9] DeVita VT., 2001, CANC PRINCIPLES PRAC
  • [10] DONEHOWER RC, 1992, SEMIN ONCOL, V19, P11