Clinical endocrinology · 1997
Does growth hormone treatment increase chromosomal abnormalities?
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Bozzola M, Tettoni K, Severi F, Capra E, Danesino C, Scappaticci S
Аннотация
OBJECTIVE: The relationship between growth hormone (GH) therapy and malignancy, including leukaemias, remains controversial. In order to study this possible relationship further, we have investigated whether GH treatment induces chromosomal abnormalities in peripheral blood lymphocytes.
DESIGN: Open, prospective study in a University Hospital to examine peripheral blood mononuclear cells in subjects with GH-deficiency (GHD) before and during GH treatment.
SUBJECTS: Twelve idiopathic GHD patients, aged 1.8-12.5 years, were evaluated before and after 3, 6 and 12 months of GH therapy (0.6 IU/kg per week subcutaneously). Two additional GHD patients, aged 16.6 and 18 years, were studied 1 year after long-term GH therapy had been discontinued, and 12 age-matched healthy subjects were evaluated as controls.
METHODS: We examined the incidence of chromosome and chromatid breaks, fragments, structural rearrangements and aneuploidies in 100 metaphases for each blood sample. A total of 5300 cells was analysed in the 14 patients.
RESULTS: The proportion of cells with chromatid and chromosome breaks ranged from 0% to 6% in patients before treatment and from 1% to 5% in controls. During GH therapy the incidence of aneuploid metaphases ranged from 0% to 7% and was comparable with values observed in controls. Chromosomal loss and gain was random.
CONCLUSIONS: We observed no increase in chromosomal abnormalities in GH-treated patients when compared with age-matched healthy controls.
DESIGN: Open, prospective study in a University Hospital to examine peripheral blood mononuclear cells in subjects with GH-deficiency (GHD) before and during GH treatment.
SUBJECTS: Twelve idiopathic GHD patients, aged 1.8-12.5 years, were evaluated before and after 3, 6 and 12 months of GH therapy (0.6 IU/kg per week subcutaneously). Two additional GHD patients, aged 16.6 and 18 years, were studied 1 year after long-term GH therapy had been discontinued, and 12 age-matched healthy subjects were evaluated as controls.
METHODS: We examined the incidence of chromosome and chromatid breaks, fragments, structural rearrangements and aneuploidies in 100 metaphases for each blood sample. A total of 5300 cells was analysed in the 14 patients.
RESULTS: The proportion of cells with chromatid and chromosome breaks ranged from 0% to 6% in patients before treatment and from 1% to 5% in controls. During GH therapy the incidence of aneuploid metaphases ranged from 0% to 7% and was comparable with values observed in controls. Chromosomal loss and gain was random.
CONCLUSIONS: We observed no increase in chromosomal abnormalities in GH-treated patients when compared with age-matched healthy controls.