BONE MINERALIZATION AFTER TREATMENT OF GROWTH-HORMONE DEFICIENCY IN SURVIVORS OF CHILDHOOD MALIGNANCY

Having noted symptomatic osteoporotic vertebral collapse in young adult survivors of childhood malignancy, bone mineral density (BMD) was examined at three sites by dual-energy X-ray absorptiometry in 64 patients treated in childhood for intracranial malignancy (group 1; n = 21) or acute leukaemia (group 2; n = 43). Patients in group 1 were selected for growth hormone deficiency (GHD) by auxological and biochemical criteria before the end of puberty (Tanner stage V). Seven patients (six men; mean (+/- SEM) age at study, 28.0 +/- 2.9 years; mean age at diagnosis, 8.7 +/- 1.5 years) in this group had been treated with human pituitary growth hormone (GH) for 1-12 years; and 14 patients (nine men; mean age at study, 26.8 +/- 1.0 years; mean age at diagnosis, 10.7 +/- 1.4 years) had not received GH. Bone densities in group 1 were normal in the GH-treated patients at the femoral neck (98.4 +/- 3.8% of control), lumbar spine (100.4 +/- 6.1% of control) and Ward's triangle (101.0 +/- 6.1% of control) but markedly reduced in the untreated group (femoral neck, 81.2 +/- 2.6% of control (p = 0.002); lumbar spine, 79.1 +/- 4.1% of control (p = 0.04); Ward's triangle, 80.1 +/- 3.6% of control (p = 0.01)). The majority of patients in group 2 had been treated for acute lymphoblastic leukaemia (ALL) and were in three subgroups. Fifteen (ten men; mean age at study, 22.1 +/- 0.8 years; mean age at diagnosis, 5.7 +/- 0.8 years) had no auxological evidence of GHD, ten (six men; mean age at study, 18.8 +/- 0.7 years; mean age at diagnosis, 6.6 +/- 1.2 years) received GH therapy for a mean of 2.6 years (range, 0.5-5.0 years), while 14 patients (three men; mean age at study, 20.9 +/- 0.4 years; mean age at diagnosis, 5.1 +/- 0.8 years) had GHD but did not receive GH. A small group of four patients (three men; mean age at study, 23.2 +/- 2.1 years; mean age at diagnosis, 8.0 +/- 2.3 years) who had been treated for acute myeloid leukaemia (AML) in childhood was also studied. The patients with AML had normal bone densities at all three sites (femoral neck, 106 +/- 6.1% of control; lumbar spine, 96.5 +/- 3.0% of control; Ward's triangle, 110.8 +/- 9.3% of control), as did the patients with ALL who did not have GHD (femoral neck, 102.3 +/- 2.9% of control; lumbar spine, 98.6 +/- 1.7% of control; Ward's triangle, 108.3 +/- 3.2% of control). The patients with ALL and GHD not treated with GH had markedly reduced BMD at all three sites (femoral neck, 90.5 +/- 2.6% of control; lumbar spine, 88.4 +/- 2.5% of control; Ward's triangle, 94.5 +/- 3.7% of control), but those treated with GH had a BMD no different from control (femoral neck, 100.6 +/- 3.3% of control; lumbar spine, 95.7 +/- 4.6% of control; Ward's triangle, 106.2 +/- 4.9% of control). It is concluded that GHD during childhood and adolescence predisposes to osteopenia.