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

Having noted symptomatic osteoporotic vertebral collapse in young adul t survivors of childhood malignancy, bone mineral density (BMD) was ex amined at three sites by dual-energy X-ray absorptiometry in 64 patien ts treated in childhood for intracranial malignancy (group 1; n = 21) or acute leukaemia (group 2; n = 43). Patients in group 1 were selecte d for growth hormone deficiency (GHD) by auxological and biochemical c riteria before the end of puberty (Tanner stage V). Seven patients (si x men; mean (+/- SEM) age at study, 28.0 +/- 2.9 years; mean age at di agnosis, 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 me n; 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 nor mal in the GH-treated patients at the femoral neck (98.4 +/- 3.8% of c ontrol), lumbar spine (100.4 +/- 6.1% of control) and Ward's triangle (101.0 +/- 6.1% of control) but markedly reduced in the untreated grou p (femoral neck, 81.2 +/- 2.6% of control (p = 0.002); lumbar spine, 7 9.1 +/- 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 trea ted for acute lymphoblastic leukaemia (ALL) and were in three subgroup s. Fifteen (ten men; mean age at study, 22.1 +/- 0.8 years; mean age a t diagnosis, 5.7 +/- 0.8 years) had no auxological evidence of GHD, te n (six men; mean age at study, 18.8 +/- 0.7 years; mean age at diagnos is, 6.6 +/- 1.2 years) received GH therapy for a mean of 2.6 years (ra nge, 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; mea n 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 chil dhood was also studied. The patients with AML had normal bone densitie s at all three sites (femoral neck, 106 +/- 6.1% of control; lumbar sp ine, 96.5 +/- 3.0% of control; Ward's triangle, 110.8 +/- 9.3% of cont rol), 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; Wa rd's triangle, 108.3 +/- 3.2% of control). The patients with ALL and G HD not treated with GH had markedly reduced BMD at all three sites (fe moral neck, 90.5 +/- 2.6% of control; lumbar spine, 88.4 +/- 2.5% of c ontrol; 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 triangl e, 106.2 +/- 4.9% of control). It is concluded that GHD during childho od and adolescence predisposes to osteopenia.