GH-Deficient Survivors of Childhood Cancer: GH Replacement during Adult Life

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Abstract
Childhood survivors of cancer are prone to a number of ad- verse sequelae related to the therapeutic interventions un- dertaken to achieve remission. The endocrine system is fre- quently affected; hypothalamo-pituitary dysfunction, in particular GH deficiency, is common after cranial irradiation. It is unclear to what extent GH deficiency contributes to the abnormalities observed in adult survivors of childhood can- cer, and whether GH replacement reverses these anomalies. We compared 27 GH-deficient survivors of childhood cancer with 27 adult age- and sex-matched controls and went on to replace GH in the patient group to determine whether GH resulted in improvements of the baseline abnormalities. The GH-deficient survivors of childhood cancer had an ad- verse lipid profile (total cholesterol, 5.4 vs. 4.6 mM, P 0.004; high-density lipoprotein cholesterol, 1.05 vs. 1.6 mM, P < 0.001; and triglycerides, 1.3 vs. 1.0 mM, P < 0.001) and were os- teopenic (lumbar spine z-score, 1.53 vs. 0.31 SD score, P < 0.001; femoral neck z-score, 1.23 vs. 0.27 SD score, P 0.02); additionally, the female subgroup had an increased percent- age body fat (43.6 vs. 32.8%, P 0.016). In keeping with the selection criterion, quality of life in the patient cohort, rela- tive to the healthy controls, was severely impaired (adult GH- deficiency assessment (AGHDA), 15.5 (range, 8-25) vs. 1 (range, 0-19), P < 0.0001; psychological general well-being schedule, 67.5 (range, 18-86) vs. 89.0 (range, 51-104), P < 0.0001). After 12 months of GH replacement, small (but significant) improvements were observed in body composition in the male subgroup (waist-hip ratio, 0.871 vs. 0.863, P < 0.05); and in the female cohort, total cholesterol (6.0 vs. 5.2 mM, P 0.01) and triglyceride (2.1 vs. 1.4 mM, P 0.01) levels fell. Bone mineral density improved in only one of the four sites studied (ultra- distal radius, 1.21 vs. 1.09, P 0.048) after a median dura- tion of GH therapy of 18 months. Quality of life improved dramatically by 3 months (AGHDA, 15.5 vs. 10.0, P < 0.001), and the improvement was maintained at 12 months (AGHDA, 15.5 vs. 9.0, P < 0.001). Importantly, there was no clinical sugges- tion of tumor recurrence during the 12 months of GH replacement. The minor improvements observed in body composition, the lipid profile, and bone mineral density in GH-deficient adult survivors of childhood cancer after 12-18 months of physiological GH replacement suggest that GH deficiency may not be the major etiological factor in their pathogenesis; the converse seems to be true for the quality of life status of these individuals. We propose that, as in patients with hypo- pituitarism caused by pituitary disease, the main indication for GH replacement in GH-deficient survivors of childhood cancer should be severe impairment of quality of life. (J Clin Endocrinol Metab 87: 129 -135, 2002)

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