Previous evidence supports a role for
growth hormone (GH)-
insulin-like growth factor (
IGF)-I deficiency in the pathophysiology of
osteopenia/
osteoporosis in adult
thalassemia. Moreover, serum
IGF-II has never been studied in this clinical condition. Thus, we elected to study the GH secretory status and the levels of circulating
somatomedins, correlating these parameters with bone mineral density (BMD) and
biochemical markers of bone turnover. A hundred and thirty-nine normal weight adult thalassemic patients (72 men and 67 women) were studied. Lumbar and femoral neck BMD were measured in 106/139 patients. Sixty-eight patients underwent
growth hormone releasing hormone plus
arginine testing. Measurement of baseline
IGF-I and
IGF-II was performed in all patients, while
osteocalcin,
C-terminal telopeptide of type I collagen (CTx), and urinary cross-linked N-telopeptides of
type I collagen (NTx) were assayed in 95 of them. Femoral and lumbar
osteoporosis/Z score below the expected range for age were documented in 61.3 and in 56.6 % of patients, respectively. Severe GH deficiency (GHD) was demonstrated in 27.9 % of cases, whereas
IGF-I SDS was low in 86.3 %. No thalassemic patients displayed circulating levels of
IGF-II below the reference range. GH peaks were positively correlated with femoral, but not lumbar, Z score. No correlations were found between GH peaks and
osteocalcin, CTx and NTx. GH peaks were positively correlated with
IGF-I values, which in their turn displayed a positive correlation with
osteocalcin, CTx, and NTx. No correlations emerged between
IGF-I values and either femoral or lumbar Z scores. No correlations were found between
IGF-II and any of the following parameters: GH peaks,
osteocalcin, CTx, NTx, femoral Z score, and lumbar Z score. Our study, besides providing for the first time evidence of a normal
IGF-II production in
thalassemia, contributes to a better understanding of the involvement of the
somatotropin-
somatomedin axis in the pathophysiology of bone demineralization in this disease. In particular, the contribution of GHD to femoral
osteoporosis appears to be likely mediated by locally produced rather than circulating
IGF-I.