ECE2008 Poster Presentations Bone and calcium (42 abstracts)
Osteopenia/osteoporosis in adult thalassemic patients: contribution of growth hormone - insulin-like growth factor I deficiency
Massimo Scacchi 1 , Leila Danesi 1 , Agnese Cattaneo 1 , Elena Valassi 1 , Francesca Pecori Giraldi 1 , Crocetta Argento 2 , Emanuela D’Angelo 3 , Nadia Mirra 3 , Laura Zanaboni 4 , Benedetta Tampieri 4 , Maria Domenica Cappellini 4 & Francesco Cavagnini 1
1Chair of Endocrinology, University of Milan, IRCCS San Luca, Milan, Italy; 2Azienda Ospedaliera San Giovanni di Dio, Agrigento, Italy; 3Second Pediatric Clinic, University of Milan, Fondazione Policlinico Mangiagalli Regina Elena, Milan, Italy; 4Department of Internal Medicine, University of Milan, Milan, Italy.
GH and IGF-I exert an important role in the control of bone formation. Osteopenia and osteoporosis are a frequent recurrence in patients with thalassemia. Due to the high prevalence of GH deficiency (GHD) in adult thalassemic patients (Scacchi et al., Clin Endocrinol 2007), we investigated the possible role of GH - IGF-I abnormalities in the pathogenesis of the osteopenia/osteoporosis of this disease.
Study: Sixty-four adult thalassemic patients (23 men and 41 women, age 31.4+6.8) were studied. BMD was assessed by DEXA at lumbar spine in 62 patients and at proximal femur in 58. All patients underwent GHRH plus arginine testing. Severe GHD was defined by GH peaks lower than 9 μg/l, partial GHD by GH peaks ranging from 9 to 16.5 μg/l. Blood samples for IGF-I measurement were collected.
Results: Lumbar osteoporosis and osteopenia were demonstrated in 74.1% and 22.5% of patients, respectively. Femoral osteoporosis and osteopenia were documented in 37.9% and 55.1% of patients, respectively. Severe GHD was demonstrated in 25% of patients, while 17.1% displayed partial GHD. IGF-I SDS was low, i.e. below −1.88, in 54.6% of patients. Lumbar T-score values were not correlated with either GH peaks or IGF-I SDS values. Femoral T-score values were positively correlated with GH peaks (r=0.38, P<0.005) and IGF-I SDS (r=0.39, P<0.005). Furthermore, mean femoral T-score was significantly lower in patients with severe GHD than in those with normal GH secretion (−2.94+0.25 vs −2.15+0.12, P<0.01).
Conclusions: GH-IGF-I deficiency appears to contribute to bone demineralization of adult thalassemic patients at femural, but not lumbar level. This observation fits in well with experimental and clinical data demonstrating a greater action of GH-IGF-I on cortical rather than trabecular bone.
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Endocrine Abstracts
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