The aetiology of thalassemia major-induced osteoporosis is multifactorial. Up to now, bisphosphonates seem to be a promising therapy. Taurine is found in a high concentration in bone cells enhancing bone tissue formation and inhibiting bone loss. Recently we found a decrease taurine plasma level in children affected by osteogenesis imperfecta during neridronate (amino-bisphosphonate) therapy suggesting a possible interaction between pharmacological effect of this drug and taurine availability. On the basis of these results, we performed plasma and urine amino acid (AA) analysis in thalassemia major-induced osteoporosis before and after 12 months of neridronate treatment. Twelve patients, five males and seven females, aged from 20 to 29 years following a hypertransfusion treatment protocol were enrolled in the study. Patients were treated with neridronate infusion every one month (30 mg in 100 ml of saline). Plasma and urine specimens for AA analysis, bone mineral density, bone mineral content and vertebral project area were examined at baseline (T0) and after 12 months of treatment (T12). A significant decrease was observed for plasma level and urinary excretion of taurine (T0 vs. T12 = p < 0.01) whereas bone mineral content and vertebral projection area showed a statistical significant increase (TO vs. T12 = p < 0.05). These results and other experimental researches warrant further studies examining the long-term effect of taurine supplementation in association with neridronate treatment. (C) 2009 Elsevier Masson SAS. All rights reserved.

Taurine deficiency in thalassemia major-induced osteoporosis treated with neridronate / D'Eufemia, Patrizia; R., Finocchiaro; M., Celli; I., Raccio; Zambrano, Anna; Tetti, Martina; Smacchia, Maria Paola; Iacobini, Metello. - In: BIOMÉDECINE & PHARMACOTHÉRAPIE. - ISSN 0753-3322. - STAMPA. - 64:4(2010), pp. 271-274. [10.1016/j.biopha.2009.06.014]

Taurine deficiency in thalassemia major-induced osteoporosis treated with neridronate

D'EUFEMIA, Patrizia;ZAMBRANO, ANNA;TETTI, MARTINA;SMACCHIA, Maria Paola;IACOBINI, Metello
2010

Abstract

The aetiology of thalassemia major-induced osteoporosis is multifactorial. Up to now, bisphosphonates seem to be a promising therapy. Taurine is found in a high concentration in bone cells enhancing bone tissue formation and inhibiting bone loss. Recently we found a decrease taurine plasma level in children affected by osteogenesis imperfecta during neridronate (amino-bisphosphonate) therapy suggesting a possible interaction between pharmacological effect of this drug and taurine availability. On the basis of these results, we performed plasma and urine amino acid (AA) analysis in thalassemia major-induced osteoporosis before and after 12 months of neridronate treatment. Twelve patients, five males and seven females, aged from 20 to 29 years following a hypertransfusion treatment protocol were enrolled in the study. Patients were treated with neridronate infusion every one month (30 mg in 100 ml of saline). Plasma and urine specimens for AA analysis, bone mineral density, bone mineral content and vertebral project area were examined at baseline (T0) and after 12 months of treatment (T12). A significant decrease was observed for plasma level and urinary excretion of taurine (T0 vs. T12 = p < 0.01) whereas bone mineral content and vertebral projection area showed a statistical significant increase (TO vs. T12 = p < 0.05). These results and other experimental researches warrant further studies examining the long-term effect of taurine supplementation in association with neridronate treatment. (C) 2009 Elsevier Masson SAS. All rights reserved.
2010
osteoporosis; bisphosphonate; thalassemia major; taurine
01 Pubblicazione su rivista::01a Articolo in rivista
Taurine deficiency in thalassemia major-induced osteoporosis treated with neridronate / D'Eufemia, Patrizia; R., Finocchiaro; M., Celli; I., Raccio; Zambrano, Anna; Tetti, Martina; Smacchia, Maria Paola; Iacobini, Metello. - In: BIOMÉDECINE & PHARMACOTHÉRAPIE. - ISSN 0753-3322. - STAMPA. - 64:4(2010), pp. 271-274. [10.1016/j.biopha.2009.06.014]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/225911
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