Scintigraphic, biochemical, and clinical response to zoledronic acid treatment in patients with Paget’s disease of bone

Avramidis, Athanassios N.; Polyzos, Stergios A.; Moralidis, Efstratios; Arsos, Georgios; Efstathiadou, Zoe; Karakatsanis, K.; Grollios, Georgios; Kita, Marina

doi:10.1007/s00774-008-0852-6

Cited by 29 publications

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“…The patient was administered per os calcium and cholecalciferol supplements 10 days before ZOL infusion, as reported previously [10,11]. On physical examination before ZOL administration, her weight was 85 kg, height 1.61 m (ΒΜΙ 32.8 kg/m 2 ), and blood pressure 112/68 mm Hg.…”

Section: Case Reportmentioning

confidence: 99%

Zoledronic acid-induced transient hepatotoxicity in a patient effectively treated for Paget’s disease of bone

et al. 2010

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Bisphosphonate (BP)-induced hepatotoxicity is very rare. There are only a few reports of liver injury after BP treatment, including aledronate and risedronate in postmenopausal osteoporosis patients. We describe hereby the case of a patient with Paget's disease of bone accompanied by nonalcoholic fatty liver disease (NAFLD) who developed transient hepatotoxicity after zoledronic acid (ZOL) treatment. NAFLD had been diagnosed 1 year before presentation, based on liver ultrasonography (US). One day after infusion, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT) were increased by 8.1, 6.7, and 6.7 times, respectively, compared with pretreatment values. Serum bilirubin remained normal. US revealed hepatic mild homogenous brightness without focal lesion of the liver or biliary ducts. Subsequent biochemical and serologic investigation did not reveal a specific liver or systematic disease. The patient remained asymptomatic, and ALT, AST, and GGT were normalized 7 days post-treatment. Although the mechanism by which ZOL may cause liver damage is elusive, physicians should be aware of this possible adverse effect and ZOL cautiously administered in NAFLD patients.

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Section: Case Reportmentioning

confidence: 99%

Zoledronic acid-induced transient hepatotoxicity in a patient effectively treated for Paget’s disease of bone

et al. 2010

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“…No patient experienced symptoms or signs of hypocalcemia. Interestingly, PTH remained significantly increased by 90% (range 20-252%) 3 months (11.6±8.7 vs. 6.8±5.7 pmol/L at baseline, p<0.05) after ZOL infusion and returned to baseline levels at 12 months (7.5±4.8 pmol/L, p=ns vs. baseline), although calcium was normalized by the tenth day (2.35±0.13 mmol/L, p=ns vs. baseline) in all patients [2].It seems that PTH increase after treatment is compensatory in order to maintain normocalcemia. The ability of the parathyroid gland to react prevents long-term hypocalcemia, by increasing renal reabsorption of calcium and vitamin D production and by stimulating osteoclasts.…”

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Transient secondary hyperparathyroidism following intravenous infusion of zoledronic acid

Polyzos

Anastasilakis

Terpos

2009

Support Care Cancer

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Dear Editor, We have read with interest the paper of Sayin and Yazici [1], describing a case of secondary hyperparathyroidism following multiple intravenous zoledronic acid (ZOL) infusions in a patient with stomach lymphoma and bone metastases. The authors supported that serum parathyroid hormone (PTH) continued to increase, despite serum calcium and vitamin D normalization, until ZOL infusions were stopped.Hypocalcemia has been described after ZOL, as well as after other bisphosphonates (BPs), in various conditions, including bone metastases, Paget's disease of bone (PDB), and osteoporosis. Transient secondary hyperparathyroidism after a single ZOL infusion has previously been observed in a cohort of nine patients with active PDB [2]. These patients had normal serum calcium, magnesium, and vitamin D and no evidence of hyperparathyroidism or hypoparathyroidism at baseline. They had received calcium carbonate (1,500 mg) and vitamin D (400 IU) daily for 10 days before, as well as after the infusion, until serum calcium was normalized. ZOL effectively restricted PDB activity, as it was shown by the significant reduction in total serum alkaline phosphatase (322±211 IU/L at baseline vs. 101±36 IU/L at 3 months vs. 93±42 IU/L at 12 months) and in the scintigraphic index of involvement, a dimensionless marker for the per patient activity of the disease (14.4±7.6 vs. 7.2±1.8 vs. 5.5±2.5, respectively) and the scintigraphic ratio, a dimensionless marker for the per lesion activity of the disease (12.8±7.7 vs. 7.0±2.9 vs. 5.8±3.0, respectively) [2]. Other bone turnover markers, such as bone-specific serum alkaline phosphatase and C-terminal cross-linking telopeptide of type I collagen (CTX), follow a similar pattern of reduction, as it has been shown elsewhere [3]. However, a significant hypocalcemia [decrease of 10% (range 4-23%) in the mean serum calcium] on the third day (2.43±0.13 vs. 2.18±0.10 mmol/L at baseline, p<0.05) was observed accompanied by a mild but not statistically significant hypophosphatemia. No patient experienced symptoms or signs of hypocalcemia. Interestingly, PTH remained significantly increased by 90% (range 20-252%) 3 months (11.6±8.7 vs. 6.8±5.7 pmol/L at baseline, p<0.05) after ZOL infusion and returned to baseline levels at 12 months (7.5±4.8 pmol/L, p=ns vs. baseline), although calcium was normalized by the tenth day (2.35±0.13 mmol/L, p=ns vs. baseline) in all patients [2].It seems that PTH increase after treatment is compensatory in order to maintain normocalcemia. The ability of the parathyroid gland to react prevents long-term hypocalcemia, by increasing renal reabsorption of calcium and vitamin D production and by stimulating osteoclasts. The effect of PTH on osteoclasts is restricted in patients taking BPs, depending on the potency of the BP. The newer more potent aminobisphosphonates, such as ZOL, initially create a bone remodeling imbalance by strongly suppressing bone

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“…El control del dolor fue rápido (entre 10 días y 1 mes) y se mantuvo durante 1 año (26). El control del dolor se asocia a la reducción de la FA, pero también se han descrito casos de mejoría del dolor en pacientes con PBD evolucionada, que no presen-…”

Section: Eficacia En El Control De Las Manifestaciones Clínicasunclassified

Enfermedad de Paget. Actualización en el tratamiento médico

Bachiller‐Corral

2015

acta reuma

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ResumenLa enfermedad de Paget del hueso (EP) se caracteriza por un aumento del metabolismo óseo localizado en uno o varios focos del esqueleto. El mecanismo fisiopatológico inicial es el aumento de la resorción ósea osteoclástica, y los bifosfonatos son el tratamiento de elección. Las indicaciones aceptadas para el tratamiento de la EP incluyen el dolor óseo y las manifestaciones del sistema nervioso. También se recomienda el tratamiento antes de una cirugía ósea para prevenir el sangrado excesivo o la hipercalcemia. Los pacientes con una alta actividad metabólica (nivel de fosfatasa alcalina más de dos veces el límite superior normal) también deben ser tratados. Una indicación controvertida es el tratamiento en pacientes asintomáticos para prevenir las complicaciones evolutivas.Los nuevos bifosfonatos, como el ácido zoledrónico, con una gran potencia y afinidad de unión a la hidroxiapatita, son muy útiles para el control de la actividad de la enfermedad a corto y largo plazo. El ácido zoledrónico está indicado para EP en Europa y América en una sola dosis de 5 mg, administrado por vía intravenosa. En 2005, un ensayo controlado con risedronato, demostró una respuesta terapéu-tica en el 96% de los pacientes tratados con ácido zoledrónico, que es significativamente mayor que los resultados obtuvieron por otros bisfosfonatos. En el estudio de extensión, se demostró que la duración de la respuesta era de al menos 6 años y medio tras la infusión del fármaco.El ácido zoledrónico ha cambiado el manejo de la enfermedad de Paget. Queda pendiente demostrar si el control metabólico eficaz y prolongado que se consigue con los nuevos fármacos, reducirá el riesgo de complicaciones tales como la deformidad, las fracturas, la sordera y la artropatía secundaria.

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Scintigraphic, biochemical, and clinical response to zoledronic acid treatment in patients with Paget’s disease of bone

Cited by 29 publications

References 29 publications

Zoledronic acid-induced transient hepatotoxicity in a patient effectively treated for Paget’s disease of bone

Zoledronic acid-induced transient hepatotoxicity in a patient effectively treated for Paget’s disease of bone

Transient secondary hyperparathyroidism following intravenous infusion of zoledronic acid

Enfermedad de Paget. Actualización en el tratamiento médico

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