Increased vertebral morphometric fracture in patients with postsurgical hypoparathyroidism despite normal bone mineral density

Mendonça, Maira Lupatelli; Pereira, Fernanda Aparecida Castro; Nogueira-Barbosa, Marcello Henrique; Monsignore, Lucas Moretti; Teixeira, Sara Reis; Watanabe, Plauto Christopher Aranha; Maciel, Léa Maria Zanini; Paula, Francisco José Albuquerque de

doi:10.1186/1472-6823-13-1

Cited by 73 publications

(63 citation statements)

References 37 publications

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“…Despite the tendency for higher BMD, its impact on longer term fracture risk has not been established in thalassemia. Indeed, in a group of nonthalassemic patients with surgical hypoparathyroidism, there was an increased frequency of morphometric vertebral fractures (141).…”

Section: H Hypoparathyroidismmentioning

confidence: 99%

Bone Disease in Thalassemia: A Molecular and Clinical Overview

et al. 2016

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Thalassemia bone disease is a common and severe complication of thalassemia-an inherited blood disorder due to mutations in the α or β hemoglobin gene. In its more severe form, severe anemia is present, and treatment with frequent red blood cell transfusion is necessary. Because the body has limited capacity to excrete iron, concomitant iron chelation is required to prevent the complications of iron overload. The effects of chronic anemia and iron overload can lead to multiple end-organ complications such as cardiomyopathy, increased risks of blood-borne diseases, and liver, pituitary, and bone disease. However, our understanding of thalassemia bone disease is incomplete and is composed of a complex piecemeal of risk factors that include genetic factors, hormonal deficiency, marrow expansion, skeletal dysmorphism, iron toxicity, chelators, and increased bone turnover. The high prevalence of bone disease in transfusion-dependent thalassemia is seen in both younger and older patients as life expectancy continues to improve. Indeed, hypogonadism and GH deficiency contribute to a failure to achieve peak bone mass in this group. The contribution of kidney dysfunction to bone disease in thalassemia is a new and significant complication. This coincides with studies confirming an increase in kidney stones and associated accelerated bone loss in the thalassemia cohort. However, multiple factors are also associated with reduced bone mineral density and include marrow expansion, iron toxicity, iron chelators, increased bone turnover, GH deficiency, and hypogonadism. Thalassemia bone disease is a composite of not only multiple hormonal deficiencies but also multiorgan diseases. This review will address the molecular mechanisms and clinical risk factors associated with thalassemia bone disease and the clinical implications for monitoring and treating this disorder.

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Section: H Hypoparathyroidismmentioning

confidence: 99%

Bone Disease in Thalassemia: A Molecular and Clinical Overview

et al. 2016

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“…Mendonça and cols. (19) recently performed a small study assessing the impact of hypoparathyroidism on BMD, frequency of subclinical vertebral fracture, and mandible morphometry. This study evaluated 33 postmenopausal women, 16 of whom had hypoparathyroidism, and 17 of whom were healthy controls matched for age, weight and height.…”

Section: Fracturesmentioning

confidence: 99%

Bone disease in hypoparathyroidism

Clarke

2014

Arq Bras Endocrinol Metab

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Hypoparathyroidism is a rare disorder that may be acquired or inherited. Postsurgical hypoparathyroidism is responsible for the majority of acquired hypoparathyroidism. Bone disease occurs in hypoparathyroidism due to markedly reduced bone remodeling due to the absence or low levels of parathyroid hormone. Chronically reduced bone turnover in patients with hypoparathyroidism typically leads to higher bone mass than in age-and sex-matched controls. Whether this increased bone density reduces fracture risk is less certain, because while increased bone mineralization may be associated with increased brittleness of bone, this does not appear to be the case in hypoparathyroidism. Treatment of hypoparathyroidism with recombinant parathyroid hormone may reduce bone mineral density but simultaneously strengthen the mechanical properties of bone. Arq Bras Endocrinol Metab. 2014;58(5):545-52 Keywords Hypoparathyroidism; bone disease; bone mineral density; bone histomorphometry; fractures; skeleton RESUMO O hipoparatireoidismo é uma enfermidade rara que pode ser adquirida ou herdada. Dentre as causas adquiridas dessa doença, destaca-se como maior responsável o hipoparatireoidismo pós-cirúrgico. As manifestações ósseas dessa patologia decorrem devido a uma diminuição marcada no remodelamento ósseo causada pela diminuição ou ausência do hormônio da paratireoide. Esse remodelamento ósseo cronicamente reduzido leva a um aumento da massa óssea, evidenciado quando indivíduos com hipoparatireoidismo são comparados a controles de mesma idade e sexo. Entretanto, não se sabe se esse aumento de massa óssea reduz o risco de fratura. Apesar de o aumento da massa óssea estar associado a um aumento da fragilidade óssea em algumas situações, este não parece ser o caso no hipoparatireoidismo. O tratamento com hormônio recombinante da paratireoide pode reduzir a densidade mineral óssea ao mesmo tempo em que melhora as propriedades mecânicas do osso. Arq Bras Endocrinol Metab. 2014;58(5):545-52Descritores

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“…29 In keeping with the importance of PTH for maintenance of trabecular bone, an increased prevalence of subclinical vertebral fractures indicative of vertebral fragility has been reported in patients with hypoparathyroidism. 30 Fracture healing studies have not, however, been reported in patients with hypoparathyroidism.…”

Section: Anabolic Effectsmentioning

confidence: 97%

Physiologic Actions of PTH I

Goltzman

2015

The Parathyroids

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Increased vertebral morphometric fracture in patients with postsurgical hypoparathyroidism despite normal bone mineral density

Cited by 73 publications

References 37 publications

Bone Disease in Thalassemia: A Molecular and Clinical Overview

Bone Disease in Thalassemia: A Molecular and Clinical Overview

Bone disease in hypoparathyroidism

Physiologic Actions of PTH I

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