Active acromegaly enhances spontaneous parathyroid hormone pulsatility

Mazziotti, Gherardo; Cimino, Vincenzo; Menis, Ernesto De; Bonadonna, Stefania; Bugari, Giovanna; Marinis, Laura De; Veldhuis, Johannes D.; Giustina, Andrea

doi:10.1016/j.metabol.2006.01.009

Cited by 13 publications

(6 citation statements)

References 42 publications

(57 reference statements)

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“…There is evidence suggesting lower peripheral bioavailability of vitamin D in acromegaly because of an increase in serum levels of vitamin D-binding protein (102,103). GH excess influences PTH pulsatility with prolongation of pulse duration and increase in pulse mass (104); however, the skeletal implications of these effects are unclear.…”

Section: Effects Of Gh Excess On Calcium and Phosphate Metabolismmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Bone disorders associated with acromegaly: mechanisms and treatment

Mazziotti

Lania

Canalis

2019

European Journal of Endocrinology

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Growth hormone (GH) and insulin-like growth factor-I (IGF-I) exert physiological actions on the skeleton throughout life, by stimulating longitudinal bone growth in children, the acquisition of bone mass during adolescence and the maintenance of skeletal architecture in adults. When GH and IGF-I are secreted in excess, bone remodeling is enhanced leading to deterioration of bone microstructure and impairment of bone strength. Indeed, acromegaly causes skeletal fragility, and vertebral fractures are reported in a remarkable number of subjects exposed to GH and IGF-I excess. The management of skeletal fragility in acromegaly is a challenge, since the awareness of this complication is low, the prediction of fracture risk is difficult to ascertain, the risk of fractures remains after the control of acromegaly and the effectiveness of bone-active drugs is unknown. This review is an update on bone disorders associated with acromegaly and provides a perspective of possible therapeutic approaches based on emerging pathophysiological and clinical information.

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Section: Effects Of Gh Excess On Calcium and Phosphate Metabolismmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Bone disorders associated with acromegaly: mechanisms and treatment

Mazziotti

Lania

Canalis

2019

European Journal of Endocrinology

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“…13,17,30,31 Due to the intrinsic characteristics of PTH physiological secretion with very frequent and small pulses, PTH pulsatility studies are complex to perform and this explains in part the lack of published data on this topic. PTH is measured with immunoradiometric assays (sensitivity about 1 pg·mL −1 ; intra- and inter-assay coefficients of variation between 4% and 6%).…”

Section: Assessment Of Pth Pulsatilitymentioning

confidence: 99%

“…49,50 Mazziotti et al . 31 evaluated whether GH excess in acromegaly could modify spontaneous pulsatile PTH secretion (Table 1). Five male patients with newly diagnosed active acromegaly and eight healthy subjects were evaluated by 3-min blood sampling for 6 h. Plasma PTH concentrations were evaluated by multiparameter deconvolution analysis and plasma PTH release profiles were also subjected to an approximate entropy estimate.…”

Section: Pth Pulsatility In Skeletal Diseasesmentioning

confidence: 99%

Parathyroid hormone pulsatility: physiological and clinical aspects

2015

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Parathyroid hormone (PTH) secretion is characterized by an ultradian rhythm with tonic and pulsatile components. In healthy subjects, the majority of PTH is secreted in tonic fashion, whereas approximately 30% is secreted in low-amplitude and high-frequency bursts occurring every 10–20 min, superimposed on tonic secretion. Changes in the ultradian PTH secretion were shown to occur in patients with primary and secondary osteoporosis, with skeletal effects depending on the reciprocal modifications of pulsatile and tonic components. Indeed, pathophysiology of spontaneous PTH secretion remains an area potentially suitable to be explored, particularly in those conditions such as secondary forms of osteoporosis, in which conventional biochemical and densitometric parameters may not always give reliable diagnostic and therapeutic indications. This review will highlight the literature data supporting the hypothesis that changes of ultradian PTH secretion may be correlated with skeletal fragility in primary and secondary osteoporosis.

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“…On the other hand, there may be subtle, but important effects of glucocorticoids on PTH secretory dynamics, with a decrease in the tonic release of PTH and an increase in pulsatile bursts of the hormone (19). These changes may lead to adverse effects on bone metabolism (20), not unlike potential effects of PTH in postmenopausal osteoporosis (21). Moreover, glucocorticoids may enhance the sensitivity to PTH by changing the number of PTH receptors and their affinity for PTH (22).…”

Section: Extraskeletal Effects Of Glucocorticoids On Bone Metabolismmentioning

confidence: 99%

Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects

Mazziotti¹,

Giustina²,

Canalis³

et al. 2007

Arq Bras Endocrinol Metab

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Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. Glucocorticoids have direct and indirect effects on the skeleton. They impair the replication, differentiation, and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are the most effective of the various therapies that have been assessed for the management of GIO. Anabolic therapeutic strategies are under investigation. Teriparatide seems to be also efficacious for the treatment of patients with GIO. RESUMO Osteoporose Induzida por Glicocorticóides: Aspectos Clínicos e Terapêuticos.A osteoporose induzida por glicocorticóides (OIG) é a forma mais comum de osteoporose secundária. Fraturas, que são freqüentemente assintomáticas, podem ocorrer em até 30-50% dos pacientes recebendo terapia glicocorticóide crônica. Fraturas vertebrais ocorrem logo após exposição aos glicocorticóides, ocasião em que a densidade mineral óssea (DMO) diminui rapidamente. As fraturas tendem a ocorrer mais com níveis elevados de DMO do que em mulheres com osteoporose da pós-menopausa. Os glicocorticóides têm efeitos diretos e indiretos sobre o esqueleto: eles impedem a replicação, a diferenciação e a função dos osteoblastos e induzem apoptose dos osteoblastos maduros e osteócitos. Esses efeitos levam à supressão da formação óssea, uma manifestação central da patogênese da OIG. Os glicocorticóides também favorecem a osteoclastogênese e, como conseqüência, aumentam a reabsorção óssea. Os bisfosfonatos são a mais efetiva das várias terapias que têm sido avaliadas para o manuseio da OIG. Estratégias terapêuticas com anabolizantes estão sendo investigadas. O teriparatídeo parece também ser eficaz no tratamento de pacientes com OIG. (Arq Bras Endocrinol Metab 2007;51/8

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Active acromegaly enhances spontaneous parathyroid hormone pulsatility

Cited by 13 publications

References 42 publications

MANAGEMENT OF ENDOCRINE DISEASE: Bone disorders associated with acromegaly: mechanisms and treatment

MANAGEMENT OF ENDOCRINE DISEASE: Bone disorders associated with acromegaly: mechanisms and treatment

Parathyroid hormone pulsatility: physiological and clinical aspects

Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects

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