Parathyroid hormone pulsatility: physiological and clinical aspects
Silvia Chiavistelli , Andrea Giustina , Gherardo Mazziotti
Bone Research ›› 2015, Vol. 3 ›› Issue (1) : 14049
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.
Osteoporosis: Altered hormone secretion may influence skeletal fragility
Further research is needed into changes in hormone secretion which may be associated with increased bone fragility in osteoporosis. Parathyroid hormone (PTH) is secreted by the parathyroid gland, and regulates levels of calcium in blood and bones. In young healthy individuals, around 70% of PTH secretion is continuous (to maintain a baseline level), while 30% of secretion is pulsatile – the hormone is released in short bursts, every 10–20 minutes. In a review of recent research, Andrea Guistina and co-workers at the University of Brescia, Italy, suggest that alterations to this normal pattern of secretion may exacerbate bone fragility, particularly in forms of osteoporosis triggered by hormonal alterations. The team found only a few studies linking PTH with bone disease progression, primarily because of difficulties in assessing spontaneous PTH secretion accurately.
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