​aspx Accessed 17 Dec 2012 99 Ganda K, Puech M, Chen JS, Speerin

​aspx Accessed 17 Dec 2012 99. Ganda K, Puech M, Chen JS, Speerin R, Bleasel J, Center JR, Eisman JA, March L, Seibel MJ (2013) Models of care for the secondary PF-01367338 prevention of osteoporotic fractures: a systematic review and meta-analysis. Osteoporos Int 24:393–406 100. Little EA, Eccles MP (2010) A systematic review of the effectiveness of interventions to improve post-fracture investigation and management of patients at risk of osteoporosis. Implement Sci: IS 5:80PubMedCrossRef 101. International Osteoporosis

Foundation (2012) Stop at One: Make your first break your last-events. http://​www.​worldosteoporosi​sday.​org/​events-eng Accessed 16 Nov 2012 102. Global Coalition on Aging (2012) Welcome to the Global Coalition on Aging. http://​www.​globalcoalitiono​naging.​com/​ Accessed 16 Nov 2012″
“Introduction Adaptations in maternal calcium homeostasis

and balance selleckchem occur during late pregnancy and lactation to meet requirements for foetal bone mineralisation and calcium secretion into breast milk. In Western women, intestinal calcium absorption increases in pregnancy [1–3]. Little change in the maternal bone mineral status (bone mineral density or content) is observed, although an increase in bone remodelling is reported [3, 4]. During lactation, bone resorption and renal calcium conservation are increased in both Western and Gambian women with concomitant decreases in bone mineral status [1, 5–7]. selleck screening library changes P-type ATPase in maternal bone mineral status and bone resorption during pregnancy and lactation appear to be independent of calcium intake in populations with a wide range of habitual calcium intakes [3, 4]. Uncertainty exists about how maternal calcium metabolism and balance are regulated, particularly in women with very low calcium intakes. During pregnancy and early lactation, plasma PTH concentration (pPTH) is suppressed, but plasma 1,25-dihydroxyvitamin D (p1,25(OH)2D) is similar or elevated compared to non-pregnant, non-lactating women (NPNL) [3, 8, 9]. This may be explained partly by the increase in the plasma

concentration of PTH-related peptide (PTHrP). The role of PTHrP in the regulation of maternal calcium and bone metabolism is unclear, however, as it does not appear to respond to changes in plasma calcium [2, 4, 10], unlike PTH which remains responsive to changes in calcium metabolism during pregnancy and lactation despite its lower concentration [1, 11]. Earlier studies in Australia and USA applied calcium-loading (or oral calcium-tolerance) tests to investigate changes in calcium homeostasis in pregnant and lactating women with calcium intakes close to recommendations [1, 2]. The calcium-loading test utilizes a single oral dose of calcium and is designed to test the response of the calciotropic hormones and calcium handling in the intestine and kidney to provide a proxy measure of the rate of calcium absorption and renal calcium excretion [2, 12].

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