Hypercalcemia is a relatively common clinical problem and a frequent laboratory finding, both in hospital and out-of-hospital practice. Calcium ions play a critical role in many cellular functions. Parathyroid hormone (PTH) and vitamin D are the most important hormones for regulating calcium. The main sources of serum calcium are intestinal absorption, stimulated by active vitamin D metabolites, and bone resorption, usually stimulated by PTH. Therefore, hypercalcemia can be classified as PTH-dependent (due to increased secretion of PTH by the parathyroid glands) and independent of PTH. The latter cases are attributable to increased bone resorption and/or increased intestinal absorption of calcium, induced by factors other than PTH. Among them, PTH-related protein (PTHrP) and locally produced cytokines are factors that often cause hypercalcemia in cancer patients [1]. Unregulated extrarenal synthesis of 1,25-dihydroxyvitamin D can also cause hypercalcemia, particularly in patients with chronic granulomatous disorders and in some patients with lymphoma [2].

Atherosclerosis, arteriosclerosis, vascular calcification and osteoporosis are common age-related disorders associated with high morbidity and mortality [1,2]. Due to the increased life expectancy in the Spanish population, these disorders are expected to become more and more frequent in the coming decades. Although recent work has been carried out on the development of non-invasive techniques for the early detection of vascular calcifications, such as pulse wave velocity and non-contrast carotid ultrasound, serum biochemical parameters continue to be the most widely used option for monitoring patients with bone metabolic disorders [3-5].

The Wnt signalling pathway is involved in a wide range of processes, including bone development and homeostasis [1]. In accordance with this, mutations have been identified in various components of the Wnt pathway that cause different musculoskeletal diseases [2]. The canonical Wnt pathway begins with the formation of a heterotrimeric complex between a co-receptor, LRP5/6, a ligand, WNT, and a receptor, FZD, which produces an accumulation of β-catenin that, once in the nucleus will activate the transcription of numerous important target genes for bone [1]. This activation is finely regulated by a series of extracellular inhibitors such as DKK1 and sclerostin that bind to LRP5/6, preventing the formation of the heterotrimeric complex. For DKK1 and sclerostin to exert their inhibitory activity, they must form another heterotrimeric complex with LRP5 and KREMEN1/2 or LRP4, respectively. Although in the case of DKK1 the presence of KREMEN does not seem to be necessary to carry out a correct inhibition, the presence of LRP4 is essential for the inhibitory function of sclerostin [3,4].

Proximal extremity fractures of the femur are a very common problem in today’s society and of great importance as there has been an increased incidence in the population. This increase is explained by the longer life expectancy in recent years, thus increasing the elderly population and, therefore, related diseases. This is particularly relevant in Spain which has, of late, seen a severe aging of the population [1].
Several epidemiological studies describe the incidence of hip fracture in Spain. In most cases these are local studies and carried out over short periods of time. National studies have been carried out, although to a lesser extent [2]. According to the Ministry of Health and Social Policy’s 2010 report “Hip fracture care in the hospitals of the National Health System” [3], a total of 487,973 cases of fracture were recorded between 1997 and 2008. In these figures and in those carried out in various local studies2, a predominance of cases in the female sex and an increase in the incidence in age over the years has been found.