The importance of nutrition factors such as calcium, vitamin D and vitamin K for the integrity of the skeleton is well known. Moreover, bone health is positively influenced by certain elements (e.g., zinc, copper, fluorine, manganese, magnesium, iron and boron). Deficiency of these elements slows down the increase of bone mass in childhood and/or in adolescence and accelerates bone loss after menopause or in old age. Deterioration of bone quality increases the risk of fractures. Monitoring of homeostasis of the trace elements together with the measurement of bone density and biochemical markers of bone metabolism should be used to identify and treat patients at risk of non-traumatic fractures. Factors determining the effectivity of supplementation include dose, duration of treatment, serum concentrations, as well as interactions among individual elements. Here, we review the effect of the most important trace elements on the skeleton and evaluate their clinical importance.
The protective role of nutrition factors such as calcium, vitamin D and vitamin K for the integrity of the skeleton is well understood. In addition, integrity of the skeleton is positively influenced by certain trace elements (e.g. zinc, copper, manganese, magnesium, iron, selenium, boron and fluoride) and negatively by others (lead, cadmium, cobalt). Deficiency or excess of these elements influence bone mass and bone quality in adulthood as well as in childhood and adolescence. However, some protective elements may become toxic under certain conditions, depending on dosage (serum concentration), duration of treatment and interactions among individual elements. We review the beneficial and toxic effects of key elements on bone homeostasis.
Objective: Apolipoprotein E (ApoE) is believed to play an important role in lipid metabolism and has been found to be related to diseases associated with ageing, the important characteristic of which is decline in circulating sex steroids, including androgen. Design: To find the relationships of levels of serum testosterone and its precursor, dehydroepiandrosterone (DHEA), to ApoE polymorphism in 113 postmenopausal Caucasian women. Methods: The ApoE genotype was assessed by polymerase chain reaction and CfoI endonuclease digestion. ApoE genotype distribution was as follows: E2/3, 15%; E3/3, 71.7%; E2/4, 1.8%; E3/4, 10.6; and E4/4, 0.89%. The differences in serum androgen levels between genotypes were evaluated by ANCOVA and least significant difference (LSD) multiple comparisons test after adjustment for body mass index, age and/or years since menopause. Results: Significant intergroup differences between the most frequent allele combination (2/3, 3/3 and 3/4) in serum DHEA levels were found (P , 0:05; ANCOVA). DHEA levels were higher in women with the E3/4 allele combination than in the E3/3 genotype (P , 0:01; LSD multiple comparisons). In serum testosterone levels, borderline intergroup differences were found (P , 0:07; ANCOVA). Higher testosterone levels were found in the E3/4 allele combination as compared with E3/3 (P , 0:05; LSD multiple comparisons). Dose effect of E4 allele analysis indicated higher serum DHEA and testosterone levels in women with the E4 allele present than in women with the E4 allele absent (P , 0:003 for DHEA, P , 0:007 for testosterone, ANCOVA). Conclusions: Circulating testosterone and DHEA are associated with the ApoE genotype, which may render women missing the allele E4 more susceptible to the development of some diseases associated with ageing and menopause.
The metabolic pathways that contribute to maintain serum calcium concentration in narrow physiological range include the bone remodeling process, intestinal absorption and renal tubule resorption. Dysbalance in these regulations may lead to hyper- or hypocalcemia. Hypercalcemia is a potentionally life-threatening and relatively common clinical problem, which is mostly associated with hyperparathyroidism and/or malignant diseases (90 %). Scarce causes of hypercalcemia involve renal failure, kidney transplantation, endocrinopathies, granulomatous diseases, and the long-term treatment with some pharmaceuticals (vitamin D, retinoic acid, lithium). Genetic causes of hypercalcemia involve familial hypocalciuric hypercalcemia associated with an inactivation mutation in the calcium sensing receptor gene and/or a mutation in the CYP24A1 gene. Furthermore, hypercalcemia accompanying primary hyperparathyroidism, which develops as part of multiple endocrine neoplasia (MEN1 and MEN2), is also genetically determined. In this review mechanisms of hypercalcemia are discussed. The objective of this article is a review of hypercalcemia obtained from a Medline bibliographic search.
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