Revista de Osteoporosis y Metabolismo Mineral

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Author: Romm

Osteoporosis in men and steroids

Osteoporosis is a bone disease characterized by a decrease in bone mineral density (BMD) and an increased risk of fragility fractures. Osteoporotic fractures, particularly hip fractures, cause significant mortality and morbidity in men and lead to considerable social costs in this population, including direct medical costs and indirect costs resulting from reduced quality of life, disability and death[1].
Of all osteoporotic fractures, it is hip fractures that contribute to the highest morbidity and mortality in men. Each year about 80,000 men will have a hip fracture. Of these, one in three will die during the first year after this hip fracture and another third will fracture again[2]. However, there is a lack of awareness among healthcare professionals about the need to screen men for osteoporosis so that male osteoporosis remains largely underdiagnosed and untreated.

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FGF-23 and pth, mirror hormones. Their role in bone metabolism

Conventionally, calcium, phosphorus, calcitriol and PTH were considered the only regulators of bone and mineral metabolism. In recent years, this axis of regulation has been complicated due to emergence of other factors with a crucial role in bone and mineral metabolism, such as fibroblast growth factor 23 (FGF-23) and the so-called klotho anti-aging protein.

Biological actions of FGF-23 and PTH
Biological action of FGF-23
FGF-23 is a 251 amino acid protein synthesized and secreted by bone cells, mainly osteoblast[1]. FGF-23 has been identified as the main regulatory factor of phosphorus metabolism, a critical element for maintaining skeletal integrity and for the development of multiple enzymatic processes[2]. In addition, in the last decade it has been attributed a notable role in the pathophysiology of vascular calcifications[3] and cardiovascular disease (CV), both in the general population[4-6] and in patients with chronic kidney disease[7].

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Anti-resorptives in the management of osteoporosis

Antiresorptive (or antiresorptive) drugs are the cornerstone of osteoporosis treatment. For decades, they have been considered the first step in treating this disease, although more recently some have been discontinued as indication. Others do not always have to be used as the first therapy in the current sequential treatments supported by the main scientific societies. There are five classes of purely antiresorptive drugs: bisphosphonates (BF), estrogen, selective estrogen receptor modulators (SERMs), calcitonin, and monoclonal antibodies against the activating receptor for nuclear factor κB ligand (RANKL) such as denosumab. For its part, a dual-action antiresorptive and osteoforming drug (strontium ranelate) was widely used from 2004 until its marketing cessation in 2017 in Europe for the reasons that will be detailed later. The treatments to be developed here are based on studies in postmenopausal women, although they can be extrapolated to men and to glucocorticoid-induced osteoporosis, although with less evidence[3].

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Health and economic impact of the use of vitamin D/calcium for fracture prevention: literature review

Osteoporotic fractures, especially those of the hip, are one of the main causes of disability in the elderly population, triggering a considerable decrease of life quality and lifespan. Besides, more than 30% of people die during the first year after suffering one of these fractures[1]. In 2010, the European Union recorded nearly 3.5 million fragility-induced fractures that led to 43,000 deaths. From an economical point of view, these fractures meant an expenditure of 37 billion euros, a sum that is expected to rise by 52% in 2025[2].
Vitamin D and calcium are essential compounds for bone metabolism and prevention of osteoporotic fractures. Two recent meta-analyses have reported that low levels of 25(OH)D are related to the increase of fragility-induced fractures due to bone mass loss and bone structure deterioration[3,4].

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Anabolic treatment of osteoporosis

Sodium fluoride (FNa) was used in the past as a bone-forming drug. Administering fluoride causes the number of osteoblasts to increase as the proliferation of osteoblastic precursors is stimulated, which leads to increased activity. In addition, it has antiresorptive capacity. The combination of osteogenic effect and inhibition of bone resorption leads to an increase in bone mineral density (BMD)[1].
Although the number of randomized clinical trials conducted with FNa is relatively limited, the salt types and dosages used in them, as well as their combination with calcium and vitamin D, make every trial very different from each other and therefore the global assessment of the results turns very difficult.
There are some studies that have shown an increase in BMD and a reduction in the risk of vertebral fractures, but in general the published results have been disappointing. Despite almost uniformly observing a statistically significant increase of BMD, these studies do not record a reduction in the risk of fractures[2].

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Generic selectors
Solo mostrar coincidencias exactas
Buscar en títulos
Buscar en cuerpo de texto
Buscar en artículos
Buscar en secciones de
Filtrar por categorías
11
12
120181004-en
120191101-en
120191102-en
120191104-en
120201201-en
120201202-en
120201203-en
120201204-en
120211301-en
120211302-en
13
920191101-en
920211301-en
920211302-en
Brief Original
Clinical Notes
Committees
Editorial
English
Index of Authors
Index of Communications
Letter to the Director
Letter to the Editor
Oral Communications
Original Articles
Osteology images
Position Paper
Poster Communications
Presentation
Reviews
SIBOMM News
Special Article
Special Documents

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