Clinical calcium最新文献

Pregnancy- and lactation-associated osteoporosis is a rare disease. Although researchers have reported a few cases, there are no established diagnostic criteria for pregnancy- and lactation-associated osteoporosis. However, a diagnosis can be easily obtained by an accurate medical interview, physical examination, imaging studies, and laboratory data, including bone mineral density measurement. This disease should be suspected when a woman presents with severe back pain in the late stages of pregnancy or the early postpartum period. An accurate and prompt diagnosis helps with appropriate treatment and prevents the progression of the disease.

Calcium metabolism changes dramatically during pregnancy and lactation because offspring needs a supply of calcium. Approximately 30g of calcium, which passes through the placenta, is accumulated in a fetus during pregnancy mostly in the third trimester, and 220-340mg/day of calcium is supplied via breast milk during lactation. However, there are elaborate mechanisms to maintain maternal calcium homeostasis, which differs during pregnancy and lactation. Extra required calcium supply to the offspring in neither pregnancy nor breastfeeding normally do not cause any adverse consequences to the maternal skeleton even if any oral intake of calcium or vitamin D are increased. This article reviews the adaptation in calcium kinetics during pregnancy and lactation. Vitamin D, calciotropic hormones, and bone metabolism are also reviewed.

In young women, why bone and calcium become a problem, it is because it is possible to delay the reach of the fracture threshold, even if the bone density in the future is acquired high bone density(bone mineral density:BMD)in the young period. In addition, the acquisition of maximum bone mass(peak bone mass:PBM)is an effective intervention to prevent future osteoporosis for around 18 years old before the age of 18. Factors that affect bone density include nutrition, dietary habits, physical activity, load movement, UV irradiation, estrogen deficiency, aging, and lifestyle-related diseases. In this section, it explains the condition and the disease which causes estrogen deficiency by low weight at an important time for the metabolism of the bone and calcium of young woman.

Pregnancy-associated osteoporosis is a rare condition characterized by a transient but significant reduction in bone mineral density. To date, the underlying pathophysiological mechanisms remain unclear. Related symptoms include severe back or hip pain secondary to vertebral fractures and/or transient osteoporosis of the hip, which typically occur during the third trimester or during lactation. Although most women are managed conservatively, a few women need surgery. Prompt diagnosis and appropriate treatment is important not only for pain control, but also to improve the woman's future quality of life.

We had called the various bone disorder in chronic kidney disease(CKD)as a "ROD:renal osteodystrophy" until last decade. However the concept of ROD have changed into the chronic kidney disease-mineral and bone disease(CKD-MBD)within this decade. This concept is containing systemic disorder affected mortality. Vascular calcification is an independent risk factor for the development of cardiovascular disease and mortality. The best strategy to prevent and treat vascular calcification would consist of the CKD-MBD management. It is expected that the treatment of preventing directly vascular calcification to appear by finding the detailed mechanism in the future.

Bone erosions develop early in the course of rheumatoid arthritis(RA)and are predictive of a worse prognosis. They deteriorate gradually and cause joint damage, resulting in impaired functional capacity and disability. Lately, a considerable number of studies have increased our understanding of the pathogenic mechanisms participating in the development of bone erosions in RA. Osteoclasts are responsible cells and multiple factors have been identified to stimulate their differentiation and function. RANKL(receptor activator of NF-κB ligand)and other cytokines have been known for a long time to enhance osteoclastogenesis, but the role of other pathways has also been revealed recently. Besides to excessive ostaoclastogenesis, impair osteoblast differentiation and function also plays part in bone erosion formation in RA. Inflamed synovial membrane products increased levels of cytokines and antagonists of the canonical Wnt signaling pathway, which inhibit osteoblast differentiation and function. It seems that downregulation of this pathway leads to impaired osteoblast differentiation and activity and consequently, to reduced capacity of bone erosion to repair. Preclinical studies show that these findings could have implications in RA treatment, although more studies are required in this direction.

Wnt signaling is known to be involved in metabolic bone disorders. Serum levels of sclerostin, a bone-specific protein that inhibits Wnt signaling, have been investigated in a variety of metabolic bone disorders. Serum sclerostin levels are positively correlated with bone mineral density in patients with osteoporosis. Elderly women with high serum sclerostin levels, however, are at increased risk of bone fractures. Since serum sclerostin levels are low in primary hyperparathyroidism and high in hypoparathyroidism, parathyroid hormone could be classified as a factor that regulates sclerostin levels. Serum sclerostin levels are high in glucocorticoid-induced osteoporosis and diabetes mellitus, which feature reduced bone formation. Finally, serum sclerostin levels increase with decreasing renal function. These findings highlight the potential of serum sclerostin levels as a new index for bone assessments which are different in nature from bone mineral density and bone metabolic markers.

Identification of responsible genes for skeletal dysplasias evidences their critical roles in the skeletal development and maintenance. Mutations in the genes encoding the components of Wnt canonical pathway, which include WNT1, LRP5, LRP4, SOST and WTX, cause the disorders characterized by abnormal in bone mass. On the other hand, mutations in the genes for the components of Wnt non-canonical pathway such as WNT5A, ROR2, DVL1 and DVL3 are associated with dysmorphic skeletal disorders which manifest short limbs and facial anomalies. Thus, both canonical and non-canonical pathways of Wnt signaling play substantial roles in the human skeletons, and it is suggested that the former mainly controls bone mass while the latter regulates skeletal morphogenesis.

Romosozumab is a humanized anti-sclerostin monoclonal antibody that has just been approved for the treatment of osteoporosis in Japan. Romosozumab causes both transient stimulation of bone formation and continuous suppression of resorption, thereby increasing bone mineral density and decreasing fracture incidence. Because the effect of romosozumab is reversible, sequential therapy with anti-resorptives after romosozumab will be necessary. This overview summarizes the results of ARCH study demonstrating superior efficacy of romosozumab compared to alendronate and effect of sequential therapy with alendronate. Possible adverse effect of romosozumab on cardiovascular diseases will also be discussed.