{"title":"[Epidemiology of FGF23-related hypophosophatemic diseases].","authors":"Itsuro Endo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Through the studies of patients with hypophosphatemic rickets/osteomalacia, fibroblast growth factor 23(FGF23)has emerged as a humoral factor that reduces serum phosphate. Discovery of FGF23 as an essential regulator of phosphate homeostasis has markedly improved our understanding of phosphate homeostasis and hypophosphatemic or hyperphosphatemic disorders. A nationwide epidemiologic survey of FGF23-related hypophosphatemic diseases indicated that the patients showed FGF23 levels of above 30 pg/mL by intact assay in the presence of hypophosphatemia. The survey also showed that prevalence and biochemical data before and after treatment of the diseases. Novel therapeutic methods for these disorders may be developed by elucidation of the mechanism of action of FGF23.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"223-31"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Pathogenesis and clinical condition of hyperphosphatemic diseases].","authors":"Naoto Hamano, Masafumi Fukagawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Phosphorus is essential mineral to life, which has the multiple roles like postural maintenance or production of energy in the cells. Phosphate overload is harmful and compensatory mechanisms exist. Phosphate is abolished through kidneys and target organ of the compensatory mechanism is also kidneys. It is necessary to evaluate renal function and source of phosphate for estimating the cause of hyperphosphatemia. Acute hyperphosphatemia may cause severe acute kidney injury and avoidance of massive phosphate overload is needed. Chronic hyperphosphatemia have an impact on prognosis because the risk of cardiovascular event increases. Adequate restriction of phosphate intake and use of phosphate absorbent is needed for improvement of prognosis of patients with chronic kidney disease.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"207-13"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138816149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-].","authors":"Keiichi Ozono","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitamin D deficiency causes rickets or osteomalacia, which is associated with hypomineralization of bone and chondrocytes, and/or hypocalcemia. Accumulating evidence indicates increase in frequency of vitamin D deficiency due to insufficient intake of vitamin D and calcium and decrease in sunshine. It is necessary for clinician to diagnose vitamin D deficiency accurately and treat patients with vitamin D deficiency adequately. For the purpose, clinical guideline or expert opinion on vitamin D deficiency has been reported.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"215-22"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Pathogenesis of hypophosphatemia].","authors":"Yasuhiro Takeuchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic hypophosphatemia is seriously involved in several disorders of musculoskeletal system. Symptoms of patients are usually non-specific, such as pain with or without muscle weakness on lower extremities and are often hard to be correctly diagnosed. It is clinically important for physicians to understand pathogenesis and clinical features of hypophosphatemia and its related diseases.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"199-205"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Regulatory mechanism of circulating inorganic phosphate].","authors":"Toshimi Michigami","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Circulating level of phosphate is altered by age and diet, and is also controlled by several hormones such as parathyroid hormone(PTH), 1,25-dihydroxyvitamin D[1,25(OH)2D]and fibroblast growth factor 23(FGF23). The main function of PTH and 1,25(OH)2D is maintaining calcium homeostasis, while FGF23 plays a central role in phosphate metabolism. PTH suppresses phosphate reabsorption in the proximal tubules to increase the renal phosphate wasting, while 1,25(OH)2D facilitates the intestinal phosphate absorption. FGF23 increases the renal phosphate wasting and reduces the production of 1,25(OH)2D. Of note, these hormones mutually regulate one another. The production of FGF23 is also regulated by various local factors. The mechanism for sensing the phosphate availability still remains unknown, and further investigation is required.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"193-8"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Steroids-induced osteoporosis due to the treatment for Pulmonary diseases.]","authors":"Nobuyuki Horita, Takeshi Kaneko","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Corticosteroids are key medications to treat pulmonary diseases. A variety of medications, doses, administration route, and duration of corticosteroids were chosen for each of pulmonary diseases. Although corticosteroids are potent medications, they often cause serious adverse effects such as osteoporosis, diabetes, and immunosuppression. Thus, physicians have to properly assess the risk of adverse effects to prevent them. In this review, we discuss the risk of osteoporosis by corticosteroids that are prescribed for pulmonary diseases. Inhaled corticosteroids are not serious risk factors of osteoporosis. If systemic corticosteroids are planned to be administrated in the prednisolone equivalent dosage of 5 mg/day or more for three months or longer, risk of bone fracture have to be assessed regardless of the primary pulmonary disease. If necessary, prophylactic agent such as bisphosphonates should be prescript.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 10","pages":"1459-1465"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Design of mechanobio-materials for cell manipulation and its application for stem cell manipulation.]","authors":"Satoru Kidoaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Recently, control of mechanobiologic response of cells has been a strong attractive issue for biomaterials sciences in relation to the requirements for optimization of cell-materials interactions. In this mini-review, we survey the typical parameters for designing the biomaterials to manipulate cell mechanobiology, i.e., mechanobio-materials. In addition, from the view of regenerative biomedical engineering, we introduce our recent approaches on the development of mechanobio-materials for stem cell manipulation that ensures the high-qualified stemness.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 12","pages":"1773-1778"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Topics for basic and clinical research in ASBMR 2015].","authors":"Ippei Kanazawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This is a brief report on selected topics in 37th Annual meeting of ASBMR held in Seattle on October 9-12, 2015. I focused on several interesting presentations of basic and clinical research.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 1","pages":"133-5"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}