Nihon rinsho. Japanese journal of clinical medicine
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Only bisphosphonates have reliable evidence to decrease the risk of vertebral fractures in patients taking glucocorticoids. Relative risk at 1 year treatment with bisphosphonates for incident vertebral fractures and non-vertebral fractures were 0.46 (95% confidence interval: 0.28-0.77) and 0.77 (95% confidence interval: 0.39-1.51), respectively. Two year extension of the alendronate trial showed that relative risk for incident vertebral fractures was 0.10 (95% confidence interval: 0.01-0.90). The bisphosphonates have been recommended as first-line drugs and active vitamin D3 and vitamin K2 have been recommended as second-line drugs in Japanese guidelines on the management and treatment of glucocorticoid-induced osteoporosis of The Japanese Society for Bone and Mineral Research (2004 edition).
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The aim of the pharmacotherapy for osteoporosis is to prevent osteoporotic fractures. It is important to identify the patients who have the risk for fractures and to assess how high the risk is. The Japanese guideline for prevention and treatment of osteoporosis showed the criteria to start the pharmacotherapy of osteoporosis. ⋯ Those factors are patients' history of femoral neck fractures, excessive alcohol or tobacco smoker. Recently 10-year absolute risk for fractures can be estimated by fracture risk assessment tool by WHO group, which is named as FRAX. The way of clinical application of this tool should be discussed in each country.
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Diabetes is one of the most important risk factors for mortality along with hypertension. Recently, it has emerged that ARB is a suitable anti-hypertensive drug for diabetic patients, because ARB has some features to prevent the progression of atherosclerosis in diabetic patients. Here, we summarize the evidences suggesting that ARB couldprevent not only macroangiopathy but also microangiopathy in diabetic patients. We conclude that ARB might be an ideal anti-hypertensive drug for diabetic patients.
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The autoinflammatory syndromes include a group of inherited diseases that are characterized by 1) seemingly unprovoked episodes of systemic inflammations, 2) absence of high titer of autoantibody or auto-reactive T cell, and 3) inborn error of innate immunity. In this article, we will focus on the clinical features, the pathogenesis related the genetic defects, and the therapeutic strategies in the representative disorders including familial Mediterranean fever (FMF), TNF receptor associated periodic syndrome (TRAPS), cryopyrin-associated periodic syndrome (CAPS), hyper-IgD with periodic fever syndrome (HIDS), syndrome of pyogenic arthritis with pyoderma gangrenosum and acne (PAPA), and Blau syndrome. Recent advances in genetics and molecular biology have proceeded our understanding of the pathogenesis of autoinflammatory syndromes.
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Pulmonary involvement is a common future in patient with collagen diseases. Some of the pulmonary involvements are a resistant of current available treatment and a fetal condition. These conditions include interstitial pneumonitis in scleroderma, acute diffuse alveolar damage (DAD) in polymyositis/dermatomyositis (PM/DM), alveolar hemorrhage, and pulmonary hypertension in collagen disease. ⋯ Combination therapy with high dose corticosteroids and immunosuppressive drugs (cyclosporin A, cyclophosphamide) is sometimes available therapy. Diffuse alveolar hemorrhage sometimes occurred in collagen disease including antineutrophilic cytoplasmic antibody (ANCA) associated vasculitis, systemic lupus erythematosus. Intensive treatment need to inhibit hemorrhage.