Bailliere's clinical rheumatology最新文献

{"title":"5 How do you know who needs prevention or treatment?","authors":"MD Jean-Pierre Devogelaer (Professor and Head of Arthritis Unit)","doi":"10.1016/S0950-3579(97)80019-2","DOIUrl":"10.1016/S0950-3579(97)80019-2","url":null,"abstract":"<div><p>Osteoporosis is preventable with the various therapeutic options available today. It is therefore important to reach the patient who needs to be treated. If based only on clinical risk factors there is much room for therapeutic misassignation in both directions: too many and too few treatments. Generally speaking, only bone mass measurement can yield the correct risk for future fracture, and clinical factors taken alone might be misleading. Clinical factors can be used to modulate the therapeutic intervention based on assessment of bone mass. In very elderly people with several risk factors (poor vision, poor balance and awkward gait, use of psychotropic drugs, etc), bone mass measurements probably become less crucial in therapeutic decision, because factors other than bone mineral have also to be actively assessed. All in all, the use of cut offs of bone mineral density balanced with the clinical decision based on an individual examination, will allow assessment of the therapeutic level in a particular patient. A therapeutic intervention will never be an all or nothing phenomenon based on computerized data.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 539-563"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80019-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20297808","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":"9 Osteoporosis in men","authors":"BSc, MBBS, MD, FRACP Ego Seeman (Associate Professor of Medicine and Endocrinologist)","doi":"10.1016/S0950-3579(97)80023-4","DOIUrl":"10.1016/S0950-3579(97)80023-4","url":null,"abstract":"<div><p>Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20–30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocrotical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 613-629"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80023-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20298896","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":"6 Can we prevent fractures?","authors":"MD, MSc, MRCPI Terence O'Neill (Senior Lecturer),&nbsp;MD, PhD Socrates Papapoulos (Associate Professor of Medicine and Director of Bone and Mineral Research)","doi":"10.1016/S0950-3579(97)80020-9","DOIUrl":"10.1016/S0950-3579(97)80020-9","url":null,"abstract":"<div><p>The primary aim of any intervention in osteoporosis is the prevention of fractures in individuals who have not yet fractured or the prevention of the progression of the disease in individuals with fragility fractures. There is currently insufficient evidence to recommend either a population-based prevention strategy or a strategy based on general screening with treatment of those individuals identified at high risk. Identification of subjects with strong clinical risk factors for osteoporotic fractures with subsequent measurement or not of bone mineral density as well as those with fragility fractures constitute at present the most rational approach to fracture prevention. Current measures to prevent osteoporotic fractures aim mainly at influencing bone mass and bone turnover and reducing the risk and impact of falls. Interventions that can reduce effectively the frequency of osteoporotic fractures in subjects at risk are available and new or alternative interventions are being developed. Issues related to the impact of these interventions on public health and health economics need to be addressed and methods to calculate the clinical outcomes in a way allowing comparison with outcomes of interventions in other common diseases should be developed.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 565-582"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80020-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20298893","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":"Introduction How can we reduce the burden of osteoporosis?","authors":"BSc, MBBS, FRCP Anthony D. Woolf (Consultant Rheumatologist),&nbsp;MD, PhD Pierre D. Delmas (Professor of Medicine and Director)","doi":"10.1016/S0950-3579(97)80014-3","DOIUrl":"10.1016/S0950-3579(97)80014-3","url":null,"abstract":"","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 451-457"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80014-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20297798","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":"8 How do we manage specific types of osteoporosis?","authors":"MBBS, FRACP, MD, LLB Philip N. Sambrook (Professor of Rheumatology),&nbsp;MBBS, FRACP Vasi Naganathan (Research Fellow)","doi":"10.1016/S0950-3579(97)80022-2","DOIUrl":"10.1016/S0950-3579(97)80022-2","url":null,"abstract":"<div><p>Osteoporosis in children, adolescents and corticosteroid-treated patients represent a particular problem for clinicians. In children and adolescents, the main management question is whether any specific interventions can influence attainment of peak bone mass and so decrease the chance of osteoporosis in later adult life. The role of physical activity and calcium in particular are reviewed. In adolescence, osteoporosis is usually due to idiopathic juvenile osteoporosis or secondary to amenorrhoea or anorexia nervosa. These entities, as well as the management of corticosteroid-induced osteoporosis at all ages, are discussed.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 597-612"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80022-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20298895","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":"10 How do we increase awareness of osteoporosis?","authors":"BA(Hons), Dip CAMMIPR Linda Edwards (Director),&nbsp;BSc(Hons)Pharm, Graduate Diploma in Marketing Mary Fraser (Director)","doi":"10.1016/S0950-3579(97)80024-6","DOIUrl":"10.1016/S0950-3579(97)80024-6","url":null,"abstract":"<div><p>In the UK and throughout Europe 10 years ago, osteoporosis was not a word that existed in the vocabulary of the general public. The majority of doctors had dismissed osteoporosis as a normal process of ageing, affecting only the very elderly and about which nothing could be done. Why should it matter that awareness of osteoporosis was so low among the general public and the medical professions?</p><p>For the newly launched National Osteoporosis Society in the UK, several questions needed to be answered: if osteoporosis was not an inevitable part of growing old, was it really a disease and how could action be implemented to treat it and prevent it? If fracture numbers and their costs were so much higher than had been thought, who should be informed of this? And if there were ways of treating and preventing osteoporosis, who should be made more aware, what should they be told, and how could such awareness-raising be done and paid for? Before real action could be undertaken, a considerable awareness programme would be needed to radically alter traditional beliefs about bone health.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 631-644"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80024-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20298897","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":"4 Bone markers","authors":"PhD Patrick Garnero (Research Scientist),&nbsp;MD, PhD Pierre D. Delmas (Professor of Medicine and Director)","doi":"10.1016/S0950-3579(97)80018-0","DOIUrl":"10.1016/S0950-3579(97)80018-0","url":null,"abstract":"<div><p>The recent development of specific and sensitive biochemical markers reflecting the overall rate of bone formation and bone resorption, has markedly improved the non-invasive assessment of bone turnover in various metabolic bone diseases, especially osteoporosis. The immunoassay of human osteocalcin recognizing the intact molecule and its major proteolytic fragment, along with that of bone alkaline phosphatase, are currently the most sensitive markers to assess bone formation. For bone resorption, the total urinary excretion of pyridinoline crosslinks measured by high pressure liquid chromatography has shown its superiority over all other markers for the clinical assessment of osteoporosis. The recent development of immunoassays recognizing either the free pyridinoline crosslinks or pyridinoline crosslinked-type I collagen peptides in urine and serum should allow a broad use of this sensitive resorption marker. Recent studies, some of them still in progress, define the clinical use of these markers: first, to improve the prognostic assessment of post-menopausal women in combination with bone mass measurement, i.e. their risk of developing osteoporosis and, ultimately, fractures and, second, to monitor the efficacy of anti-resorption drugs.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 517-537"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80018-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20297806","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":"1 What is the impact of osteoporosis?","authors":"MD, PhD Olof Johnell (Professor of Orthopaedics),&nbsp;MD, PhD Karl J. Obrant (Associate Professor of Orthopaedics)","doi":"10.1016/S0950-3579(97)80015-5","DOIUrl":"10.1016/S0950-3579(97)80015-5","url":null,"abstract":"<div><p>A body of evidence points towards a close connection between susceptibility to fractures and osteoporosis. The incidence of osteoporotic fractures, both in absolute figures and in age-specific figures, has increased worldwide throughout this century. Although some reports show that the age-specific incidence is levelling-off, there will be a continuously increasing number of individuals with such fractures that will have implications from an economical point of view not only for the affected individual but for society as a whole. The outcome after such fractures, especially those of the hip, is by no means always favourable, partly due to insufficient results after orthopaedic treatment and partly due to an already high comorbidity. Therefore, trying to prevent osteoporotic fractures by non-pharmacological or pharmacological regimens is of utmost importance.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 459-477"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80015-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20297799","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":"7 Hormone replacement therapy","authors":"MD, FRCPath, FRCP Juliet E. Compston (Senior Research Associate and Honorary Consultant Physician)","doi":"10.1016/S0950-3579(97)80021-0","DOIUrl":"10.1016/S0950-3579(97)80021-0","url":null,"abstract":"<div><p>Oestrogen deficiency at the menopause leads to bone loss primarily as a result of increased bone turnover and an increase in the activity of osteoclasts. Hormone replacement therapy (HRT) reverses these changes, preventing menopausal bone loss and reducing fracture risk at the spine, hip, and wrist, although the magnitude of this reduction has not been accurately established. The optimal duration of therapy for the prevention of osteoporosis is uncertain but there is increasing evidence that life-long treatment after the menopause may be required to maintain maximum protection against fracture. The extraskeletal effects of long-term oestrogen therapy include protection against cardiovascular disease and a possible increase in the risk of breast cancer; the persistence of these effects after therapy is withdrawn is uncertain although there is some evidence that the increase in risk of breast cancer is seen only in current users. Furthermore, there is increasing evidence that the use of progestogens in combined formulations does not substantially alter either the cardiovascular benefits or the increased risk of breast cancer, although further studies are needed in this area. The emergence of ‘no-bleed’ preparations in recent years has increased the acceptability of HRT for some women, particularly those in older age groups. Finally, the development of tissue-selective oestrogen agonists is an exciting advance which may enable life-long therapy after the menopause to protect against cardiovascular and bone disease in the absence of significant side-effects.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 3","pages":"Pages 583-596"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80021-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20298894","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":"7 Other forms of vasculitis and pseudovasculitis","authors":"MD Vedat Hamuryudan (Associate Professor),&nbsp;MD Huri Özdogğan (Professor),&nbsp;MD Hasan Yazıcı (Professor and Chief)","doi":"10.1016/S0950-3579(97)80049-0","DOIUrl":"10.1016/S0950-3579(97)80049-0","url":null,"abstract":"<div><p>Behçet's syndrome can involve all sizes and kinds of blood vessels. There is an association between arterial involvement and venous thrombosis. Pulmonary arterial aneurysms and neurological involvement have a definite influence on mortality. Male sex and young age are indicators of a more severe disease course. Immunosuppressive treatment early in the disease may affect the long term prognosis favourably. Patients with familial Mediterranean fever may develop manifestations of vasculitis. The most common associations are with Schönlein-Henoch purpura and polyarteritis nodosa. In some patients the diagnosis of vasculitis precedes that of familial Mediterranean fever. Kawasaki disease, although rare, can be seen in adults. The coronary sequela of childhood disease can affect the prognosis later in life. Many conditions, like myxoma, cholesterol embolism, and calciphylaxis may mimic vasculitic syndromes. These conditions should always be kept in mind because their pathophysiology and treatment are different from true vasculitides.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"11 2","pages":"Pages 335-355"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(97)80049-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20164509","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}