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Recent studies show comparable results of arthroscopic shoulder stabilization techniques compared with the gold standard open Bankart reconstruction. Great technical advances and ever-increasing surgeon experience have rendered pathology once deemed an indication for open surgery as treatable by arthroscopic means. With this movement toward a more universal application of all-arthroscopic techniques, we might consider the following question: Is there ever a need to open? To answer this question, we must first consider normal anatomy and then appreciate the contribution of deranged pathoanatomy to recurrent instability in each individual case. The surgeon must then determine whether this is best addressed via an arthroscopic or open technique. Arthroscopy, as compared with open stabilization procedures, holds the potential benefits of decreased morbidity rates, early functional rehabilitation, and improved range of motion. Despite potential advantages, arthroscopic stabilization is clearly contraindicated when a significant pathologic lesion contributing to recurrent instability cannot be adequately addressed as a result of the limitations of current techniques or instrumentation. On the basis of this principle, we believe that sizable glenohumeral bone defects remain the only absolute contraindication to an all-arthroscopic approach. Many complicating issues, such as attenuated capsule, humeral avulsion of the glenohumeral ligament lesions, cases of revision surgery, and collision or contact athletes, exist and warrant close attention. We prefer to think of these situations as “challenges” for which both arthroscopic and open surgery should be considered, rather than as true contraindications to arthroscopic shoulder stabilization. We are, by no means, advocating arthroscopic treatment in all cases of shoulder instability, because this would represent a gross oversimplification of the issues at hand. However, we do acknowledge that the steadfast contraindications to arthroscopic shoulder stabilization are decreasing every day. 相似文献
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Cora E Lewis Susan K Ewing Brent C Taylor James M Shikany Howard A Fink Kristine E Ensrud Elizabeth Barrett-Connor Steven R Cummings Eric Orwoll 《Journal of bone and mineral research》2007,22(2):211-219
We examined determinants of nonvertebral fracture in elderly men from six U.S. communities followed an average of 4.1 years. Six clinical risk factors predicted fracture risk independent of hip BMD: tricyclic antidepressant use, previous fracture, inability to complete a narrow walk trial, falls in previous year, age > or =80 years, and depressed mood. INTRODUCTION: There are few prospective studies of fracture determinants in men. We examined the associations between a comprehensive set of clinical risk factors and risk of nonspine fracture in older men and whether determinants of fracture risk were independent of total hip BMD. MATERIALS AND METHODS: A total of 5995 men > or =65 years of age were recruited from six communities in the Unites States and followed prospectively for an average of 4.1 years. Baseline assessments of demographic, lifestyle, medical history, functional status, anthropometry, and cognitive, visual, and neuromuscular function were assessed by questionnaire or examination. Triannual mailed questionnaires ascertained incident fracture; reported fractures were adjudicated by physicians using medical records and X-ray reports. Proportional hazards models were used to develop multivariable models, selecting variables and controlling for BMD. RESULTS: Of 5876 men, 4.7% (N = 275) reported an incident nonspine fracture during follow-up (11.46/1000 person-years). Tricyclic antidepressant use (hazard ratio [HR], 2.36; 95% CI, 1.25-4.46), history of fracture at or after age 50 (HR, 2.07; 95% CI, 1.62-2.65), inability to complete a narrow walk trial (HR, 1.70; 95% CI, 1.23-2.34), falls in previous year (HR, 1.59; 95% CI, 1.23-2.05), age > or =80 years (HR, 1.33; 95% CI, 1.01-1.76), depressed mood (HR, 1.72; 95% CI, 1.00-2.95), and decreased total hip BMD (HR, 1.53; 95% CI, 1.34-1.74) were independently related to increased risk. Compared with having none (48.0% of men), having three or more of the clinical risk factors (4.9% of men) increased fracture risk 5-fold, independent of BMD. Having three or more risk factors and being in the lowest tertile of BMD was associated with a 15-fold greater risk than having no risk factors and being in the highest BMD tertile. CONCLUSIONS: Several clinical risk factors were independently associated with nonspine fractures in elderly men. The combination of multiple risk factors and low BMD was a very powerful indicator of fracture risk. 相似文献
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Liesbeth Vandenput Fernand Labrie Dan Mellstr?m Charlotte Swanson Thomas Knutsson Ralph Peeker Osten Ljunggren Eric Orwoll Anna L Eriksson Jan-Erik Damber Claes Ohlsson 《Journal of bone and mineral research》2007,22(2):220-227
Androgens are important regulators of bone and prostate health in elderly men. The role of serum levels of glucuronidated androgen metabolites as predictors of BMD and prostate volume in men is unclear. We show that specific glucuronidated androgen metabolites predict BMD and prostate volume in elderly men. INTRODUCTION: Androgens are important regulators of bone and prostate health in elderly men. Local synthesis and degradation of androgens are likely to be important parameters of biological action of androgens in androgen-responsive tissues. The aim of this study was to determine the role of serum levels of glucuronidated androgen metabolites as predictors of BMD and prostate volume in elderly men. MATERIALS AND METHODS: A subsample of the population-based Swedish part of the MrOS study (n = 631, average age = 75.9 years) was investigated. Bone parameters were measured using DXA. Serum levels of total testosterone (T) and dihydrotestosterone (DHT) were measured by gas chromatography/mass spectroscopy (GC-MS); androstane-3alpha,17beta-diol-3glucuronide (3G) and androstane-3alpha,17beta-diol-17glucuronide (17G) were measured by liquid chromatography/mass spectroscopy. Prostate volume (n = 159) was measured by transrectal ultrasound. RESULTS: The general pattern is that two of the glucuronidated androgen metabolites, namely 17G and 3G, are stronger positive predictors of BMD than the bioactive androgens (T and DHT). In addition, 17G is a clear positive predictor of prostate volume, explaining 4.5% of the variance in prostate volume, whereas the bioactive androgens do not display any association with prostate volume. CONCLUSIONS: Serum levels of specific glucuronidated androgen metabolites predict BMD and prostate volume in elderly men. Future studies should determine if the glucuronidated androgen metabolites also reflect other biological correlates of androgenic activity, including prostate cancer, and if low levels might be a marker of general androgen deficiency in men. 相似文献
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Alfred E Buxton Hugh Calkins David J Callans John P DiMarco John D Fisher H Leon Greene David E Haines David L Hayes Paul A Heidenreich John M Miller Athena Poppas Eric N Prystowsky Mark H Schoenfeld Peter J Zimetbaum Paul A Heidenreich David C Goff Frederick L Grover David J Malenka Eric D Peterson Martha J Radford Rita F Redberg 《Journal of the American College of Cardiology》2006,48(11):2360-2396
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Eric A Schwartz Peter D Reaven 《Endocrinology & Metabolism Clinics of North America》2006,35(3):525-49, viii
Although the prevalence of cardiovascular complications is increased in insulin-resistant individuals, the underlying causes of this link have been elusive. Recent work suggests that several intracellular signal transduction pathways are inappropriately activated by hyperinsulinemia, hyperglycemia, increased free fatty acids, dyslipidemia, various inflammatory cytokines and adipokines--factors that are increased in insulin resistance. Once activated, substantial cross talk occurs between these pathways, especially a self-reinforcing cascade of vascular inflammation and cell dysfunction, greatly increasing the risk and severity of atherosclerosis in the insulin-resistant individual. We review several key cell-signalling pathways, describe how they are activated in they insulin-resistant state and the damage they induce, and discusses possible therapeutic approaches to limit vascular damage. 相似文献