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The high prevalence of inadequate serum vitamin D levels and implications for bone health.

BACKGROUND: Inadequate serum vitamin D is associated with secondary hyperparathyroidism, increased bone turnover, and bone loss, which increased fracture risk. Osteomalacia has also been observed in severe cases. Indeed, vitamin D and calcium are essential components of management strategies for the prevention and treatment of osteoporosis. Despite this, many people currently do not have adequate vitamin D levels. This problem has been documented in many studies around the world, regardless of age, health status, or latitude, and is especially common among older adults, who are also likely to have osteoporosis. Factors that contribute to low vitamin D include low exposure to sunlight, decreased synthesis in skin and reduced intestinal absorption related to aging, and limited dietary sources. Supplementation is the most effective means of correcting poor vitamin D nutrition. However, few patients with osteoporosis currently take sufficient vitamin D supplements. SCOPE: This review article discusses the role of vitamin D in osteoporosis and skeletal health, and summarizes what is known about the high prevalence of inadequate serum vitamin D and recommendations for supplementation. CONCLUSION: Greater awareness of the importance of vitamin D for skeletal health and more aggressive supplementation efforts are urgently needed to address this important public health problem.

Bone Resorption↗

Contributions of basal and post-prandial hyperglycaemia to micro- and macrovascular complications in people with type 2 diabetes.

BACKGROUND: People with Type 2 diabetes mellitus are at high risk of cardiovascular disease and microvascular complications. A number of epidemiological studies have shown a strong relationship between the prevalence of vascular complications and raised levels of plasma glucose and glycated haemoglobin (HbA(1c)). Accumulating evidence supports the superior independent prognostic importance of the post-challenge glucose level, measured either 1 or 2 h after a glucose load. Thus, data from studies conducted in Europe, the USA, and particularly the Pacific rim and South Asia suggest that 2-h glucose is a better predictor of cardiovascular and all-cause mortality than pre-breakfast glucose, both in people with diabetes and those with pre-diabetic impaired glucose tolerance (IGT). Pathophysiological studies suggest that post-prandial rises in hyperglycaemia can trigger endothelial damage through multiple mechanisms, including increased oxidative stress and the increased expression of atherogenic circulating adhesion molecules and inflammatory cytokines that induce and regulate cell recruitment, migration, growth, and proliferation. Optimal pharmacological control of meal-time glucose levels can help to lower the HbA(1c) and thus may reduce the incidence of vascular complications in many people with diabetes. Moreover, emerging evidence suggests that reducing meal-time hyperglycaemia may delay the progression from pre-diabetic states toward overt diabetes. SCOPE: This review (based on MEDLINE searches, 1980-2005) examines the evidence linking the microvascular and macrovascular complications of diabetes and glycaemic control, assesses the relative contributions of basal and meal-time concentrations, and considers the implications for optimal treatment for people with Type 2 diabetes or with prediabetic IGT.

Arteriosclerosis↗

Can thiazolidinediones delay disease progression in type 2 diabetes?

BACKGROUND: Type 2 diabetes results from increasing insulin resistance coupled with progressive loss of beta-cell function. Further deterioration of beta-cell function is associated with progression of diabetes and the potential development of microvascular and macrovascular complications. SCOPE: This review examines current knowledge of beta-cell function and uses this information to assess how the results of ongoing trials could increase our understanding of disease progression and potential interventions. Data were derived from a Medline search using the search terms 'beta-cell dysfunction', 'IGT', 'thiazolidinediones', 'metformin', and 'sulfonylurea'. RESULTS: The mechanisms that underlie beta-cell dysfunction are complex and most likely involve the interplay of a range of factors that reduce both beta-cell mass and secretory function. These include detrimental effects associated with hyperglycemia itself, elevated free fatty acids, and inflammatory responses linked to adipocyte-derived cytokines, with apoptosis a key underlying mechanism. Early intervention with treatments that address these defects, and preserve beta-cell function while improving insulin sensitivity, may delay disease progression in patients with type 2 diabetes and also prevent the development of diabetes in 'at-risk' individuals. Two of the studies examining the effects of interventions on development and progression of diabetes that are due to report shortly are ADOPT (A Diabetes Outcome Progression Trial), comparing a thiazolidinedione, metformin and a sulfonylurea in patients with type 2 diabetes not previously treated with oral hypoglycemic agents, and DREAM (Diabetes REduction Assessment with ramipril and rosiglitazone Medication), assessing the effects of a thiazolidinedione and an angiotensin-converting enzyme inhibitor in subjects with impaired glucose tolerance and/or impaired fasting glucose. CONCLUSIONS: Although we do not have a full understanding of the mechanisms driving progression of type 2 diabetes, there is growing evidence that we may be able to modulate them and thereby improve patient outcomes.

Diabetes Complications↗

Improving macrovascular outcomes in type 2 diabetes: Outcome studies in cardiovascular risk and metabolic control.

BACKGROUND: Type 2 diabetes is accompanied by a host of potentially modifiable cardiovascular disease risk factors. Consequently, people with type 2 diabetes have a higher risk of macrovascular disease than the non-diabetic population, and a poor prognosis following an event. Several large-scale primary and secondary outcome studies have included large diabetes subgroups for post-hoc analysis, and a limited number of studies have focused specifically on type 2 diabetes. SCOPE: This review provides an overview of macrovascular outcome studies in type 2 diabetes and discusses potential new targets for therapy based upon a MEDLINE literature search from January 1990 to April 2006. FINDINGS: Large cardiovascular outcome studies show that treating cardiovascular disease risk factors significantly reduces the risk of primary and secondary macrovascular events in patients with type 2 diabetes. The evidence for targeting hypertension (using renin-angiotensin system inhibitors), dyslipidemia (statins), and coagulation factors (aspirin) appears robust. However, the macrovascular benefits of improved glucose control remain to be proven definitively, although metformin may have advantages over other glucose-lowering agents. Nevertheless, these studies reveal that significant excess residual risk remains, highlighting the need for new therapies. It is also apparent that some agents (e.g. metformin, statins, renin-angiotensin system inhibitors) may also have pleiotropic mechanisms. Newer strategies are investigating other lipid targets (especially HDL cholesterol) or using agents, such as thiazolidinediones, that address multiple established and emerging risk factors. A recent study with pioglitazone suggests that macrovascular risk can be reduced in very high-risk patients with type 2 diabetes who are already receiving contemporary lipid, anti-hypertensive, and anti-platelet therapy. CONCLUSION: The core therapeutic paradigm targeting glycemia, hypertension, dyslipidemia, and coagulation factors has failed to remove excess residual risk in patients with type 2 diabetes completely. Emerging data, and on-going trials, should provide better guidance on new therapeutic opportunities in this high-risk patient group.

Cardiovascular Diseases↗

Metformin and pioglitazone: Effectively treating insulin resistance.

BACKGROUND: Insulin resistance has a complex etiology, with multiple manifestations across the organ systems involved in glucose homeostasis. Glucose-lowering drug therapies that target insulin resistance can therefore utilize different mechanistic approaches. Two key classes of insulin-sensitizing agents--the biguanides (principally metformin) and thiazolidinediones (pioglitazone and rosiglitazone)--have distinct molecular mechanisms of action and differing effects on metabolic dysfunction. This provides an opportunity for complementary beneficial effects in the treatment of type 2 diabetes and on the potential consequences of insulin resistance, such as dyslipidemia and atherosclerosis. SCOPE: This review (based upon EMBASE and MEDLINE searches from January 1990 to April 2006) highlights the mechanistic distinctions and clinical data that support the rationale for thiazolidinedione/metformin combination therapy in patients with type 2 diabetes. FINDINGS: The different insulin-sensitizing mechanisms of metformin and the thiazolidinediones are manifest in partially distinct effects on hepatic and peripheral glucose homeostasis, and clinical studies show improved glucose control with combination therapy. Both metformin and thiazolidinediones may also have pancreatic beta-cell preserving properties. Furthermore, they have different beneficial effects on several other metabolic risk markers and risk factors for cardiovascular disease. Whereas the thiazolidinediones (particularly pioglitazone) have greater effects on multiple aspects of dyslipidemia, metformin has anorexigenic properties. They also have distinct effects on levels of mediators involved in inflammation and endothelial dysfunction, and outcome studies suggest that either pioglitazone or metformin may reduce the risk of macrovascular events. CONCLUSION: The distinct, but complementary, mechanisms of action of the thiazolidinediones and metformin provide the opportunity for effective combination therapy with two insulin-sensitizing agents. Such an approach has consequences, not only for improved glucose control, but also for reducing metabolic risk and potentially improving major cardiovascular disease outcomes.

Diabetes Mellitus, Type 2↗

Restoration of vestibular function: basic aspects and practical advances for rehabilitation.

BACKGROUND: Normal balanced functioning of the human vestibular system is required to achieve an upright stance and locomotion, head and eye stabilization and internal spatial representation; any lesion in this system will disrupt these functions. SCOPE: This review synthesizes previous work performed by the author and his research group in both animal models and vestibular defective patients over the last three decades. The author presents both an updated view on the basic mechanisms underlying the two main theories of vestibular compensation and his views on the principles that should guide management and rehabilitation of patients with vestibular loss. FINDINGS: Static deficits, following the loss or disruption of vestibular functions, are fully compensated; this is explained by the vestibulo-centric theory that suggests different plastic changes occurring in the vestibular nuclei complexes. In contrast, dynamic deficits remain poorly compensated; the restoration of dynamic vestibular functions results from substitution processes and vicarious strategies. The practical advances in the rehabilitation of vestibular defective patients are as follows: (1) perform rehabilitation at an early stage; (2) favour active retraining; (3) do not use stereotyped rehabilitation programs but adapt exercises to the patients; (4) examine patients in standardized environments; (5) use both static and dynamic tests; and (6) avoid drugs with sedative effects (or limit them to the very acute stage only) and prescribe those accelerating the recovery process (e.g. betahistine dihydrochloride). CONCLUSION: Recovery of vestibular function is greatest when early active retraining and adequate pharmacological treatments are used in combination.

Animals↗

A fixed-dose combination of pioglitazone and metformin: A promising alternative in metabolic control.

BACKGROUND: When type 2 diabetes is managed with glucose-lowering monotherapy, glycemic control ultimately deteriorates due to the inability of the beta-cell to overcome insulin resistance. Combining drugs with different complementary mechanisms of action improves long-term glycemic control and may lower the risk of vascular complications. A fixed-dose combination of pioglitazone (a thiazolidinedione) and metformin has been approved for use in the US (Actoplus met) and in Europe (Competact). SCOPE: This review (based upon MEDLINE and EMBASE searches from January 1990 to April 2006) discusses the potential benefits of co-formulating metformin and pioglitazone with respect to compliance and targeting glycemia, as well as other metabolic parameters. FINDINGS: Pioglitazone increases insulin sensitivity, while metformin reduces hepatic gluconeogenesis and improves peripheral glucose uptake. Both agents reduce hyperglycemia and hyperinsulinemia, and appear to protect beta-cell function. Their similar pharmacokinetic time profiles have facilitated a co-formulation bioequivalent to their separate administration. In randomized studies, pioglitazone and metformin administered separately provided significantly better glycemic control than metformin monotherapy or metformin plus gliclazide. Pioglitazone and metformin have complimentary benefits on diabetic dyslipidemia; pioglitazone primarily improves high-density lipoprotein cholesterol and triglyceride levels (to a greater extent than rosiglitazone does), while metformin mainly improves total cholesterol. Pioglitazone and metformin also modulate other atherosclerosis biomarkers, including inflammatory mediators, coagulation thrombosis components, and carotid intima media thickness. Together, these pleiotropic effects have the potential to confer a reduced risk of cardiovascular disease in patients with type 2 diabetes. Pioglitazone and metformin are well tolerated in combination, with low rates of hypoglycemia, and the convenience of a single tablet may be expected to aid dosing compliance. CONCLUSION: The co-formulation of pioglitazone and metformin is a rational approach that maximizes the established, complimentary benefits of these agents, while potentially improving compliance.

Cardiovascular Diseases↗

Management of cSSTIs: the role of daptomycin.

BACKGROUND: Skin and soft tissue infections (SSTIs) and complicated SSTIs (cSSTIs), particularly those caused by Gram-positive pathogens, are among the most common human bacterial infections. The emergence of resistance to antibiotics such as methicillin and vancomycin has compromised treatment options for these infections and stimulated the search for new antimicrobial therapies. Daptomycin, the first in a class of agents known as cyclic lipopeptides, is a novel antibiotic with potent activity against most Gram-positive pathogens, including methicillin-resistant Staphylococcus aureus. SCOPE: This review examines the novel properties of daptomycin and describes its therapeutic efficacy and tolerability, particularly in the treatment of cSSTIs. The data search strategy included identification of original research papers, review articles, meeting reports and editorials by searches of MEDLINE and references from relevant articles. FINDINGS: In vitro studies have demonstrated that daptomycin has superior bactericidal activity compared with vancomycin and the newer anti-Gram-positive agents, quinupristin/dalfopristin and linezolid. Robust, randomised, phase III clinical trials have shown daptomycin to be effective and well tolerated for the treatment of cSSTIs caused by Gram-positive bacteria, with equivalent clinical success rates and a similar safety profile to those of comparator agents. Data from these studies suggest a trend toward shorter duration of therapy and faster resolution of symptoms with daptomycin. CONCLUSIONS: Given the pressing need for new antibiotics to combat infections caused by Gram-positive organisms, and to overcome the problem of resistance to conventional antibiotics, daptomycin is a welcome addition to the treatment options for the management of cSSTIs.

Anti-Bacterial Agents↗

Carotid intima-media thickness as a surrogate marker for cardiovascular disease in intervention studies.

BACKGROUND: Cardiovascular trials using clinical endpoints to assess efficacy typically require follow-up of large numbers of participants for 3-5 years. This disadvantage has encouraged the search for well-validated surrogate markers for cardiovascular disease (CVD). These markers may provide earlier indications of efficacy in trials involving fewer participants. One approach gaining interest in recent years is the measurement of atherosclerotic progression, a major underlying cause of CVD. SCOPE: This review article aims to further substantiate the evidence supporting the use of measurement of carotid intima-media thickness (CIMT) as a surrogate marker for atherosclerosis and cardiovascular risk. FINDINGS: CIMT has consistently been related to future CVD events in population studies. CIMT is significantly related with other markers for CVD risk, such as elevated levels of risk factors and presence of atherosclerosis in the coronary arteries. Furthermore, almost all lipid-lowering trials and a large number of blood pressure lowering trials have consistently shown a reduction in progression of CIMT. In addition, the ultrasound technique for measuring CIMT is safe and highly reproducible. CONCLUSION: Thus, CIMT may be used as a surrogate endpoint in clinical trials to enable the benefits of new therapies or regimens to be more rapidly translated into clinical practice.

Biomarkers↗

Screening and selecting for optimized antiretroviral drugs: rising to the challenge of drug resistance.

BACKGROUND: Resistance to antiretroviral (ARV) drugs constitutes one of the greatest limitations to effective long-term therapy for human immunodeficiency virus (HIV) infection--a problem alleviated, but by no means overcome, by the application of carefully selected, sequential combination regimens. The rational development of novel therapeutics with the ability to suppress viraemia effectively and also address the complex problems of resistance offers a useful way forward for HIV therapy. The investigational drug TMC114 (darunavir) was designed to be active against both wild-type HIV and strains that are resistant to currently available protease inhibitors. SCOPE: This review describes the challenges posed by HIV drug resistance and the novel approach taken in the design and selection of TMC114. Articles were identified by searching MEDLINE in September 2005 (search limits: 1995-2006) using the terms: TMC114, darunavir, resistance, screening, selection, ARV therapy, HIV and HAART. Additional data included bibliographies from identified articles. FINDINGS: With the continuing problem of resistance, ARV drugs must be designed with broad-spectrum activity forming a central part of their development and screening. Drugs must not only be able to treat existing resistant strains, but must also possess more intrinsic resilience to the development of resistance. TMC114 was designed and selected with strong emphasis on potent activity across a range of both wild-type and resistant HIV strains and high binding affinity to HIV protease. CONCLUSION: This review illustrates that future treatment strategies should include screening against multiple-resistant strains to optimize the identification of novel therapeutic agents for the treatment of HIV.

Anti-HIV Agents↗

Endothelin receptor antagonism in pulmonary arterial hypertension--a role for selective ET(A) inhibition?

BACKGROUND: Pulmonary arterial hypertension (PAH) develops from an abnormal interaction between the endothelium and smooth muscle cells in the pulmonary arteries and is characterized by a progressive increase in pulmonary vascular resistance resulting from vascular remodeling, vasoconstriction, and cellular proliferation. A rapidly progressive disease with limited therapeutic options, PAH may progress to right ventricular failure and death. Endothelin (ET-1), a potent vasoconstrictor, has vascular remodeling properties that contribute to the acceleration of the disease. ET-1 predominantly binds to two receptors, endothelin-A (ET(A)) and endothelin-B (ET(B)) receptors. ET(A) receptors are found on smooth muscle cells only and, when activated, induce vasoconstriction and cellular proliferation. ET(B) receptors on smooth muscle cells, when activated, cause vasoconstriction, whereas those on endothelial cells produce vasodilation and clear circulating ET-1. Therefore, a clinically important question arises as to whether selective ET(A) receptor antagonism is superior to nonselective dual-receptor antagonism in the treatment of PAH. SCOPE: To review clinical trials that studied safety and efficacy of various endothelin receptor antagonists (ETRAs) for the treatment of PAH and address the rationale for the use of either a nonselective or a selective ETRA. FINDINGS: Nonselective blockade of both ET receptors with the ETRA bosentan has demonstrated benefit in PAH, as have sitaxsentan and ambrisentan, two investigational agents with more selectivity for the ET(A) receptor. Data from placebo-controlled studies and long-term, open-label studies suggest that all ETRAs have similar efficacy, though there is some evidence suggesting that selective ETRAs may have a safer profile. CONCLUSION: Both selective and nonselective ETRAs have proven to be efficacious in treatment of PAH patients, and selective ETRAs may have a slightly safer profile. However, because PAH is a rare disease and trials have relatively small numbers of patients, it is difficult to quantify the magnitude of the difference between the different agents.

Clinical Trials as Topic↗

An overview of the prevalence of 25-hydroxy-vitamin D inadequacy amongst elderly patients with or without fragility fracture in the United Kingdom.

BACKGROUND: Many studies have investigated the prevalence of 25-hydroxy-vitamin D inadequacy throughout the world and found a high prevalence of 25-hydroxy-vitamin D inadequacy in older patients, particularly those with fragility fracture. SCOPE: To review the findings from vitamin D audits from six units across the UK and compare with previously published data from around the world. Results from four units have been previously published (Belfast, Glasgow, London and Medway) and this paper presents new data from Southampton and Carshalton, and further sub-analysis of the data from Medway. FINDINGS: Three audits of patients attending metabolic bone clinics (Carshalton, Medway and Southampton) identified 954 patients, of which overall 49% had a prior fragility fracture. Mean 25-hydroxy-vitamin D levels ranged from 47.7 nmol/L to 62.4 nmol/L. Of these patients 72.9-88.9% had a 25-hydroxy-vitamin D level < 80 nmol/L, 68.8-83.3% < 70 nmol/L and 37.5-59.1% < 50 nmol/L. The mean age of patients ranged from 60.0 to 67.5 years. Sub-analysis of the data by fracture status revealed that patients with fracture had lower mean levels of 25-hydroxy-vitamin D compared with patients without fracture. This was statistically significant in the sub-analysis of the Medway data (45.3 nmol/L versus 49.9 nmol/L, p < 0.005). Three audits identified 330 patients with fragility fracture. Audits from Glasgow and Belfast specifically identified patients with fragility fracture. A subgroup of patients with fracture aged over 50 years from the Medway audit was also included in this group. Mean levels of 25-hydroxy-vitamin D ranged from 40.0 nmol/L to 52.3 nmol/L. 83.7-96.4% of patients had a 25-hydroxy-vitamin D level < 80 nmol/L, 73.3-89.7% < 70 nmol/L and 55.8-73.2% < 50 nmol/L. The mean age of patients ranged from 65.3 to 68.6 years. The audits carried out in Belfast and Medway were also divided by supplementation status. Mean 25-hydroxy-vitamin D levels were 48.1 nmol/L in Belfast and 40.5 nmol/L in Medway in the patients not receiving supplements and 53.8 nmol/L and 59.9 nmol/L, respectively in the patients receiving supplements. The difference was statistically significant in the Medway audit (p < 0.0001), but not in the smaller Belfast audit (p = 0.216). As would be expected, the prevalence of 25-hydroxy-vitamin D inadequacy was higher in the patients not receiving supplements, for example at the 70 nmol/L threshold: 82.6% versus 67.1% in Belfast and 89.6% versus 72.7% in Medway. Three audits specifically identified 694 patients with hip fracture (Belfast, Glasgow and London). Mean levels of 25-hydroxy-vitamin D ranged from 24.7 nmol/L to 36.1 nmol/L. Of these patients 90.7-99.0% had a 25-hydroxy-vitamin D level < 80 nmol/L, 88.4-98.0% < 70 nmol/L and 81.6-92.7% < 50 nmol/L. The mean age of patients ranged from 73.4 to 80.5 years. CONCLUSION: Inadequate 25-hydroxy-vitamin D levels are extremely common in the elderly and particularly so in patients with fragility fracture - specifically in those with hip fracture. Although the differing audit specifications and assay techniques used make direct comparisons difficult, the data do provide a snapshot of 25-hydroxy-vitamin D status across the UK and are consistent with those previously observed elsewhere in Europe and the rest of the world.

Aged↗

Thirteen-year follow-up of deliberate self-harm, using linked data.

BACKGROUND: We describe a national cohort of individuals surviving an episode of deliberate self-harm (DSH). Subsequent admissions for DSH and mortality over the following 13 years were studied. METHOD: In 1981, 8304 individuals were discharged from Scottish general hospitals with a diagnosis of attempted suicide (E950-959). They were followed-up to the end of 1994 using the Scottish Linked Data Set. Mortality was compared to the Scottish population using person-years analysis. RESULTS: 2624 people (31.6%) were readmitted with further episodes of DSH. The median number of readmissions was 1, range 1-137. The observed:expected ratio for all-cause mortality was 2.26 (95% CI 2.13-2.26). One hundred and sixty-eight people (2%) died from suicide, and 46 (0.6%) from undetermined causes. The observed:expected ratio for suicide plus undetermined deaths was 12.17 (95% CI 10.64-13.91). Accidental deaths in men and homicide deaths in men and women were elevated. The pattern of deaths from other causes suggested that alcohol misuse was a contributory factor. CONCLUSIONS: People admitted to general hospitals in Scotland after attempted suicide are at high risk of readmission for further episodes of DSH. Long-term follow-up of such large cohorts is impractical, but services should review the scope for intervention in alcohol misuse following DSH.

Adolescent↗

[Nature and scope of the examination and review of the quality of care].

The quality is a dynamic and multidirectional phenomenon that depends on many factors. It changes in the time in relation to the variation of the cultural and social behaviours, of the scientific and technologic knowledges and to the change of the natural resources.

Attitude to Health↗

Recommendations for improving the quality of care through stroke centers and systems: an examination of stroke center identification options: multidisciplinary consensus recommendations from the Advisory Working Group on Stroke Center Identification Options of the American Stroke Association.

BACKGROUND AND PURPOSE: The American Stroke Association (ASA) assembled a multidisciplinary group of experts to develop recommendations regarding the potential effectiveness of establishing an identification program for stroke centers and systems. "Identification" refers to the full spectrum of models for assessing and recognizing standards of quality care (self-assessment, verification, certification, and accreditation). A primary consideration is whether stroke center identification might improve patient outcomes. METHODS: In February 2001, ASA, with the support of the Stroke Council's Executive Committee, decided to embark on an evaluation of the potential impact of stroke center identification. HealthPolicy R&D was selected to prepare a comprehensive report. The investigators reported on models outside the area of stroke, ongoing initiatives within the stroke community (such as Operation Stroke), and state and federal activities designed to improve care for stroke patients. The investigators also conducted interviews with thought leaders in the stroke community, representing a diverse sampling of specialties and affiliations. In October 2001, the Advisory Working Group on Stroke Center Identification developed its consensus recommendations. This group included recognized experts in neurology, emergency medicine, emergency medical services, neurological surgery, neurointensive care, vascular disease, and stroke program planning. RESULTS: There are a variety of existing identification programs, generally falling within 1 of 4 categories (self-assessment, verification, certification, and accreditation) along a continuum with respect to intensity and scope of review and consumption of resources. Ten programs were evaluated, including Peer Review Organizations, trauma centers, and new efforts by the National Committee on Quality Assurance and the Joint Commission on the Accreditation of Healthcare Organizations to identify providers and disease management programs. The largest body of literature on clinical outcomes associated with identification programs involves trauma centers. Most studies support that trauma centers and systems lead to improved mortality rates and patient outcomes. The Advisory Working Group felt that comparison to the trauma model was most relevant given the need for urgent evaluation and treatment of stroke. The literature in other areas generally supports the positive impact of identification programs, although patient outcomes data have less often been published. In the leadership interviews, participants generally expressed strong support for pursuing some form of voluntary identification program, although concerns were raised that this effort could meet with some resistance. CONCLUSIONS: Identification of stroke centers and stroke systems competencies is in the best interest of stroke patients in the United States, and ASA should support the development and implementation of such processes. The purpose of a stroke center/systems identification program is to increase the capacity for all hospitals to treat stroke patients according to standards of care, recognizing that levels of involvement will vary according to the resources of hospitals and systems.

Accreditation↗

Certificate of need: the Massachusetts experience.

Certificate of Need legislation is one of several regulatory programs designed to control the allocation of health care delivery resources. This paper examines the Massachusetts experience with Certificate of Need, focusing on two major administrative law controversies--the extent of the regulatory agency's power to participate actively in the planning process, and the scope of review of agency decisions permitted under a non-judicial appeals mechanism. The study concludes that any Certificate of Need program may be strengthened by accurately defining the roles of the participants and by providing for safeguards within the system itself.

Decision Making↗