Veterans Health Administration

About: Veterans Health Administration is a government organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Population & Veterans Affairs. The organization has 63820 authors who have published 98417 publications receiving 4835425 citations. The organization is also known as: VHA.

Multiple-Organ-Failure Syndrome

Abstract: INCIDENCE AND PROBLEMS OF MULTIPLE-ORGAN-FAILURE SYNDROMES The panelists for the discussion were C. James Carrico, MD, from Seattle; Jonathan Meakins, MD, DSc, FRCSC, FACS, from Montreal; Donald Fry, MD, from Cleveland; and Ronald V. Maier, MD, from Seattle. Dr Carrico: Multiple-organ-failure (MOF) syndrome is a process that occurs following 7% to 22% of emergency operations and between 30% and 50% of operations for intra-abdominal sepsis; MOF syndrome carries a mortality that varies from 30% to 100% depending on the number of organs involved. Treatment usually involves support of the organ (system) function and control of sepsis. 1,2 In developing a clinical description, we can use a classic description of respiratory failure from the late 1960s as a model. Rather than a single organ we need to describe the function of several systems and follow the changes through a series of stages, beginning with the patient who has recently experienced one

Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease

Abstract: Profound neuronal dysfunction in the entorhinal cortex contributes to early loss of short-term memory in Alzheimer's disease. Here we show broad neuroprotective effects of entorhinal brain-derived neurotrophic factor (BDNF) administration in several animal models of Alzheimer's disease, with extension of therapeutic benefits into the degenerating hippocampus. In amyloid-transgenic mice, BDNF gene delivery, when administered after disease onset, reverses synapse loss, partially normalizes aberrant gene expression, improves cell signaling and restores learning and memory. These outcomes occur independently of effects on amyloid plaque load. In aged rats, BDNF infusion reverses cognitive decline, improves age-related perturbations in gene expression and restores cell signaling. In adult rats and primates, BDNF prevents lesion-induced death of entorhinal cortical neurons. In aged primates, BDNF reverses neuronal atrophy and ameliorates age-related cognitive impairment. Collectively, these findings indicate that BDNF exerts substantial protective effects on crucial neuronal circuitry involved in Alzheimer's disease, acting through amyloid-independent mechanisms. BDNF therapeutic delivery merits exploration as a potential therapy for Alzheimer's disease.

Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial.

Abstract: ContextA low plasma level of high-density lipoprotein cholesterol (HDL-C) is a major risk factor for coronary heart disease (CHD). A secondary prevention study, the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT), demonstrated that CHD events were significantly reduced during a median follow-up of 5.1 years by treating patients with the fibric acid derivative gemfibrozil when the predominant lipid abnormality was low HDL-C.ObjectiveTo determine if the reduction in major CHD events with gemfibrozil in VA-HIT could be attributed to changes in major plasma lipid levels.DesignMulticenter, randomized, double-blind, placebo-controlled trial conducted from September 1991 to August 1998.SettingThe Department of Veterans Affairs Cooperative Studies Program, in which 20 VA medical centers were participating sites.ParticipantsA total of 2531 men with a history of CHD who had low HDL-C levels (mean, 32 mg/dL [0.83 mmol/L] ) and low low-density lipoprotein cholesterol (LDL-C) levels (mean, 111 mg/dL [2.88 mmol/L]).InterventionParticipants were randomly assigned to receive gemfibrozil, 1200 mg/d (n = 1264), or matching placebo (n = 1267).Main Outcome MeasureRelation of lipid levels at baseline and averaged during the first 18 months of gemfibrozil treatment with the combined incidence of nonfatal myocardial infarction and CHD death.ResultsConcentrations of HDL-C were inversely related to CHD events. Multivariable Cox proportional hazards analysis showed that CHD events were reduced by 11% with gemfibrozil for every 5-mg/dL (0.13-mmol/L) increase in HDL-C (P = .02). Events were reduced even further with gemfibrozil beyond that explained by increases in HDL-C values, particularly in the second through fourth quintiles of HDL-C values during treatment. During gemfibrozil treatment, only the increase in HDL-C significantly predicted a lower risk of CHD events; by multivariable analysis, neither triglyceride nor LDL-C levels at baseline or during the trial predicted CHD events.ConclusionsConcentrations of HDL-C achieved with gemfibrozil treatment predicted a significant reduction in CHD events in patients with low HDL-C levels. However, the change in HDL-C levels only partially explained the beneficial effect of gemfibrozil.

Recommendations for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis

Abstract: Glucocorticoid-induced bone loss should be prevented, and if present, should be treated (Table 2). Supplementation with calcium and vitamin D at a dosage of 800 IU/day, or an activated form of vitamin D (e.g., alfacalcidiol at 1 microg/day or calcitriol at 0.5 microg/day), should be offered to all patients receiving glucocorticoids, to restore normal calcium balance. This combination has been shown to maintain bone mass in patients receiving long-term low-to-medium-dose glucocorticoid therapy who have normal levels of gonadal hormones. However, while supplementation with calcium and vitamin D alone generally will not prevent bone loss in patients in whom medium-to-high-dose glucocorticoid therapy is being initiated, supplementation with calcium and an activated form of vitamin D will prevent bone loss. There are no data available to support any conclusion about the antifracture efficacy of the combination of calcium supplementation plus an activated form of vitamin D. Antiresorptive agents are effective in the treatment of glucocorticoid-induced bone loss. All of these agents either prevent bone loss or modestly increase lumbar spine bone mass and maintain hip bone mass. While there are no randomized controlled trials of prevention of glucocorticoid-induced bone loss or radiographic vertebral fracture outcomes with HRT or testosterone, patients receiving long-term glucocorticoid therapy who are hypogonadal should be offered HRT. The bisphosphonates are effective for both the prevention and the treatment of glucocorticoid-induced bone loss. Large studies have demonstrated that bisphosphonates also reduce the incidence of radiographic vertebral fractures in postmenopausal women with glucocorticoid-induced osteoporosis. Treatment with a bisphosphonate is recommended to prevent bone loss in all men and postmenopausal women in whom long-term glucocorticoid treatment at > or =5 mg/day is being initiated, as well as in men and postmenopausal women receiving long-term glucocorticoids in whom the BMD T-score at either the lumbar spine or the hip is below normal. While there is little information on the prevention or treatment of bone loss in premenopausal women, these women, too, may lose bone mass if they are being treated with glucocorticoids, so prevention of bone loss with antiresorptive agents should be considered. If bisphosphonate therapy is being considered for a premenopausal woman, she must be counseled regarding use of appropriate contraception. The therapies to prevent or treat glucocorticoid-induced bone loss should be continued as long as the patient is receiving glucocorticoids. Data from large studies of anabolic agents (e.g., PTH) and further studies of combination therapy in patients receiving glucocorticoids are eagerly awaited so additional options will be available for the prevention of this serious complication of glucocorticoid treatment.

Financial incentive-based approaches for weight loss: a randomized trial.

Abstract: Context Identifying effective obesity treatment is both a clinical challenge and a public health priority due to the health consequences of obesity. Objective To determine whether common decision errors identified by behavioral economists such as prospect theory, loss aversion, and regret could be used to design an effective weight loss intervention. Design, Setting, and Participants Fifty-seven healthy participants aged 30-70 years with a body mass index of 30-40 were randomized to 3 weight loss plans: monthly weigh-ins, a lottery incentive program, or a deposit contract that allowed for participant matching, with a weight loss goal of 1 lb (0.45 kg) a week for 16 weeks. Participants were recruited May-August 2007 at the Philadelphia VA Medical Center in Pennsylvania and were followed up through June 2008. Main Outcome Measures Weight loss after 16 weeks. Results The incentive groups lost significantly more weight than the control group (mean, 3.9 lb). Compared with the control group, the lottery group lost a mean of 13.1 lb (95% confidence interval [CI] of the difference in means, 1.95-16.40; P=.02) and the deposit contract group lost a mean of 14.0 lb (95% CI of the difference in means, 3.69-16.43; P =.006). About half of those in both incentive groups met the 16-lb target weight loss: 47.4% (95% CI, 24.5%-71.1%) in the deposit contract group and 52.6% (95% CI, 28.9%-75.6%) in the lottery group, whereas 10.5% (95% CI, 1.3%- 33.1%; P = .01) in the control group met the 16-lb target. Although the net weight loss between enrollment in the study and at the end of 7 months was larger in the incentive groups (9.2 lb; t = 1.21; 95% CI, −3.20 to 12.66; P = .23, in the lottery group and 6.2 lb; t = 0.52; 95% CI, −5.17 to 8.75; P = .61 in the deposit contract group) than in the control group (4.4 lb), these differences were not statistically significant. However, incentive participants weighed significantly less at 7 months than at the study start (P = .01 for the lottery group; P = .03 for the deposit contract group) whereas controls did not. Conclusions The use of economic incentives produced significant weight loss during the 16 weeks of intervention that was not fully sustained. The longer-term use of incentives should be evaluated. Trial Registration clinicaltrials.gov Identifier: NCT00520611