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Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema.
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Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement
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Houston doctors say they may have found a way to destroy HIV | News for Austin, Texas | KVUE.com | State News
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Diagnosis and treatment of vitamin B12 deficiency--an update -- Hvas and Nexo 91 (11): 1506 -- Haematologica
Nice review - PDF file, downloads when link is clicked (no HTML for some reason)
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|| DukeMedNews || Blocked Brain Enzyme Decreases Appetite and Promotes Weight Loss
Activation of the enzyme CaMKK2 is just one step in the appetite stimulation pathway located in the hypothalamus section of the brain. An empty stomach releases the hormone ghrelin, which launches a cascade of signals that ultimately results in increased appetite.
Means and colleagues believed that CaMKK2 in the ghrelin pathway might be a likely candidate for study, because it activates AMPK, an enzyme that stimulates animals to eat and gain weight. They tested their theory in several ways, the results of which are published in the May issue of Cell Metabolism. The work was funded by NIH grants, as well as by the Australian Research Council, National Heart Foundation and the National Health and Medical Research Council of Australia.
First they blocked CaMKK2 in mice with a specialized molecule inhibitor and then measured food intake. These mice ate significantly less food than untreated mice during the six days in which they were evaluated, and also lost body weight, which led the scientists to think they might be on to something.
Next they studied a group of mice that normally do not make CaMKK2 and found that the molecule inhibitor did not change feeding behavior or reduce weight. "The fact that blocking CaMKK2 worked in normal mice to make them eat less and lose weight, but not in mice missing the enzyme, provides compelling evidence that CaMKK2 signaling is a requirement for appetite control," Means said.
They also studied both normal mice and mice missing CaMKK2 to learn how these types responded to low-fat and high-fat diets. After nearly 30 weeks on the specific diets, the normal mice on the high-fat diet became diabetic – they were unable to respond to insulin and weren't able to manage blood sugar levels well. In contrast, the normal mice on a low-fat diet stayed healthy.
In mice missing CaMKK2, the scientists found that they stayed healthy regardless of whether they were on a low-fat or high-fat diet. The CAMKK2-negative mice apparently were protected from changes that lead to diabetes in a high-fa
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The Danish multicentre randomized study of fibrino...[Eur Heart J. 2008] - PubMed Result
Background The DANAMI-2 trial showed that in patients with ST-elevation myocardial infarction (STEMI), a strategy of inter-hospital transfer for primary angioplasty was superior to on-site fibrinolysis at 30 days follow-up. This paper reports on the pre-specified long-term composite endpoint at 3 years follow-up in DANAMI-2. Methods and results We randomized 1572 patients with STEMI to primary angioplasty or intravenous alteplase; 1129 patients were enrolled at 24 referral hospitals and 443 patients at 5 angioplasty centres. Ninety-six percent of inter-hospital transfers for angioplasty were completed within 2 h. No patients were lost to follow-up. The composite endpoint (death, clinical re-infarction, or disabling stroke) was reduced by angioplasty when compared with fibrinolysis at 3 years (19.6 vs. 25.2%, P =0.006). For patients transferred to angioplasty compared with those receiving on-site fibrinolysis, the composite endpoint occurred in 20.1 vs. 26.7% (P = 0.007), death in 13.6 vs. 16.4% (P = 0.18), clinical re-infarction in 8.9 vs. 12.3% (P = 0.05), and disabling stroke in 3.2 vs. 4.7% (P = 0.23). Conclusion The benefit of transfer for primary angioplasty based on the composite endpoint was sustained after 3 years. For patients with characteristics as those in DANAMI-2, primary angioplasty should be the preferred treatment strategy when inter-hospital transfer can be completed within 2 h.
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Sensitivity and Specificity of a Single Emergency Department Measurement of Urinary Neutrophil Gelatinase-Associated Lipocalin for Diagnosing Acute Kidney Injury -- Nickolas et al. 148 (11): 810 -- Annals of Internal Medicine
Background: A single serum creatinine measurement cannot distinguish acute kidney injury from chronic kidney disease or prerenal azotemia.
Objective: To test the sensitivity and specificity of a single measurement of urinary neutrophil gelatinase–associated lipocalin (NGAL) and other urinary proteins to detect acute kidney injury in a spectrum of patients.
Design: Prospective cohort study.
Setting: Emergency department of Columbia University Medical Center, New York, New York.
Participants: 635 patients admitted to the hospital with acute kidney injury, prerenal azotemia, chronic kidney disease, or normal kidney function.
Measurements: Diagnosis of acute kidney injury was based on the RIFLE (risk, injury, failure, loss, and end-stage) criteria and assigned by researchers who were blinded to experimental measurements. Urinary NGAL was measured by immunoblot, N-acetyl-β-d-glucosaminidase (NAG) by enzyme measurement, {alpha}1-microglobulin and {alpha}1-acid glycoprotein by immunonephelometry, and serum creatinine by Jaffe kinetic reaction. Experimental measurements were not available to treating physicians.
Results: Patients with acute kidney injury had a significantly elevated mean urinary NGAL level compared with the other kidney function groups (416 µg/g creatinine [SD, 387]; P = 0.001). At a cutoff value of 130 µg/g creatinine, sensitivity and specificity of NGAL for detecting acute injury were 0.900 (95% CI, 0.73 to 0.98) and 0.995 (CI, 0.990 to 1.00), respectively, and positive and negative likelihood ratios were 181.5 (CI, 58.33 to 564.71) and 0.10 (CI, 0.03 to 0.29); these values were superior to those for NAG, {alpha}1-microglobulin, {alpha}1-acid glycoprotein, fractional excretion of sodium, and serum creatinine. In multiple logistic regression, urinary NGAL level was highly predictive of clinical outcomes, including nephrology consultation, dialysis, and admission to the intensive care unit (odds ratio, 24.71 [CI, 7.69 to 79.42]).
Limitations: All patients came from a single center. Few kidney biop
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Meta-analysis: Subclinical Thyroid Dysfunction and the Risk for Coronary Heart Disease and Mortality -- Ochs et al. 148 (11): 832 -- Annals of Internal Medicine
Background: Data on the association between subclinical thyroid dysfunction and coronary heart disease (CHD) and mortality are conflicting.
Purpose: To summarize prospective evidence about the relationship between subclinical thyroid dysfunction and CHD and mortality.
Data Sources: MEDLINE (1950 to January 2008) without language restrictions and reference lists of retrieved articles were searched.
Study Selection: Two reviewers screened and selected cohort studies that measured thyroid function and then followed persons prospectively to assess CHD or mortality.
Data Extraction: By using a standardized protocol and forms, 2 reviewers independently abstracted and assessed studies.
Data Synthesis: Ten of 12 identified studies involved population-based cohorts that included 14 449 participants. All 10 population-based cohort studies examined risks associated with subclinical hypothyroidism (2134 CHD events and 2822 deaths), whereas only 5 examined risks associated with subclinical hyperthyroidism (1392 CHD events and 1993 deaths). In a random-effects model, the relative risk (RR) for subclinical hypothyroidism for CHD was 1.20 (95% CI, 0.97 to 1.49; P for heterogeneity = 0.14; I2 = 33.4%). Risk estimates were lower when higher-quality studies were pooled (RR, 1.02 to 1.08) and were higher among participants younger than 65 years (RR, 1.51 [CI, 1.09 to 2.09] for studies with mean participant age <65 years and 1.05 [CI, 0.90 to 1.22] for studies with mean participant age ≥65 years). The RR was 1.18 (CI, 0.98 to 1.42) for cardiovascular mortality and 1.12 (CI, 0.99 to 1.26) for total mortality. For subclinical hyperthyroidism, the RR was 1.21 (CI, 0.88 to 1.68) for CHD, 1.19 (CI, 0.81 to 1.76) for cardiovascular mortality, and 1.12 (CI, 0.89 to 1.42) for total mortality (P for heterogeneity >0.50; I2 = 0% for all studies).
Limitations: Individual studies adjusted for different potential confounders, and 1 study provided only unadjusted data. Publication bias or selective reporting of outcomes could not be excluded
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Are Intensivists Safe? -- Rubenfeld and Angus 148 (11): 877 -- Annals of Internal Medicine
In this issue, Levy and colleagues (10) explore the effects of ICU physician staffing models on mortality in Project IMPACT, a consortium of ICUs that receive benchmarking data in an effort to improve their care. Their findings not only refute the claim that intensivist-staffed ICUs improve outcomes but raise the possibility that intensivists are actually harmful. It is a complex study made more so by combining 2 separate research questions: one on the effect of intensivist care in choice ICUs and the other on intensivist care in no-choice ICUs.
Most of the patients in this cohort received care in choice ICUs, where someone, presumably a physician, decided whether to involve an intensivist. The investigators found that elective management by an intensivist in choice ICUs was associated with increased mortality. Elective management by an intensivist in a choice ICU should not be confused with intensivist staffing. The choice ICUs would all be classified as low-intensity staffed ICUs because intensivist involvement with a patient's care was discretionary. The effect of intensivists in low-intensity–staffed ICUs has not been studied extensively, but Levy and colleagues are not the first to raise concerns about this model of care. Treggiari and colleagues (11) demonstrated that elective consultation by a pulmonologist in open ICUs was associated with no benefit in patients with acute lung injury. These authors attributed the lack of association to indication bias, arguing that physicians would be more likely to seek help in cases that they judged to have worse prognosis. Because physicians' predictions of outcome contribute to prognoses generated by mathematical models, indication bias is difficult to eliminate from observational studies with regression models (12). Estimates of prognosis probably affect the decision to involve an intensivist, making the analysis of the choice ICUs susceptible to the same bias. Despite these limitations, these 2 studies certainly raise concerns that elective intensivist consultation
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Cardiovascular Consequences of Subclinical Thyroid Dysfunction: More Smoke but No Fire -- Ladenson 148 (11): 880 -- Annals of Internal Medicine
On the basis of our knowledge of human biology, thyroid hormone deficiency and excess could increase risks for atherosclerosis, heart failure, and cardiac dysrhythmias (6). The thyroid hormones alter cholesterol and homocysteine metabolism, endovascular functions, and coagulability; they influence systolic and diastolic myocardial performance; and they affect the cardiac conducting system, particularly the sinoatrial node and potentially aberrant atrial region pacemaker cells. Sensitive serologic markers, imaging techniques, and electrophysiologic measurements demonstrate these effects. Clinical investigators have used various research designs: case–control studies, small controlled trials, cross-sectional epidemiologic analyses, prospective observational studies, and in recent years, meta-analyses of these studies to determine whether these effects cause clinical disease. In this issue, Ochs and colleagues (7) report a meta-analysis of selected population-based cohort studies, in which researchers have tested the hypothesis that disorders of thyroid function increase coronary heart disease (CHD) events and mortality. Ten studies reported risks associated with subclinical hypothyroidism, and 5 examined risks associated with subclinical thyrotoxicosis.
For subclinical hypothyroidism, the relative risks for CHD events and cardiovascular and overall mortality were 1.2, 1.2, and 1.1, respectively, with 95% CIs that, in each case, extended slightly below 1.0. Limiting analyses to studies with the most rigorous methodologies slightly decreased these risk estimates, whereas including studies that used convenience samples of patients increased them. On the basis of these studies, the independent CHD risk that subclinical hypothyroidism poses seems to be very modest, if it exists at all.
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Escitalopram and Problem-Solving Therapy for Prevention of Poststroke Depression: A Randomized Controlled Trial, May 28, 2008, Robinson et al. 299 (20): 2391
Context Depression occurs in more than half of patients who have experienced a stroke. Poststroke depression has been shown in numerous studies to be associated with both impaired recovery in activities of daily living and increased mortality. Prevention of depression thus represents a potentially important goal.
Objective To determine whether treatment with escitalopram or problem-solving therapy over the first year following acute stroke will decrease the number of depression cases that develop compared with placebo medication.
Design, Setting, and Participants A multisite randomized controlled trial for prevention of depression among 176 nondepressed patients was conducted within 3 months following acute stroke from July 9, 2003, to October 1, 2007. The 12-month trial included 3 groups: a double-blind placebo-controlled comparison of escitalopram (n = 59) with placebo (n = 58), and a nonblinded problem-solving therapy group (n = 59).
Main Outcome Measures The main outcome measure was the development of major or minor poststroke depression based on symptoms elicited by the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) (DSM-IV) and the diagnostic criteria from DSM-IV for depression due to stroke with major depressive-like episode or minor depression (ie, research criteria).
Results Patients who received placebo were significantly more likely to develop depression than individuals who received escitalopram (11 major and 2 minor cases of depression [22.4%] vs 3 major and 2 minor cases of depression [8.5%], adjusted hazard ratio [HR], 4.5; 95% confidence interval [CI], 2.4-8.2; P < .001) and also more likely than individuals who received problem-solving therapy (5 major and 2 minor cases of depression [11.9%], adjusted HR, 2.2; 95% CI, 1.4-3.5; P < .001). These results were adjusted for history of mood disorders and remained significant after considering possible confounders such as age, sex, treatment site, and severity of impairment in the mo
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JAMA -- CCB/ACE Inhibitor Dual Therapy for Hypertension Lowers Cardiovascular Risk, May 21, 2008, Mitka 299 (19): 2263
The randomized double-blind ACCOMPLISH trial enrolled 11 462 patients in the United States and Nordic countries. Participants, who were aged 55 years or older (average age was 68 years) and who were at high risk for cardiovascular disease (systolic blood pressure ≥160 mm Hg, or currently on antihypertensive therapy and who had evidence of cardiovascular or renal disease), were to be followed up for 36 months before the trial was halted. Patients were randomly assigned to receive a pill containing both benazepril (an ACE inhibitor) and amlodipine (a CCB) or a pill containing both benazepril and hydrochlorothiazide (a diuretic). The study was funded by Novartis Pharmaceuticals Corp, East Hanover, NJ, which manufactures a CCB/ACE inhibitor combination therapy in a range of doses.
At 30 months, blood pressure of patients in both treatment groups decreased to a mean of about 130 mm Hg systolic and about 80 mm Hg diastolic, but those receiving the CCB/ACE inhibitor combination experienced 20% less cardiovascular morbidity and mortality (defined as cardiovascular deaths, myocardial infarctions, stroke, hospitalization for unstable angina, and revascularization) compared with the other group.
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