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Natural Cure For High Blood PressureMonitoring and tracking your blood pressure on a daily basis may be the only way that you know if your plan of medical treatment is working. When Blood Pressure Goes Too Low - Health Essentials from Cleveland ClinicThis application records the blood pressure of every day. This doc shows the true team work of Nutanix with multiple team members contributing to the paper. Testimonials From Current Subscribers "Mike Adams is the best health and natural products writer on the scene today." - Ronnie Cummins, founder, Organic Consumers Association "Your newsletter is even better than books I've paid for!" - S. Here is a list of 10 factors that can temporarily cause significant deviations in your blood pressure measurements. Long-Term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study.
Effect of CPAP on Glycemic Control in Patients with Obstructive Sleep Apnea and Type 2 Diabetes. Stabilization of Glycemic Control and Improved Quality of Life Using a Shared Medical Appointment Model in Adolescents with Type 1 Diabetes in Suboptimal Control.
Diabetes and Risk of Community-Acquired Staphylococcus aureus Bacteremia: a Population-Based Case-Control Study. Incident Type 2 Diabetes and the Effect of Early Regression to Normoglycaemia in a Population with Impaired Glucose Regulation. Effect of Antihypertensive Treatment at Different Blood Pressure Levels in Patients with Diabetes Mellitus: Systematic Review and Meta-Analyses.
Dipeptidyl Peptidase-4 Inhibitors and Risk of Heart Failure in Type 2 Diabetes: Systematic Review and Meta-Analysis of Randomised and Observational Studies. Physical Fitness Among Swedish Military Conscripts and Long-Term Risk for Type 2 Diabetes Mellitus: a Cohort Study.
Effects of a Mindfulness-Based Weight Loss Intervention in Adults with Obesity: a Randomized Clinical Trial.
Perinatal Lead (Pb) Exposure Alters Gut Microbiota Composition and Results in Sex-Specific Bodyweight Increases in Adult Mice. Genome-Wide Association Analysis Identifies Three New Susceptibility Loci for Childhood Body Mass Index. Weight Loss and Variation of Levothyroxine (L-T4) Requirements in Hypothyroid Obese Patients After Bariatric Surgery. We present a selection of interesting endocrinology articles for the month of March in the following slides.
This patient with type 1 diabetes noted a painful erosion at the site of tattoo she had gotten several days earlier.
The study also includes the newer drugs in this class namely luseogliflozin, ipragliflozin and tofogliflozin. The newest class of drugs for type 2 diabetes are the sodium glucose co-transporter 2 receptor (SGLT-2) inhibitors.
In addition to the SGLT-2 transport system in the kidney, there is also a related transport system in the gut, SGLT-1. In-process and EMBASE from January 2005 to September 2014 using search strategies given in online supplementary appendix S1. The studies were screened for inclusion and exclusion by one author and checked by a second. RR.10 The model convergence was assessed using trace plots and the Brooks-Gelman-Rubin statistic.
We excluded the Bolinder 2012 trial11 of dapagliflozin because it recruited patients with very good baseline HbA1c (mean 7.2%) who would have less to gain.
We used a software called DigitizeIt to calculate SD from a published figure for an outcome mean change in HbA1c for a study13 assessing efficacy of canagliflozin in patients inadequately controlled with diet and exercise.
100a€…mg come from Inagaki 2014 where the 100 and 200a€…mg doses of canagliflozin were used. As aforementioned, for other outcomes, some SGLT-2 inhibitors could not be included in the analysis due to inadequate information. Canagliflozin 300a€…mg gave the largest reduction in HbA1c (a?’1.23%) compared with placebo. 2.6a€…mma€…Hg for empagliflozin 10a€…mg, though (figure 8) in some cases CIs were wide and the reductions were not statistically significant. For dual therapy, we undertook sensitivity analyses by including Kashiwagi et al24 (ipragliflozin), Henry et al12 (dapagliflozin) and Bolinder et al11 (dapagliflozin). All SGLT-2 inhibitors were significantly more effective than placebo for achieving HbA1c <7% (figure 9), reducing HbA1c (%) from baseline (figure 10), weight loss (figure 11) and reducing SBP (figure 12). For mean change in SBP, inclusion of the Kashiwagi (ipragliflozin) and Henry studies (dapagliflozin) caused contrasting results. In monotherapy, the reduction in weight was greatest with canagliflozin 100a€…mg (a?’3a€…kg). When interpreting weight changes, the baseline body mass indices (BMIs) need to be considered. The primary outcomes of both canagliflozin studies were reported at 26a€…weeks instead of 24a€…weeks. The usual first drug for type 2 diabetes is metformin, with sulfonylurea in those who cannot tolerate metformin.
Our New BMJ website does not support IE6 please upgrade your browser to the latest version or use alternative browsers suggested below. Being able to view the data as a table oThis doc shows the true team work of Nutanix with multiple team members contributing to the paper.
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Effects of Blood Pressure Reduction in Mild Hypertension: A Systematic Review and Meta-analysis.
Sundstrom was funded by the Swedish Heart-Lung Foundation (grant 20041151), Kjell och Marta Beijers Stiftelse, and the Swedish Research Council (grants 2007-5942 and 2010-1078). There was no need for a third reviewer to resolve any disagreements regarding inclusion or exclusion.
After removing 73 duplicate articles, there were 462 articles left for title and abstract screening.
Six studies11 ,12 ,14 ,16 ,19 ,24 compared flozins with placebo in dual therapy in patients failing to achieve glycaemic control on metformin alone.
Bolinder et al11 study was included in the sensitivity analysis of mean change in HbA1c and weight.
The results were slightly different when the trials by Kashiwagi et al24 and Henry et al12 were included, as discussed later.
There were no statistically significant differences between the two doses of canagliflozin and the two doses of empagliflozin. The CIs around ipragliflozin are very wide because no patients in the placebo group achieved HbA1c under 7%.
Those with a poor response to the 100a€…mg dose might also have a poor response to 300a€…mg.


All the SGLT-2 inhibitors reduced SBP, though wide CIs meant that differences were not always statistically significant.
Today I was prescribed Lisinoprl 5mg twice a day along with the my metoprolol 25mg twce a day. National Institute for Health Research (NIHR Oxford Biomedical Research Centre and NIHR Career Development Fellowship). Patterns were similar for attained systolic blood pressure.Conclusions Antihypertensive treatment reduces the risk of mortality and cardiovascular morbidity in people with diabetes mellitus and a systolic blood pressure more than 140 mm Hg.
Woodward are supported by National Health and Medical Research Council of Australia Senior Research Fellowships. This work received partial funding support from a National Health and Medical Research Council of Australia Program Grant.
All previous systematic reviews only analysed previously published data.7 8 13We assessed the effect of blood pressure lowering treatment in people with diabetes mellitus, including previously unpublished data. Although people with diabetes have been included in many trials of blood pressure lowering treatment, for most of these trials data on people with diabetes have not been published separately.
We contacted authors, pharmaceutical companies, and authorities to get access to this data. To assess the effect of treatment at different blood pressure levels, we stratified meta-analyses according to baseline and attained SBP. Baseline SBP is important because it reflects the clinical situation better than attained SBP.
Although blood pressure before treatment is known, the attained blood pressure with treatment may vary substantially. We included randomised controlled trials with a mean follow-up of 12 months or more and including 100 or more participants with diabetes mellitus.
Trials had to compare any antihypertensive agent against placebo, any two agents against one, or any blood pressure target against another. We excluded strictly comparative trials, evaluating one agent against another, as well as trials with combined interventions.During February 2013, we searched CENTRAL, Medline, Embase, and BIOSIS using broad strategies to maximise sensitivity.
CENTRAL was searched using the MeSH terms “antihypertensive agent” and “blood pressure”, exploded and combined, without restrictions in publication year or language (see the web appendix for full search strategies in each database). We also browsed reference lists in, and citations of, systematic reviews and guidelines in the discipline, including a more recently updated review.7 8 13 15 16 17 Using EndNote reference software, we combined the search results and removed duplicate records.
Both authors independently checked the abstracts and full text articles for eligibility and resolved any disagreements by discussion. Data were extracted into specially designed Excel sheets, pretested on 10 included trials and then modified to increase functionality. Given the poor reporting of adverse events and quality of life in the original trials, we excluded these outcomes before extraction of any data.
We collected data on baseline characteristics at trial level and blood pressure data for the intervention and control groups separately. When any data required according to the protocol were missing, but the trial was potentially eligible, we contacted the authors. Where data were available, we calculated relative risks for each outcome in each trial, and pooled results using random effects meta-analysis. We chose the random effects model over the fixed effects model because the included trials differed to some extent, both clinically and methodologically. The results of random and fixed effects models in analyses with low heterogeneity are the same, and if heterogeneity is present the random effects model is generally more conservative. Prespecified stratified analyses were performed based on mean baseline SBP and diastolic blood pressure (DBP) in all participants, mean in-treatment SBP and DBP for the intervention group, and mean differences in SBP and DBP between groups during follow-up. Cochran Q statistics were used to assess the interaction between blood pressure levels and treatment effect on outcomes, testing the null hypothesis that there is no difference between groups. We carried out prespecified metaregression analyses between each blood pressure variable and the treatment effect on each outcome.In the stratified analyses, we excluded trials predominantly including patients with heart failure because of the risk of assessing effects independent of blood pressure.
Also, we were unable to stratify analyses of amputation and blindness because too few trials reported these outcomes. For reasons of power, we excluded the baseline stratum for SBP less than 135 mm Hg and for attained SBP greater than 150 mm Hg. DBP stratification was done to achieve as equal a number of trials in each stratum as possible. Because SBP has the strongest association with cardiovascular disease, explaining more than 95% of events,19 we report on this in the review. DBP is problematic because it might be confounded by differences in pulse pressure, as seen between included trials. When heterogeneity was present, we scrutinised baseline characteristics, blood pressure data, and risk of bias assessments of the included trials for possible explanations. If such explanations were found, we carried out sensitivity analyses if we suspected a potential effect on the main results.
Publication bias was assessed using funnel plots for all outcomes separately, and for mortality in the stratified analyses. Analyses were performed using STATA v12.Patient involvementNo patients were involved in setting the research question or the outcome measures, nor were they involved in developing plans for design or implementation of the study. The mean difference in SBP between baseline and follow-up in the intervention groups was 10.2 mm Hg. Because of this, the trials included in each baseline SBP strata generally ended up in the strata for 10 mm Hg lower attained SBP. Relative risk is expressed as change in treatment effect for each 10 mm Hg lower baseline SBP. See table for results of all outcomes (those with significant results also presented as graphs). Each circle represents one trial and the size of each circle represents the weight given to the trial in metaregressionAll cause mortality was reduced if SBP before treatment was more than 140 mm Hg and if SBP with treatment was 130-140 mm Hg. Results were not significant for the attained SBP analyses but showed similar patterns, towards risk reduction if SBP was more than 130 mm Hg and towards harm if SBP was less than 130 mm Hg. If SBP was less than 140 mm Hg at baseline or less than 130 mm Hg during treatment, however, there was no association between treatment and risk. The lowest SBP stratum, for both baseline and attained SBP, had wide confidence intervals, reflecting low numbers of events. Both interaction analyses and metaregression analyses were not significant for both baseline and attained SBP.The risk of heart failure decreased with treatment if baseline SBP was more than 140 mm Hg and attained SBP was more than 130 mm Hg. For end stage renal disease, the only subgroup showing a positive effect of treatment was that with a baseline SBP of more than 150 mm Hg.
For both the baseline and attained analyses, the point estimate in the lowest strata was close to 1. Interaction tests and metaregression analyses were negative for heart failure and end stage renal disease.The web appendix presents non-stratified meta-analyses, meta-analyses stratified according to baseline and in-treatment DBP, and meta-analyses stratified according to differences in SBP and DBP between groups.
There was a significant interaction between baseline and attained DBP and cardiovascular mortality. Metaregression showed the risk of cardiovascular mortality to increase by 28 percentage points for each 10 mm Hg lower baseline DBP (P=0.013), crossing from benefit towards harm at 78 mm Hg.
One trial (DIabetic REtinopathy Candesartan Trials-Protect 2, DIRECT-P2) was judged to have high risk of bias in three domains.


This shifted the effect measures of all cause and cardiovascular mortality slightly more towards harm, but did not change the significance level for any outcome.DiscussionThis systematic review and meta-analyses confirms that blood pressure lowering treatment is associated with reduced mortality and cardiovascular morbidity in people with diabetes mellitus, if systolic blood pressure (SBP) before treatment is more than 140 mm Hg.
If SBP is less than 140 mm Hg, however, we found no benefit, but potential harm, with an increased risk of cardiovascular death. Treatment reduced the risk of all cause mortality, myocardial infarction, stroke, and heart failure, if SBP was treated to 130-140 mm Hg, but was associated with a non-significant increase in all cause and cardiovascular mortality if SBP was lowered to less than 130 mm Hg. The results are further supported by metaregression analyses showing that treatment effect on cardiovascular mortality and myocardial infarction is worse for each unit decrease in baseline SBP, and harmful below certain levels.Strengths and limitations of this reviewThis review has some limitations that are general to meta-analyses without access to individual patient data, including not being able to account for patient characteristics in a sophisticated way or analyse blood pressure levels within trials. Firstly, we identified more potentially eligible trials than could be included in the final analyses. These were trials in which we either knew there were people with diabetes but did not receive data on these participants, or trials in which there were no data on inclusion but participation by people with diabetes could not be excluded. Secondly, our analyses are stratified on mean baseline and attained blood pressure within trials. One way to reduce this risk of bias would have been to stratify on eligibility criteria or blood pressure targets instead of on measured values.
However, the blood pressure range accepted in each trial is usually wide, with great overlap between trials, making stratification on this variable virtually impossible. Thirdly, we see no increase in the risk of myocardial infarction or stroke, corresponding to the increase in cardiovascular mortality in the lowest SBP strata. Case fatality might increase with intensive treatment, reflecting lower margins to handle an event with lower blood pressure.
It could also reflect stricter definitions for myocardial infarction and stroke in the included trials than those used for cardiovascular mortality. For example, all unexpected deaths, deaths out of hospital, and deaths without known causes, usually qualify as cardiovascular mortality, but not as any specific event. Fourthly, most of the included trials were not designed to test different blood pressure targets but rather randomised patients to drug versus placebo. Thus, if blood pressure independent drug effects were present, they could affect our results. A recent systematic review showed no difference in treatment effect between drug classes for all cause and cardiovascular mortality.73 Also, all trials that randomised patients to specific drugs in the lowest blood pressure strata used renin angiotensin system (RAS) blockers. It has been suggested that these agents have a positive effect beyond that of blood pressure lowering,48 but still the main results in this stratum were negative. It is thus unlikely that the observed treatment effects in this review are related to drug class. Fifthly, the ALiskiren Trial In Type 2 Diabetes Using Cardio-Renal Endpoints (ALTITUDE) is given large weight in all meta-analyses within the baseline SBP stratum of less than 140 mm Hg. Importantly, this did not change the point estimate but widened the confidence intervals, indicating that the treatment effect is consistent across trials but that the power to establish such an effect is insufficient without ALTITUDE. In line with this, the shift in significance for cardiovascular mortality and stroke, between the baseline and attained SBP analyses, can also be attributed to ALTITUDE. Although baseline SBP was less than 140 mm Hg, this trial did not lower SBP to below 130 mm Hg. Sixthly, the majority of participants in the included trials in our meta-analyses had type 2 diabetes and were already treated with one or more antihypertensive agents. Firstly, we show an increased risk of cardiovascular death, an outcome not analysed by Emdin and colleagues.
Secondly, Emdin and colleagues showed a decreased risk of stroke, even if baseline SBP was less than 140 mm Hg, which we do not. Thirdly, Emdin and colleagues showed a decreased risk of albuminuria, an outcome we did not analyse. In the case of stroke, the difference in results between the two reviews can be explained by the standardisation used by Emdin and colleagues. Even if the best possible scenario, with respect to confidence intervals for end stage renal disease, was true, the absolute number of cardiovascular deaths exceeds that of end stage renal disease, and hence the numbers needed to treat would exceed the numbers needed to harm. The absence of a beneficial effect on stroke if baseline SBP is less than 140 mm Hg also differs compared with another review, including both people with diabetes and people with impaired fasting glucose.8 It is reasonable to think that the vessels of people with impaired fasting glucose are less affected than those of people with manifest diabetes, and hence they might be less sensitive to, and perhaps more helped by, additional blood pressure lowering. Recently, the results of the Systolic Blood Pressure Intervention Trial (SPRINT) were published.74 This was a randomised controlled trial comparing a systolic blood pressure target of less than 120 mm Hg with one less than 140 mm Hg, in high risk patients with moderately elevated blood pressure. The trial was stopped preterm owing to a highly significant reduction in all cause mortality, suggesting that this population might benefit from very aggressive blood pressure treatment. Impaired myocardial perfusion, compared with the superior autoregulation of cerebral blood flow, could also explain the different effects of blood pressure levels on myocardial infarction and stroke. Another potential explanation for our findings is that low blood pressure leads to less coronary collateral circulation. Results from the analyses stratified by baseline SBP are largely consistent with those stratified by attained SBP. The interaction between blood pressure and treatment effect is reproducible across exposure variables and outcomes, indicating a robust dose-response relation. Together with a possible biological mechanism, our results suggest that SBP before treatment modifies the effect of treatment in a causal way.The results are important both conceptually for research on hypertension and for clinicians. Firstly, we show that not only the absolute, but also the relative benefit of blood pressure lowering is attenuated at lower blood pressures. This suggests that the linear relation between blood pressure and cardiovascular disease seen in some observational studies cannot be extrapolated to assumed benefit of treatment. Stretching this further, we show, based on randomised comparisons, that treatment below a certain blood pressure level might be harmful. Secondly, and contrary to what has previously been recommended, our results, combined with those from the SPRINT trial, suggest that blood pressure treatment goals should be less aggressive in people with diabetes than without diabetes. This review strongly supports blood pressure treatment in people with diabetes mellitus if SBP is more than 140 mm Hg. When should antihypertensive drug treatment be initiated and to what levels should systolic blood pressure be lowered?
Effects of intensive blood pressure control in the management of patients with type 2 diabetes mellitus in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. 2007 Guidelines for the management of arterial hypertension - The task force for the management of arterial hypertension of the European society of hypertension (ESH) and of the European society of cardiology (ESC). Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Effects of intensive blood pressure reduction on myocardial infarction and stroke in diabetes: a meta-analysis in 73,913 patients. Clinical practice guidelines for the management of hypertension in the community a statement by the American Society of Hypertension and the International Society of Hypertension.
2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8).



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