Pharma Care Tweet from @tonybluu
@tonybluu: Pharmacists Find New Ways to Improve Care Transitions http://t.co/Gw56pP84Vd
...an email.
Sunday, April 21, 2013
Weight loss...
Looking for that extra boost to help with your weight loss? http://bit.ly/SYSuiy
...an email.
Licking Your Own Wounds...
Licking your own wounds actually speed up the healing process -- Human saliva contains many antibacterial compounds.
...a BB® email
Wednesday, March 20, 2013
World Water Day - (wikipaedia)
World Water Day
From Wikipedia, the free encyclopedia
| World Water Day | |
|---|---|
| Observed by | All UN member states |
| Date | 22 March |
World Water Day has been observed on 22 March since 1993 when the United Nations General Assembly declared 22 March as World Day for Water.[1]
This day was first formally proposed in Agenda 21 of the 1992 United Nations Conference on Environment and Development (UNCED) in Rio de Janeiro, Brazil. Observance began in 1993 and has grown significantly ever since; for the general public to show support, it is encouraged for the public to not use their taps throughout the whole day, the day has become a popular Facebook trend.
The UN and its member nations devote this day to implementing UN recommendations and promoting concrete activities within their countries regarding the world's water resources. Each year, one of various UN agencies involved in water issues takes the lead in promoting and coordinating international activities for World Water Day. Since its inception in 2003, UN-Water has been responsible for selecting the theme, messages and lead UN agency for the World Day for Water.
In addition to the UN member states, a number of NGOs promoting clean water and sustainable aquatic habitats have used World Day for Water as a time to focus public attention on the critical water issues of our era. Every three years since 1997, for instance, the World Water Council has drawn thousands to participate in its World Water Forum during the week of World Day for Water. Participating agencies and NGOs have highlighted issues such as a billion people being without access to safe water for drinking and the role of gender in family access to safe water. In 2003, 2006 and 2009, the UN World Water Development Report was launched on the occasion of the World Water Day. The fourth Report is expected to be released around 22 March 2012.
World Water Day
International Year of Water Cooperation - 22 Maech 2013
Water cooperation
Good management of water is especially challenging due to some of its unique characteristics: it is unevenly distributed in time and space, the hydrological cycle is highly complex and perturbations have multiple effects. Rapid urbanization, pollution and climate change threaten the resource while demands for water are increasing in order to satisfy the needs of a growing world population, now at over seven billion people, for food production, energy, industrial and domestic uses. Water is a shared resource and its management needs to take into account a wide variety of conflicting interests. This provides opportunities for cooperation among users.
In designating 2013 as the UN International Year of Water Cooperation, the UNGA recognizes that cooperation is essential to strike a balance between the different needs and priorities and share this precious resource equitably, using water as an instrument of peace. Promoting water cooperation implies an interdisciplinary approach bringing in cultural, educational and scientific factors, as well as religious, ethical, social, political, legal, institutional and economic dimensions.
Source: http://www.unwater.org/water-cooperation-2013/water-cooperation/en/
Masked Hypertension in Diabetes Mellitus
Masked Hypertension in Diabetes Mellitus
Treatment Implications for Clinical Practice
Abstract
Although distinguishing features of masked hypertension in diabetics are well known, the significance of antihypertensive treatment on clinical practice decisions has not been fully explored. We analyzed 9691 subjects from the population-based 11-country International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes. Prevalence of masked hypertension in untreated normotensive participants was higher (P<0.0001) among 229 diabetics (29.3%, n=67) than among 5486 nondiabetics (18.8%, n=1031). Over a median of 11.0 years of follow-up, the adjusted risk for a composite cardiovascular end point in untreated diabetic-masked hypertensives tended to be higher than in normotensives (hazard rate [HR], 1.96; 95% confidence interval [CI], 0.97–3.97; P=0.059), similar to untreated stage 1 hypertensives (HR, 1.07; CI, 0.58–1.98; P=0.82), but less than stage 2 hypertensives (HR, 0.53; CI, 0.29–0.99; P=0.048). In contrast, cardiovascular risk was not significantly different in antihypertensive-treated diabetic-masked hypertensives, as compared with the normotensive comparator group (HR, 1.13; CI, 0.54–2.35; P=0.75), stage 1 hypertensives (HR, 0.91; CI, 0.49–1.69; P=0.76), and stage 2 hypertensives (HR, 0.65; CI, 0.35–1.20; P=0.17). In the untreated diabetic-masked hypertensive population, mean conventional systolic/diastolic blood pressure was 129.2±8.0/76.0±7.3 mm Hg, and mean daytime systolic/diastolic blood pressure 141.5±9.1/83.7±6.5 mm Hg. In conclusion, masked hypertension occurred in 29% of untreated diabetics, had comparable cardiovascular risk as stage 1 hypertension, and would require considerable reduction in conventional blood pressure to reach daytime ambulatory treatment goal. Importantly, many hypertensive diabetics when receiving antihypertensive therapy can present with normalized conventional and elevated ambulatory blood pressure that mimics masked hypertension.
Source / Read more: http://hyper.ahajournals.org/content/early/2013/03/11/HYPERTENSIONAHA.111.00289
A Step toward Personalized Asthma Treatment
A Step toward Personalized Asthma Treatment
Jeffrey M. Drazen, M.D.
Inhaled glucocorticoids are used every day by millions of patients with asthma. As with all asthma-controller treatments, there is marked patient-to-patient variability in the therapeutic response1; about one in three patients with asthma who use inhaled glucocorticoids may not benefit from this treatment. It would be advantageous if we could identify, in advance, patients who would respond to such treatment, but we have not been able to do so, despite major efforts during the past decade. In this issue of the Journal, Tantisira and colleagues appear to have made progress toward reaching this goal with the identification of a genetic variant associated with the response to inhaled glucocorticoids in the treatment of asthma.2
To identify this genetic variant, the group first used the clinical data and DNA resources from patients enrolled in the Childhood Asthma Management Program (CAMP), sponsored by the National Heart, Lung, and Blood Institute.3 Children 5 through 12 years of age who had asthma of moderate severity were enrolled in CAMP and were treated for 5 years with budesonide (an inhaled glucocorticoid), nedocromil sodium, or placebo. The frequent measurements of lung function and careful monitoring for asthma exacerbations resulted in a rich database of clinical information for use in the genetic studies. But what made the cohort most useful to these investigators was the availability of DNA from the children with asthma and from their parents — so-called DNA trios. Armed with one sample from an affected child and one sample from each of the child's parents, the investigators were able to use family-based statistics to identify 13 single-nucleotide–polymorphism (SNP) candidates from the hundreds of thousands of SNPs they had genotyped.4 The authors then tested these potential candidates in four replication populations and identified a variant in the glucocorticoid-induced transcript 1 gene (GLCCI1), rs37972, associated with a decrease in forced expiratory volume in 1 second (FEV1) in response to treatment with inhaled glucocorticoids. To offer additional reassurance that they had identified a causative SNP, the investigators provided data from isolated cell systems containing the pharmacogenetically identified SNP (and rs37973, which is in complete linkage disequilibrium with rs37972) to show that the presence of these sequence variants was associated with biologic changes that would be consistent with a decreased response to these agents.
Read more/ Source: http://www.nejm.org/doi/full/10.1056/NEJMe1102469
Effect of Bronchoconstriction on Airway Remodeling in Asthma
Effect of Bronchoconstriction on Airway Remodeling in Asthma
Christopher L. Grainge, Ph.D., Laurie C.K. Lau, Ph.D., Jonathon A. Ward, B.Sc., Valdeep Dulay, B.Sc., Gemma Lahiff, B.Sc., Susan Wilson, Ph.D., Stephen Holgate, D.M., Donna E. Davies, Ph.D., and Peter H. Howarth, D.M.
BACKGROUND
Asthma is a common chronic respiratory condition characterized clinically by an excessive tendency toward reversible airway narrowing. This may arise in response to everyday environmental exposure and is worsened both by intercurrent infection and, in sensitized persons, by allergen exposure. In pathological terms, asthma is characterized by airway inflammation and by structural changes in airway tissues, such as epithelial goblet-cell hyperplasia, subepithelial collagen deposition, and smooth-muscle hypertrophy — collectively referred to as airway remodeling.1-3 Since an inhaled-allergen challenge in atopic asthma induces eosinophilic inflammation of the airway and changes in the extracellular matrix,4 and since a reduction in airway eosinophils has been reported to reduce certain markers of airway remodeling,5 such structural changes in the tissues have been considered a consequence of eosinophilic airway inflammation.6 This paradigm, however, fails to account for the potential contribution of airway narrowing to airway remodeling. Bronchoconstriction generates excessive mechanical forces within the airways that distort tissue cells,7,8 and mechanical forces within other organs are known to induce tissue remodeling.9-11 In vitro studies in a variety of models have shown that ex vivo compression of the airway epithelium results in changes that mimic those identified and associated with remodeling in vivo.12-15 We therefore hypothesized that the airway narrowing induced by allergen exposure in vivo in patients with asthma may in itself be a sufficient stimulus for the development of airway remodeling and that such remodeling is not solely dependent on induced recruitment of airway eosinophils.
Asthma is a common chronic respiratory condition characterized clinically by an excessive tendency toward reversible airway narrowing. This may arise in response to everyday environmental exposure and is worsened both by intercurrent infection and, in sensitized persons, by allergen exposure. In pathological terms, asthma is characterized by airway inflammation and by structural changes in airway tissues, such as epithelial goblet-cell hyperplasia, subepithelial collagen deposition, and smooth-muscle hypertrophy — collectively referred to as airway remodeling.1-3 Since an inhaled-allergen challenge in atopic asthma induces eosinophilic inflammation of the airway and changes in the extracellular matrix,4 and since a reduction in airway eosinophils has been reported to reduce certain markers of airway remodeling,5 such structural changes in the tissues have been considered a consequence of eosinophilic airway inflammation.6 This paradigm, however, fails to account for the potential contribution of airway narrowing to airway remodeling. Bronchoconstriction generates excessive mechanical forces within the airways that distort tissue cells,7,8 and mechanical forces within other organs are known to induce tissue remodeling.9-11 In vitro studies in a variety of models have shown that ex vivo compression of the airway epithelium results in changes that mimic those identified and associated with remodeling in vivo.12-15 We therefore hypothesized that the airway narrowing induced by allergen exposure in vivo in patients with asthma may in itself be a sufficient stimulus for the development of airway remodeling and that such remodeling is not solely dependent on induced recruitment of airway eosinophils.
To test this hypothesis, we performed repeated challenges with exposure to either allergen (to induce bronchoconstriction with airway eosinophil recruitment) or methacholine (to induce bronchoconstriction alone) in volunteers who had mild atopic asthma. Two additional groups of volunteers with asthma served as controls, undergoing repeated challenges with either saline placebo (to control for the challenge procedures) or methacholine after they had received albuterol to prevent bronchoconstriction (to control for any additional nonbronchodilator, receptor-mediated actions of methacholine within the airways). The effect of these challenges on the airway was evaluated by assessing changes in markers of airway remodeling in endobronchial tissue obtained by fiberoptic bronchoscopy before and after the challenge.
>>>Read more: http://www.nejm.org/doi/full/10.1056/NEJMoa1014350#t=articleBackground
Treating Asthma
Treating asthma
The aim of treatment is to get your asthma under control and keep it that way. Everyone with asthma should be able to lead a full and unrestricted life. The treatments available for asthma are effective in most people and should enable you to be free from symptoms.
What is good asthma care?
Your doctor or nurse will tailor your asthma treatment to your symptoms. Sometimes, you may need to be on higher levels of medication than at other times.
You should be offered:
- care at your GP surgery provided by doctors and nurses trained in asthma management
- full information about your condition and how to control it
- involvement in making decisions about your treatment
- regular checks to ensure your asthma is under good control and your treatment is right for you (which should be at least once a year)
- a written personal asthma action plan agreed with your doctor or nurse
It is also important that your GP or pharmacist teaches you how to properly use your inhaler as this is an important part of good asthma care. See 'taking asthma medicines' below for a video on inhaler techniques.
Source / Read More:
http://www.nhs.uk/Conditions/Asthma/Pages/Treatment.aspx
Have we found a cure for HIV?
Have we found a cure for HIV? Child born with virus is now free of infection after 'miraculous' treatment
- Child's mother was only diagnosed as HIV positive after going into labour
- Baby was given extra-strong programme of medication to 'blast' the virus
- This prevented the virus from taking hold in the baby's cells
- Two years after beginning treatment, tests show no virus in the child's blood
- Breakthrough hailed as 'major landmark' in the battle to find cure
PUBLISHED:22:32, 3 March 2013| UPDATED:01:04, 5 March 2013
Miraculous: Dr Hannah Gay, a paediatric HIV specialist at the University of Mississippi, treated the two-year-old girl who is now 'cured' of the virus
Doctors have made a landmark breakthrough in the treatment of HIV after they 'cured' a baby with the virus.
The baby girl had been infected by her mother who was diagnosed as HIV positive during labour.
Because of the high infection risk, the baby was given an accelerated programme of medication.
She received three standard HIV drugs instead of the usual one when she was just 30-hours old.
This appears to have blasted the virus into remission and prevented it from taking root in the baby's cells.
Now two-years-old, the girl from Mississipi is in remission with blood tests showing no signs that the virus is present. This is known as a 'functional cure.'
Experts say the groundbreaking development paves the way for other children to be treated before the virus takes hold.
Last night at a major AIDS meeting in Atlanta, the case was declared a major landmark in the battle to find a cure for the disease.
Study leader Dr Deborah Persaud, of Johns Hopkins Children's Centre in Baltimore, said the toddler is now free from the potentially fatal disease.
Dr Anthony Fauci of the National Institutes of Health said: 'You could call this about as close to a cure, if not a cure, that we've seen.'
He added that the child, which is only the second patient ever recorded to have been 'cured' of AIDS, 'opens up a lot of doors' for the treatment of other children born with HIV.
The child's mother was rushed to a rural emergency room in July 2010 in advanced labour and tests showed she was HIV positive.
Because the mother had not had any treatment, doctors knew the child was at high risk of infection.
Normally, they would have given the newborn a low dose of the medication nevirapine in the hope that it would prevent the HIV from taking hold.
However the small hospital didn't have the right kind of liquid to give the treatment and so she was rushed to specialist centre run by Dr Hannah Gay, a paediatric HIV specialist at the University of Mississipi.
Read more: http://www.dailymail.co.uk/health/article-2287564/Have-cure-HIV-Child-born-virus-free-infection-miraculous-treatment.html#ixzz2O4Zqc6Hi
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Source: http://www.dailymail.co.uk/health/article-2287564/Have-cure-HIV-Child-born-virus-free-infection-miraculous-treatment.html
More Near-Cures for HIV
Early treatment may be key to a drug-free life for a small percentage of patients.
Last week, scientists reported that a baby had been "functionally cured" of HIV (see "A Toddler May Have Been Cured of HIV Infection"). Now, other researchers report in PLoS Pathogens that 14 HIV-infected adults—four women and 10 men—have survived with the virus in check even though they have stopped taking their antiretroviral medications.
The authors write that while combined antiretroviral drugs reduce HIV-associated illness and death, they cannot cure the infection. The 14 patients in the study are functionally cured, meaning they are not completely rid of the virus—although they have no symptoms, very low levels of HIV can still be detected in their blood. "Given the difficulty of eradicating [HIV], a functional cure for HIV-infected patients appears to be a more reachable short-term goal," they write.
But bear in mind that the 14 adults who were functionally cured were part of a larger study of 70 people who had gone off of their antiretroviral drugs. The majority of the group relapsed when their treatment stopped. The key now is to find out what makes the 14 adults different. They did not carry known protective genetic variants and actually had more severe infections and more symptoms before starting treatment. This sensitivity may have helped by prompting the patients to seek treatment sooner than most people, write the researchers who conclude that:
"These findings argue in favor of early [combined antiretroviral therapy] initiation and open up new therapeutic perspectives for HIV-1-infected patients."
Tuesday, March 19, 2013
Meta-analysis: low-dose aspirin (modestly) reduces risk of pre-eclampsia.
A large meta-analysis of patient-level data has found that low-dose aspirin given to pregnant woman at risk of pre-eclampsia modestly but consistently reduced their risk of adverse outcomes. Pre-eclampsia affects between 2% and 8% of pregnancies and can have severe adverse effects on both mother and baby. While the cause is not yet known, abnormalities of clotting and platelet function occur and suggest the potential for benefit from anti-platelet drugs: many studies have been carried out over the past two decades, but their results have not been clear-cut. Previous systematic reviews suggested a benefit overall, however there was still controversy. The authors of this meta-analysis aimed to used patient-level data from as many previous trials as possible in an attempt to clarify the situation.
They carried out a comprehensive literature search using a relevant secondary database that is regularly updated from other databases. Eligible studies were randomised controlled trials of women at risk of pre-eclampsia treated for primary prevention with one or more anti-platelet agents, against controls of placebo or no treatment. Where potentially eligible trials included both primary and secondary prevention arms, only patients in the primary prevention arm were included in the analysis. Variables for the analysis were pre-specified, and anonymised data for patients in all eligible trials was requested from the original study authors; this was re-coded if necessary, checked for consistency, corrected where necessary, and finally agreed with the original authors. Four primary outcomes were defined: pre-eclampsia, death in utero or before hospital discharge, delivery pre-term at less than 34 weeks gestation, and infant small for gestational age. These were combined as an additional composite outcome - 'pregnancy with serious adverse outcome' (pregnancy where the mother dies or develops pre-eclampsia or if any baby is preterm, small for gestational age, or does not survive to discharge from hospital). Results were analysed on an intention to treat basis, but analysis for each outcome was restricted to trials having at least 80% of the data available for that outcome. Analyses compared the effect of the anti-platelet agent against placebo or no treatment for each outcome.
There were 115 trials identified initially, of which 50 were excluded as having no comparison group or treating women with established eclampsia only and two were excluded because patients were not truly randomised. Of the 63 remaining, including a total of 38,026 women, data could not be obtained for 27 (accounting for about 10% of the total participants; trial authors not traceable n=7, refused n=1, original data lost or irretrievable n=17, or not supplied n=2). This left 36 trials involving 34,288 women for which data could be analysed. Of these, 31, including 32,217 women and their 32,819 babies, were primary prevention studies and were thus included in this analysis. In 27, accounting for the great majority of the data, aspirin was given alone (dose 50mg to 150mg daily). Three small trials used only other anti-platelet drugs, and three tested aspirin and dipyridamole in combination. Just over half the women included were in their first pregnancy, 70% were aged 20 to 35, and 90% had at least one risk factor. Overall, 8% developed pre-eclampsia.
Compared to control, treatment with an anti-platelet agent was associated with a small but robust reduction in the relative risk of both pre-eclampsia (RR 0.90, 95% CI 0.84 to 0.97, p=0.004) and preterm birth before 34 weeks' gestation (RR 0.90, 95% CI 0.83 to 0.98, p=0.011). They also reduced the risk of the composite outcome to a similar extent (RR 0.90, 95% CI 0.85 to 0.96, p=0.001). There were also similar reductions in the other two primary outcomes (baby small for age, stillborn, or died before discharge), however these were not statistically significant. Maternal outcomes were similar for the two groups, with no significant increase in bleeding in the anti-platelet group. Subgroup analyses did not reveal any subgroup in which there was particular benefit.
The authors conclude that the data shows that treatment with an anti-platelet drug, mainly aspirin, reduces the risk of pre-eclampsia and some adverse pregnancy outcomes by about 10%. It is not possible to determine from the available data whether any particular subgroup benefits, although as the risk reduction is relative the absolute benefit will depend on a woman's underlying risk. The trials recruited mainly women at low to moderate risk of pre-eclampsia, so the data for women at high risk is limited. The analysis does not suggest that aspirin treatment is associated with significant adverse effects, although because some of the data on post-partum haemorrhage is uncertain, this outcome needs to be treated with caution.
An accompanying Comment discusses the paper and its implications. They authors discuss the possible mechanism of the benefit, and suggest questions that still need answers. They agree with the trial authors that use will depend on the mother's pre-existing risk level, and should be after full discussion of the potential risks and benefits. There have been a number of media reports of this study, and UK experts caution that pregnant women should not start taking aspirin without discussion with their doctor.
They carried out a comprehensive literature search using a relevant secondary database that is regularly updated from other databases. Eligible studies were randomised controlled trials of women at risk of pre-eclampsia treated for primary prevention with one or more anti-platelet agents, against controls of placebo or no treatment. Where potentially eligible trials included both primary and secondary prevention arms, only patients in the primary prevention arm were included in the analysis. Variables for the analysis were pre-specified, and anonymised data for patients in all eligible trials was requested from the original study authors; this was re-coded if necessary, checked for consistency, corrected where necessary, and finally agreed with the original authors. Four primary outcomes were defined: pre-eclampsia, death in utero or before hospital discharge, delivery pre-term at less than 34 weeks gestation, and infant small for gestational age. These were combined as an additional composite outcome - 'pregnancy with serious adverse outcome' (pregnancy where the mother dies or develops pre-eclampsia or if any baby is preterm, small for gestational age, or does not survive to discharge from hospital). Results were analysed on an intention to treat basis, but analysis for each outcome was restricted to trials having at least 80% of the data available for that outcome. Analyses compared the effect of the anti-platelet agent against placebo or no treatment for each outcome.
There were 115 trials identified initially, of which 50 were excluded as having no comparison group or treating women with established eclampsia only and two were excluded because patients were not truly randomised. Of the 63 remaining, including a total of 38,026 women, data could not be obtained for 27 (accounting for about 10% of the total participants; trial authors not traceable n=7, refused n=1, original data lost or irretrievable n=17, or not supplied n=2). This left 36 trials involving 34,288 women for which data could be analysed. Of these, 31, including 32,217 women and their 32,819 babies, were primary prevention studies and were thus included in this analysis. In 27, accounting for the great majority of the data, aspirin was given alone (dose 50mg to 150mg daily). Three small trials used only other anti-platelet drugs, and three tested aspirin and dipyridamole in combination. Just over half the women included were in their first pregnancy, 70% were aged 20 to 35, and 90% had at least one risk factor. Overall, 8% developed pre-eclampsia.
Compared to control, treatment with an anti-platelet agent was associated with a small but robust reduction in the relative risk of both pre-eclampsia (RR 0.90, 95% CI 0.84 to 0.97, p=0.004) and preterm birth before 34 weeks' gestation (RR 0.90, 95% CI 0.83 to 0.98, p=0.011). They also reduced the risk of the composite outcome to a similar extent (RR 0.90, 95% CI 0.85 to 0.96, p=0.001). There were also similar reductions in the other two primary outcomes (baby small for age, stillborn, or died before discharge), however these were not statistically significant. Maternal outcomes were similar for the two groups, with no significant increase in bleeding in the anti-platelet group. Subgroup analyses did not reveal any subgroup in which there was particular benefit.
The authors conclude that the data shows that treatment with an anti-platelet drug, mainly aspirin, reduces the risk of pre-eclampsia and some adverse pregnancy outcomes by about 10%. It is not possible to determine from the available data whether any particular subgroup benefits, although as the risk reduction is relative the absolute benefit will depend on a woman's underlying risk. The trials recruited mainly women at low to moderate risk of pre-eclampsia, so the data for women at high risk is limited. The analysis does not suggest that aspirin treatment is associated with significant adverse effects, although because some of the data on post-partum haemorrhage is uncertain, this outcome needs to be treated with caution.
An accompanying Comment discusses the paper and its implications. They authors discuss the possible mechanism of the benefit, and suggest questions that still need answers. They agree with the trial authors that use will depend on the mother's pre-existing risk level, and should be after full discussion of the potential risks and benefits. There have been a number of media reports of this study, and UK experts caution that pregnant women should not start taking aspirin without discussion with their doctor.
Lancet, published early online 18 May 2007; DOI:10.1016/S0140-6736(07)60712-0 (link to abstract); Lancet, published early online 18 May 2007; DOI:10.1016/S0140-6736(07)60713-2 (Comment; link to full text, available to subscribers only); BBC News report.
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