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20th March 2020
Leading UK clinicians assessed the one-year data of around 80,000 people with HF as part of the analysis.
Nearly one million people in the UK live with HF, of whom around 50% may also suffer from ID. However, the investigation revealed that potentially a third of people with HF are not being screened for ID/IDA, with potentially debilitating effects on their quality of life.
IDA is one of 19 ambulatory care sensitive conditions (ACSCs), where effective community care and case management can help prevent the need for hospital admissions. It is estimated that emergency admissions for ACSCs could be reduced by up to 18%, and this study highlights that consistent management of ID/IDA, treatable comorbidities in HF, could help relieve some of the current burden on the NHS and improve the quality of life of patients.
This analysis has found that HF patients found to have ID/IDA are more likely to be re-admitted to hospital within 30 days than those without ID, 95% of whom present as emergency admissions. With an NHS deficit of £960 million reported for 2017/2018, hospital bed occupancy hitting an eight-year high in 2018, and a near 7% rise in emergency admissions to hospitals reported for 2018/19, correct management of these patients presents an opportunity for cost-savings for an over-stretched healthcare system.
Dr Rani Khatib, Consultant Pharmacist in Cardiology and Cardiovascular Research, Leeds Teaching Hospitals and co-author of the analysis published in Open Heart added, “Some evidence suggests that iron studies are conducted in less than 20% of heart failure patients admitted to NHS Trusts, which is not enough when you consider that 50% of these patients are likely to be iron deficient. The published data estimate an additional £21.5 million a year is being spent on managing co-morbid patients with heart failure and iron deficiency or iron deficiency anaemia, and this is based on the small proportion of those who were found from testing, so the true cost is likely to be much higher. There is a clear need to raise awareness about the growing evidence in this area and translate into practice accordingly.”
Across the NHS, there is a clear disparity in the care that patients with HF receive. In patients who were screened and treated for ID, data show that the amount of time they spent in hospital varied widely, with a difference of up to 18 bed days. Patients across the lowest and highest tier Clinical Commissioning Groups (CCGs) across England spent eight and 26 days in hospital respectively, with each day costing the NHS around £400 per patient. This disparity suggests that international guidance is not being consistently followed. European, Scottish and American guidance highlight the importance of managing ID/IDA in HF in order to improve patients’ quality of life and exercise capacity and reducing hospitalisations, recommending that clinicians consider available intravenous iron therapy in appropriate patients.
“Current clinical opinion widely acknowledges that the treatment of iron deficiency in heart failure not only improves patients’ functional capacity and symptoms, but most importantly, their quality of life. Treatment can also reduce time-consuming hospital visits for patients and costly readmissions for the wider healthcare economy” says Dr Simon Williams, Consultant Cardiologist, Wythenshawe Hospital, Manchester and fellow co-author of the analysis published in Open Heart. “Our colleagues in Scotland, America and Europe have guidance that provides them with recommendations for treatment of these co-morbid patients, it is disappointing that we are lagging behind and do not have such standardised recommendations to refer to here in England and Wales.”
19th March 2020
This will be renamed metabolic associated fatty liver disease (MAFLD) and researchers highlighted that the new terminology will better reflect its causes, and improve public health initiatives.
MAFLD is a condition characterised by a build-up of fat in the liver and affects over one billion people. Over time, this can lead to complications including cirrhosis, liver failure, liver cancer, and heart health issues.
The consensus panel found that both the term ‘NAFLD’ and its diagnostic criteria must be updated in order to better reflect our current understanding of the disease.
Associate Professor Mohammed Eslam, co-lead author of the paper said, “Since it was first described in 1980, we haven’t revisited the appropriateness of the name, or the criteria used to diagnose fatty liver disease.
“By updating terminology and definitions, we can shift towards more precise and personalised treatment pathways, trial design and drug development.”
Professor Jacob George, co-lead author of the paper said, “Initially, the disease was defined as fatty liver in the absence of significant alcohol intake. This definition was problematic and has resulted in a ‘one-size-fits-all’ approach to treatment, despite the significant variation we see in people affected by the disease.
“This may be one of the reasons why we are seeing relatively low response rates in our current trials.
“The proposed name and definition recognises that the disease we are looking at is associated with metabolic dysfunction. It also acknowledges that there are multiple overlapping causes and drivers of the disease.”
Researchers are now conducting further studies to characterise the different sub-types and causes of MAFLD to help design new clinical trials, and best practices for patient management.
“Ultimately, we hope that by strengthening the diagnostic criteria and language surrounding MAFLD, we can help reduce the progression of the disease, and reduce the number of people affected worldwide,” Professor George concluded.
18th March 2020
Patients with moderate-to-severe psoriasis, that is, where more than 10% of their body surface area is affected, are normally managed with a group of monoclonal antibody drugs (biologics). The biologics were introduced in the early 2000’s and the initial agents worked by inhibiting the pro-inflammatory cytokine, tumour necrosis factor which is secreted by both T cells and antigen-presenting cells within lesional skin.1 This initial group of drugs which included etanercept, infliximab and adalimumab became known as ‘first-generation’ biologics and represented a significant treatment advance for those with more widespread disease. Nevertheless, most patients failed to achieve complete clearance of their disease and more recent advances in our understanding of the pathophysiology of psoriasis led to the development of a wider range of specific cytokine inhibitors that provided a greater level of skin clearance. These ‘second-generation’ biologics such as secukinumab, izekizumab, brodalumab, guselkumab, risankizumab and ustekinumab, targeted interleukin (IL)-17 and IL-12/23.2
A greater range of treatment options is welcomed by clinicians and patients allowing shared decision-making. In order for both parties to make an informed choice about a particular treatment requires insight of the relative efficacy of the different options. While head-to-head trials are of value when comparing two agents, more information can be gleaned from meta-analyses because data is pooled from all of the available head-to-head studies and this offers a more robust efficacy estimate. However, differences in the design of trials, for example, patient inclusion criteria, prior treatment exposures, study duration and lack of comparative data for a particular intervention, can all potentially impact on the outcome of a meta-analysis. One potential solution to the problems faced by meta-analyses is to use a network meta-analysis (NMA). This technique not only compares the outcomes from head-to-head trials but also includes indirect comparisons across trials.3 In short, an NMA can be used to evaluate the comparative effectiveness of different interventions (in this case biologics) even where there are no trials in which the two agents have been compared directly.
In the February 2020 issue of JAMA Dermatology, an NMA study sought to provide greater clarity on the short and longer term efficacy of both oral and biologic therapies in psoriasis to help clinicians and patients in their decision-making process.4 The study used a NMA to examine the relative efficacy of the various treatments in the short-term (10 to 16 weeks) and then used a traditional meta-analysis to explore the longer-term (44 to 60 weeks) response rate. It included Phase II, III or IV randomised trials of treatments licensed by the US Food and Drug Administration and the European Medicines Agency for adults with moderate to severe psoriasis. This included not only all of the biologics but also oral treatments such as apremilast (Otezla) and dimethyl fumarate (Tecfidera).
The main outcome measure was a change in the Psoriasis Area and Severity Index (PASI) score, which evaluates disease severity. Typically, trials report a PASI 75, 90 or 100, which describes the improvement in disease severity attained by the intervention. For instance, a PASI 75 indicates that a patient achieved a 75% reduction in PASI score (compared to baseline) from the treatment and a PASI 100, represents complete clearance of psoriasis. The study identified 60 studies and found that after 10 to 16 weeks of treatment, the highest PASI 90 rates were achieved with four biologics, risankizumab (71.6%), brodalumab (70.8%), izekizumab (70.6%) and guselkumab (67.3%) and these differences were not statistically significant. In the longer term (weeks 44 to 60), the highest PASI 90 rates were achieved by, risankizumab (79.4%), guselkumab (76.5%), brodalumab (74.0%) and izekizumab (73.9%).
In contrast, the first generation biologics, infliximab and etanercept only achieved PASI 90 rates of 57.4% and 17.9% respectively. These improvements are impressive and serve to illustrate the benefits of these newer agents over the first-generation biologics. In practice, the results suggest that with these newer agents, after 4 months of therapy, roughly 70% of patients can expect to see a 90% reduction in disease severity and that efficacy is also retained in the longer term. The short-term efficacy (i.e. up to 16 weeks) data obtained in this study are comparable to the results observed in another NMA which found that brodalumab, Ixekinumab exhibited similar efficacies to risankizumab.5
The latest JAMA study therefore suggests that in order to achieve the greatest improvement in disease severity in both the short and longer term, biologic therapy should be restricted to one of the following; brodalumab, guselkumab, ixekinumab or risankizumab since these drugs provide the highest PASI 75, 90 and 100 rates.
This recent NMA has therefore provided an important starting point to inform the clinical decision-making discussion between clinicians and patients although whether or not the small differences in response between the biologics have real-world implications remains to be seen.
17th March 2020
The study was part-funded by the Francis Crick Institute and the Wellcome Trust in London.
The research, published in Nature Chemical Biology, found that contrary to current understanding, an antibiotic used to treat tuberculosis is unable to permanently prevent one of the enzymes it targets from functioning. By uncovering how this enzyme is re-activated, the research could lead to the development of improved versions of the drug which could be used against antibiotic resistant bacteria.
For more than 50 years, the antibiotic D-cycloserine has been used to treat cases of TB that are resistant to first-line drugs. It had been thought that this drug in part worked by irreversibly preventing an enzyme, alanine racemase, from helping to build TB bacteria’s cell walls.
However, this study found that despite being exposed to D-cycloserine, about 10% of the alanine racemase enzyme was later able to function effectively again. This enzyme is capable of regaining activity by inactivating the drug, in a process called hydrolysis. This change means the modified drug can no longer bind to and block the enzyme.
The drug however can still treat TB because it also inhibits another enzyme involved in building TB cell walls, D-Ala:D-Ala ligase.
“You could say that alanine racemase acts like Dr Jekyll and Mr Hyde. When first exposed to the drug, it’s Dr Jekyll, as it is a good target for the drug, and this stops the bacteria for a time. However, over time it turns into Mr Hyde, as it stops the drug from targeting it and so it can function again. If it weren’t for the drug also blocking a separate target, it would be ineffective against TB,” says Luiz Pedro Carvalho, group leader in the Mycobacterial Metabolism and Antibiotic Research Laboratory at the Crick.
These findings could lead to the development of new drugs. One new route, for example, would be to develop similar molecules that cannot be hydrolysed and therefore would irreversibly inhibit alanine racemase. Various bacteria have the same enzyme or a version of it, so such drugs could provide a new way to treat these diseases.
“For decades, it’s been thought this drug worked in one way, that its action could not be reversed, so it’s rather incredible that we’ve found it gets inactivated by one of its targets,” further explains Luiz Pedro Carvalho. “The fact this has been missed for so long demonstrates how important it is to work with the right protein derived from the organism you want to understand.”
Cesira de Chiara, principal laboratory research scientist in Luiz’s lab, says: “The key here is that tuberculosis takes a relatively long time to replicate, about 20 hours, so there’s enough time for this enzyme to be inhibited and then re-activated. Previous studies missed this re-activation as they haven’t studied the process of inactivation of the enzyme by the drug over such a long period.
“If we could create a tweaked version of this drug that can permanently block this family of enzymes, we could further improve its effectiveness against the raising threat of antibiotic resistant bacteria, perhaps reducing the doses and, with them, the risk of potentially toxic side-effects.”
10th March 2020
In research published in Nature Communications, the team followed babies born before 32 weeks gestation to identify different immune cell populations, the state of these populations, their ability to produce mediators, and how these features changed post-natally. They also took stool samples and analysed to see which bacteria were present.
They found that all the infants’ immune profiles progressed in a similar direction as they aged, regardless of the number of weeks of gestation at birth. Babies born at the earliest gestations – before 28 weeks – made a greater degree of movement over a similar time period to those born at later gestation. This suggests that preterm and term infants converge in a similar time frame, and immune development in all babies follows a set path after birth.
Dr Deena Gibbons, a lecturer in Immunology in the School of Immunology & Microbial Sciences, said: “These data highlight that the majority of immune development takes place after birth and, as such, even those babies born very prematurely have the ability to develop a normal immune system.”
Infection and infection-related complications are significant causes of death following preterm birth. Despite this, there is limited understanding of the development of the immune system in babies born prematurely, and how this development can be influenced by the environment post birth.
Some preterm babies who went on to develop infection showed reduced CXCL8-producing T cells at birth. This suggests that infants at risk of infection and complications in the first few months of their life could be identified shortly after birth, which may lead to improved outcomes.
There were limited differences driven by sex which suggests that the few identified may play a role in the observations that preterm male infants often experience poorer outcomes.
The findings build on previous findings studying the infant immune system.
Dr Deena Gibbons said: “We are continuing to study the role of the CXCL8-producing T cell and how it can be activated to help babies fight infection. We also want to take a closer look at other immune functions that change during infection to help improve outcomes for this vulnerable group.”
In the study, published in The Journal of Clinical Investigation, researchers at UCL Cancer Institute used next generation sequencing (NGS) to establish if they could identify prostate cancer DNA in blood plasma. Previous studies have focused on tissue samples; however, this requires an invasive biopsy.
Researchers say their successful discovery in blood represents a prostate tissue “fingerprint”, or early circulating biomarker, and when detected identifies that cancer is active and spreading. As this can be detected in a simple blood test, commonly known as a liquid biopsy, physicians could monitor cancer response to treatment regularly and in real-time.
Moving forward researchers will see if this test could complement or replace the existing prostate specific antigen test, which is used for prostate cancer diagnosis and treatment monitoring.
Lead author, Dr Anjui Wu (UCL Cancer Institute), said: “Metastatic prostate cancer – the most dangerous late stage of the disease – can vary substantially in its treatment response and clinical progression.
“We urgently need biomarkers that will help us determine how far along each patient’s cancer is, to determine the best course of treatment.
“With tumour biopsies difficult to obtain, being able to identify prostate cancer DNA signatures at the earliest opportunity in blood, will help monitor patients better and assist more effective treatment selection and combination.”
In this proof of concept study, the researchers set out to investigate a process called DNA methylation – that is, a chemical change in DNA molecules that can affect gene function and has been studied in tissues.
To do this, the methylation and genome profiles of circulating-cell free DNA (degraded DNA fragments released to the blood plasma) from 25 metastatic prostate cancer patients were concurrently profiled using NGS. As a control, four healthy blood plasma samples were also analysed.
The research group interrogated the molecular profiles to identify circulating tumour DNA (ctDNA) methylations, which can be used to sensitively track tumour content change.
Traditionally, the amount and quality of circulating cell-free DNA extracted from blood can be limited: surprisingly, researchers discovered thousands of methylation changes specific to the prostate gland in blood samples from men with prostate cancer. Using this finding, they developed these changes into a signature (a blood test that can be used in the clinic) for tracking prostate genetic material in blood to monitor cancer activity.
Corresponding author, Professor Gert Attard (UCL Cancer Institute), said: “We are now testing our new technique in trial patients to see if it can complement or substitute the traditional serum prostate specific antigen (PSA) for diagnosis, risk assignment and monitoring how well a treatment is working.
“We believe the increased sensitivity and additional information we derive, will significantly improve the outcomes of men with advanced prostate cancer.”
Professor Mark Emberton, Dean of the Faculty of Medical Sciences at UCL, said “The field of liquid biopsies has shown great potential recently to improve the diagnosis and management of cancer patients.
“This test could be the first to tell us cancer has got into blood before the spread is large enough to see on imaging. This could allow targeting of treatment for men at the highest risk of prostate cancer spread.”
Researchers have developed new methods to identify biomarkers for prostate cancer by combining information from multiple parts of urine samples.
It is hoped that the breakthrough could help large numbers of men avoid an unnecessary initial biopsy.
Prostate cancer is the most common cancer in men in the UK. It usually develops slowly and the majority of cancers will not require treatment in a man’s lifetime.
The most commonly used tests for prostate cancer include blood tests, a physical examination known as a digital rectal examination (DRE), an MRI scan or a biopsy.
Lead author Shea Connell from UEA’s Norwich Medical School, said: “Prostate cancer is more commonly a disease men die with rather than from.
“Current practice assesses a patient’s disease using a PSA blood test, prostate biopsy and MRI. But up to 60% of men with a raised PSA level are negative for prostate cancer on biopsy.
“So it is clear that there is a considerable need for additional, more accurate, tests.
Last year, the same team unveiled an experimental new test called ‘PUR’ (Prostate Urine Risk) which diagnoses aggressive prostate cancer and predicts whether patients will require treatment up to five years earlier than standard clinical methods.
The latest research combines information from two different components in urine which further improves its use for diagnosis.
Shea Connell said: “We wanted to see if other biological information from urine could be integrated together with clinical information to create a new predictive test with even greater potential.”
The team developed the ExoMeth test by studying urine samples collected from 197 patients. They used machine learning techniques to find which specific combination of biological markers could be useful for predicting the presence of prostate cancer.
ExoMeth takes a ‘holistic view’ of urine for biomarkers by considering much more than a single fraction of the urine. By integrating cell-free RNA, cellular methylation and clinical factors all together, the research team can now much more accurately discriminate the disease status of a patient without the need for an invasive biopsy.
It provides good evidence that multiple aspects of urine can be combined to determine a patient’s disease status.
Senior author Dr Daniel Brewer, from UEA’s Norwich Medical School, said: “It’s still very early days for this research, but if ExoMeth were validated in a future study with many more patients, we could see an approximate 60% reduction in unnecessary biopsies in around five years.”
The research was led by UEA, in collaboration with the Norfolk and Norwich University Hospital, the Earlham Institute, University College Dublin, and the University of Toronto.
It was funded by Movember, the Masonic Charitable Foundation, the Bob Champion Cancer Trust, the King Family, the Andy Ripley Memorial Fund, the Hargrave Foundation, the US Prostate Cancer Foundation, the Science Foundation Ireland, the Royal Irish Academy and the Irish Cancer Society.
Dr Mark Buzza, global director of biomedical research programs at men’s health charity Movember, said: “Despite advances in recent years, prostate cancer remains very difficult to diagnose and treat. That’s why we’re so excited about the Exometh test. One of the major advantages of the test is that it could remove the need for 60% of invasive biopsies.
“We are delighted to have supported this project under Movember’s Global Action Plan (GAP1) Biomarker project which fosters collaboration between researchers across the globe. Bringing researchers together to collaborate rather than compete for funding allows research findings to be fast-tracked.”
In the study of 1177 mother-infant pairs, a third of the children were exclusively breastfed until the age of three months. By the age of six years, 20.8% of children had been diagnosed with respiratory allergies and 11.3% with asthma.
Exclusive breastfeeding for three months was associated with a 23% lower relative risk of respiratory allergies at the age of six years. It was also associated with a 34% lower relative risk of asthma, but only if the children did not have a family history of asthma.
Breastfeeding for three months, but not exclusively, was insufficient to reduce the risk of respiratory allergies or asthma.
“Airway disorders such as respiratory allergies and some asthma may be prevented in some cases by encouraging exclusive breastfeeding for at least three months, as human milk was potentially beneficial in reducing the risk of airway disorders among children,” said author Galya Bigman, PhD, of the University of Maryland, Institute of Human Virology, School of Medicine.
6th March 2020
Patients given chemotherapy within three months of surgery saw the risk of their cancer coming back or spreading reduced and were much more likely to live cancer free for three years or more.
The new results are set to change clinical practice around the world – with chemotherapy being recommended after surgery for all suitable patients with a rare tumour of the urinary system that is large or just starting to spread.
Cancer of the ureter and renal pelvis is relatively rare, with nearly 1000 people being diagnosed with the disease in the UK each year.
The disease is often diagnosed at a late stage, with over half of patients dying from it, so more effective treatment options are desperately needed.
The POUT trial, led by researchers at The Institute of Cancer Research, London, and the Lancashire Teaching Hospitals NHS Foundation Trust, involved 261 people with cancer of the ureter and renal pelvis.
The trial assessed the benefit of giving people four cycles of a combination of two chemotherapies compared with the current standard of treatment, where patients are actively monitored to spot signs of their cancer coming back after having surgery.
The study was published in the Lancet Oncology and was funded by Cancer Research UK.
The researchers found that treating patients with platinum-based chemotherapy after surgery reduced the risk of dying or of ureter and renal pelvis cancer returning by 55%.
They found that 71% of patients given chemotherapy survived for three years or more after joining the trial without their disease coming back, compared with 46% of patients who were on surveillance.
As expected, more people experienced serious side-effects in the chemotherapy group compared with patients under surveillance – around 44%, similar to the rates of side-effects seen in other groups of patients treated with these drugs.
The combination treatment of gemcitabine with platinum chemotherapy used in the study is a low-cost, generic treatment option and is already routinely used on the NHS in a range of other cancers.
The researchers are now working to incorporate the trial results into international clinical practice guidelines, so that chemotherapy after surgery will become the new standard of care.
Next, the team plan to study the benefit of adding immunotherapy or targeted treatment to chemotherapy in this form of the disease.
Professor Emma Hall, Professor of Oncology Clinical Trials at The Institute of Cancer Research, London, who co-ordinated the study, said: “Our clinical trial has found a considerable benefit of giving chemotherapy to people with cancers that start in the tube leading from the kidney to the bladder – cutting the risk of dying or the disease coming back after surgery by more than half.
“Giving chemotherapy after surgery could give people with this rare form of cancer years more to spend quality time with their families. The results of our study are set to change clinical practice in the UK and internationally, and I’m hopeful that patients will start benefiting very soon.
“Running clinical trials in patients with rare cancers comes with its challenges, including finding enough people to take part – so it’s fantastic to see such clear evidence of patient benefit from this study. It shows how important it is to run studies like this to improve treatment options for patients with rarer forms of cancer.”
Dr Alison Birtle, Consultant Clinical Oncologist at Lancashire Teaching Hospitals NHS Foundation Trust and the trial’s Chief Investigator, said: “We are very grateful that our participants and the entire uro-oncology community in the UK got behind this study. It is the first to show that there is a real chance for people with upper urinary tract cancer to stay free of their disease for much longer. This type of cancer has always been forgotten and to be able to deliver this, a study that everyone said was impossible, to benefit patients is a privilege.”
5th March 2020
Atopic eczema is characterised by a defective skin barrier and often precedes the development of food allergies and other atopic diseases. Could regular emollient use from birth actually prevent the development of the condition? Rod Tucker finds out.
Atopic eczema is a highly pruritic, inflammatory skin condition which affects 20% of children.1 The condition develops during infancy and classically leads to food allergies, asthma and allergic rhinitis in what has been termed the ‘atopic march’.2 A family history of atopic disease is an important risk factor for the development of atopic eczema. In addition, the presence of atopic eczema increases the risk of IgE-mediated food allergies and for example, infants with the condition are six times more likely to develop egg allergies.3
While the precise cause of eczema remains uncertain, the condition is characterised by a defective skin barrier and there is evidence that genetically determined loss-of-function mutations in the gene that codes for filaggrin, a protein that has an important role in skin barrier function, may contribute to eczema development during infancy.4 The presence of defective skin barrier serves as a possible entry route for allergens and this has been proposed as a possible route to sensitisation and the subsequent development of a peanut allergy.5
Emollients are the cornerstone of eczema management and are recommended for all patients with the condition.6 An emollient provides a water impermeable barrier over the surface of the skin which serves to both prevent water loss and ingression of potential allergens and irritants.
Given this dual role, is it possible that treatment with emollients soon after birth could actually prevent the development of atopic eczema and the ensuing atopic march? This was the question posed in the barrier enhancement for eczema prevention (BEEP) study published in the Lancet.7
The study was based on the observations of a pilot study undertaken by the same group which found that the incidence of atopic eczema was lower (22% vs 43%) in 124 infants treated with the daily application of an emollient from birth.8 But this was not simply blue sky thinking: several lines of evidence had pointed to a role for emollients in preventing inflammation as well as work which illustrated how the barrier dysfunction in atopic eczema appeared to be a secondary phenomena to subclinical inflammation present in dry atopic skin.9
The BEEP study recruited 1,394 high-risk (that is, where at least one first-degree relative had either eczema, allergic rhinitis or asthma) babies who were randomised to either once daily application of an emollient (Diprobase or Doublebase gel) to the whole body excluding the scalp or best practice skincare advice (the control group). This latter group received advice to use mild cleansers and shampoos specifically formulated for infants but also to avoid soaps, bubble bath and baby wipes.
The primary outcome measure was a diagnosis of eczema at two years of age. The results showed no difference: eczema was present at two years of age in 23% of infants assigned to daily emollient use and 25% in the control group. There were also no significant differences in the incidence of food allergies or other allergic diseases and the authors were at a loss to explain their findings.
An alternative strategy to reducing food allergies is through early exposure to potentially allergenic foods in order to allow the development of tolerance and this was the subject of the preventing atopic dermatitis and allergies (PreventADALL) study which was also published in the same issue of The Lancet.
In PreventADALL, Norwegian researchers explored the dual approach of daily emollient use and early introduction of potential allergic foodstuffs such as peanut butter, wheat porridge and eggs10 and the incidence of eczema was recorded after 12 months.
The study had four arms: control (no advice); skin emollients; early feeding and finally combined emollient and early feeding. The incidence of eczema at 12 months was 8% (control group), 11% (emollient group), 9% (food group) and 5% (combined group) and these differences were not significant. In other words, neither a combination of daily emollient use and early introduction of potential allergenic foods reduced the development of atopic eczema at 12 months.
The results of both studies, although disappointing, recognise the limited value of these primary prevention strategies. However, these results do not undermine the importance of regular emollient use in the management of established atopic eczema.
Whether changing the composition of an emollient makes any difference remains to be seen and is the subject of the ongoing PEBBLES study.11
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