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Take a look at a selection of our recent media coverage:

Research redefines constipation

6th June 2019

Research by King’s College London, published in the American Journal of Gastroenterology,1 finds that the public’s perception of constipation differs drastically from that of doctors’ and from the formal diagnosis guidelines.
 
Researchers also identified six key sets of symptoms common to both that in the future could form the basis of a new medical definition for constipation.
 
Constipation is a very common condition. Although most people with chronic constipation do not visit a doctor, it is still diagnosed in more than one million GP consultations and 63,000 hospital admissions in the UK every year. The way it is detected, however, varies considerably. Some patients self-diagnose, some doctors diagnose pragmatically, and others use formal criteria (such as Rome IV) which specify combinations of symptoms experienced over defined periods of time.
 
Lead author Dr Eirini Dimidi, Research Associate at King’s College London said: “Previous studies have tried to estimate how many people suffer from constipation, but their results vary between 3% and 35%. One potential reason for this range is the lack of a consistent way to diagnose it. Accurately identifying a condition is at the root of good care. Currently prescription medication for constipation fails in nearly 60% of patients and almost half report not being satisfied with their treatment.
 
The team from King’s collected data from 2557 members of the public (of which 934 had self-reported constipation), 411 GPs and 365 gastroenterology specialists.
 
They found that of those who self-reported constipation, 94% met the formal diagnostic criteria (Rome IV). Surprisingly, however, of the 1623 who did not self-report constipation, 29% met these criteria too. Nearly one in three ‘healthy’ patients were, therefore, clinically constipated but did not recognise it.
 
Using case studies, the rates of correct diagnosis of constipation ranged from 99% down to 39%, depending upon the symptoms present. Infrequent bowel movements, for example, were perceived as important for diagnosing constipation by less than a third of the constipated general population, compared to 41% of GPs and as many as 65% of specialist doctors.
 
The study also highlighted six key symptom clusters which were commonly agreed upon across the study groups: abdominal discomfort, pain and bloating; rectal discomfort; infrequent bowel movements and hard stools; sensory dysfunction; flatulence and bloating; fecal incontinence.
 
Professor Kevin Whelan, Head of the Department of Nutritional Sciences at King’s College London said: “Our study has revealed that numerous symptoms are considered important for a diagnosis of constipation by the general population that are not part of any current diagnostic criteria or assessment tools, with significant differences between patients and doctors.
 
“This is important as patients who seek medical care for their constipation-related symptoms may not have their symptoms recognised as constipation by the doctor and, therefore, may not be managed as such. This could significantly impact patients’ access to care and treatment.”
 
Dr Dimidi added: “Our findings emphasise the need to re-define the current universally accepted diagnostic criteria so they reflect both patients’ and doctors’ perceptions. The six symptom clusters we have identified seem a logical place to start.”
 
Reference
  1. Dimidi E et al. Perceptions of constipation among the general public and people with constipation differ strikingly from those of general and specialist doctors and the Rome IV Criteria. Am J Gastroenterol 2019;4 June [Epub ahead of print]: doi: 10.14309/ajg.0000000000000267.

Zebinix effective as adjunctive therapy in epilepsy patients with psychiatric comorbidities

Bial and Eisai have announced clinical practice data from the Euro-Esli study demonstrating clinical effectiveness of eslicarbazepine acetate, and that it is generally well tolerated as an adjunctive therapy in focal epilepsy patients with psychiatric comorbidities, including intellectual disability, compared with people with no psychiatric comorbidities.1 
 
The data, which add to the body of evidence on eslicarbazepine acetate as adjunctive therapy from Phase III studies,2-5 were published in Journal of the Neurological Sciences.1
 
Psychiatric comorbidities, including intellectual disability and depression, are common for adults who have epilepsy.6,7 Prevalence of psychiatric comorbidities may be twofold higher in adult patients with epilepsy compared to the general public, and up to a quarter of people diagnosed with epilepsy are estimated to have an intellectual disability.6,7 Psychiatric comorbidities can exacerbate the effects and increase the impact of epilepsy.8 Furthermore, antiepileptic treatments can interfere with treatments for the psychiatric comorbidities, and thus adversely affect these psychiatric conditions.9,10 There are many considerations for treating this patient population, thereby complicating treatment choice.10
 
“The comorbidities of epilepsy represent a substantial burden for people with epilepsy. This data provides a significant insight into how eslicarbazepine acetate performs in a routine medical setting for these patients and the results are very encouraging, demonstrating eslicarbazepine acetate’s efficacy and tolerability as an adjunctive therapy in this sub-set of patients,” comments Dr Colin Doherty, Consultant Neurologist, St James’s Hospital, Dublin, Ireland, and lead author of the Euro-Esli study.
 
These newly published data includes patient populations that are sometimes excluded from clinical trials, including those with psychiatric comorbidities, specific comorbidities of intellectual disability, or depression.1,11 Adverse events reported during this sub-cut of the Euro-Esli study are consistent with eslicarbazepine acetate’s safety profile established in Phase III studies.1-5 Adverse events with eslicarbazepine acetate treatment were reported by 43.1% of people with psychiatric comorbidities (n=122/283) and 45.8% of people with intellectual disability (n=49/107). The most common adverse events were dizziness (11.4%; n=31/272), somnolence (8.8%; n=24/272) and fatigue (8.1%; n=22/272) for people with psychiatric comorbidities; and somnolence (10.1%; n=10/99), dizziness (7.1%; n=7/99) and fatigue (6.1%; n=6/99) for people with intellectual disability.1
 
References
  1. Doherty C, et al. (2019) Eslicarbazepine acetate in epilepsy patients with psychiatric comorbidities and intellectual disability: Clinical practice findings from the Euro-Esli study. Journal of the Neurological Sciences. DOI: https://doi.org/10.1016/j.jns.2019.04.040.
  2. Elger C, et al. (2009) Efficacy and safety of eslicarbazepine acetate as adjunctive treatment in adults with refractory partial onset seizures: A randomised, double-blind, placebo-controlled, parallel-group phase III study. Epilepsia. 50:454-63.
  3. Ben-Menachem E et al. Eslicarbazepine acetate as adjunctive therapy in adult patients with partial epilepsy. Epilepsy Research 2010; 89(2-3):278-85.
  4. Gil-Nagel A et al. Efficacy and safety of 800 and 1200 mg eslicarbazepine acetate as adjunctive treatment in adults with refractory partial-onset seizures. Acta Neurologica Scandinavica 2009; 120:281-87.
  5. Sperling M, et al.  Eslicarbazepine acetate as adjunctive therapy in patients with uncontrolled partial-onset seizures: Results of a phase III, double-blind, randomized, placebo-controlled trial. Epilepsia 2015;56(2):244-53.
  6. Gaitatzis A et al. The epidemiology of the comorbidity of epilepsy in the general population. Epilepsia 2004; 45(12):1613-22.
  7. Lhatoo S et al. The epidemiology of epilepsy and learning disability. Epilepsia 2001;42 Suppl 1:6-9.
  8. Gilliam F et al. Psychiatric comorbidity, health, and function in epilepsy. Epilepsy Behav 2003; 4 Suppl 4:S26-30.
  9. Kanner A. Management of psychiatric and neurological comorbidities in epilepsy. Nat Rev Neurol 2016; 12(2):106-16
  10. Mula M. Treatment issues for psychiatric comorbidities of epilepsy. Clin Pract 2013; 10(3):293-299.
  11. Tlusta E et al. Clinical relevance of patients with epilepsy included in clinical trials. Epilepsia 2008; 49, 1479-80.

Opioid analgesics increase the risk of pneumonia among persons with Alzheimer’s disease

Opioid analgesics were associated with a 30% increase in the risk of pneumonia in persons with Alzheimer’s disease, a recent study from the University of Eastern Finland shows. 
 
The risk was most pronounced in the first two months of use. This is the first study to investigate the association between opioids and pneumonia in this population. The results were published in the Journal of Alzheimer’s Disease.1
 
The risk of pneumonia was highest among those using strong opioids, such as oxycodone or fentanyl, but the risk was also increased among those using buprenorphine, tramadol or codeine. Persons with active cancer were excluded from the study, and other diseases and drug use were accounted for in the analyses. Opioids impair the cough reflex and respiratory functions and cause sedation, possibly underlying the increased risk for pneumonia.
 
Pneumonia is a severe but relatively common complication among persons with Alzheimer’s disease, and often leads to hospitalisation and even death. Opioids are important in the treatment of severe acute pain, but treatment should be initiated at a low dose and regularly assessed for both benefit and harm. The diagnosis and assessment of pain is challenging among persons with Alzheimer’s disease due to problems in communication.
 
The study is part of the MEDALZ cohort, which included 5623 persons with Alzheimer’s disease diagnosed in Finland during 2010-2011. Each person initiating opioid use was matched with a comparison person with Alzheimer’s disease who did not initiate opioid use but had the same age, gender and year of Alzheimer’s diagnosis. Data for the study were derived from Finnish nationwide registers.
 

Reference

  1. Hamina A et al. Hospital-treated pneumonia associated with opioid use among community dwellers with Alzheimer’s disease. J Alzheimer’s Dis;Published online 20 May 2019. DOI: 10.3233/JAD-181295

Expert view: How personalised is autoimmunity in 2019?

3rd June 2019

The ultimate goal of modern medicine is a personalised approach for the individual patient, that is, a tailored management based on a finely tuned definition of immunogenetics, epigenetics, microbiome, and biomarkers, to maximise results and minimise risks of treatment (particularly of new biologics and small molecules). 
 
As in the case of rheumatoid arthritis, current treatment choices are largely based on minor determinants, while a trial-and-error approach remains largely utilised. While the development of objective criteria might appear an overambitious goal, we note that our current genotyping capacity, the proteomic tools, and the examples of rheumatoid arthritis and other autoimmune diseases are strongly supporting the likelihood of the success of this hypothesis. Indeed, biomarkers are central to this pathway. Among individual factors around which to tailor the patient management are sex and age, with gender-medicine finally becoming central to the research agenda. 
 
Genetics data have thus far been of limited use in clinical practice, whereas we are expecting major developments from synovial tissue histology, which has been largely overlooked in the past years and will become central with the growing number of mechanisms of action of treatments (that is, TNF alpha, IL6R, JAK, CTLA4). Among individual factors, the role of anti-citrullinated peptide antibodies to discriminate a more aggressive and erosive disease is established, while a renewed understanding of the reproductive factors involved in rheumatoid arthritis, considering its striking predominance in females, is great news in the field. Finally, current research efforts are dedicated to lifestyle changes that might impact disease phenotype, such as weight loss or undertaking physical exercise.
 
The management and treatment of rheumatoid arthritis is becoming more individualised thanks to a special combined effort of basic scientists and clinicians, and, as a result, more answers are becoming available for patients who inquire about the progression and natural history of their condition.

New EULAR recommendations for the management of antiphospholipid syndrome in adults

2nd June 2019

EULAR has published a set of recommendations for the management of antiphospholipid syndrome in adults.
 
Based on evidence from a systematic literature review and expert opinion, overarching principles and recommendations were formulated and voted. Three overarching principles and twelve recommendations were formulated. The overarching principles are:
  • Risk stratification in aPL positive individuals should include determination of the presence of a high-risk aPL profile (multiple aPL positivity, lupus anticoagulant, persistently high aPL titers), prior history of thrombotic and/or obstetric antiphospholipid syndrome (APS), co-existence of other systemic autoimmune diseases such as systemic lupus erythematosus (SLE), and the presence of traditional cardiovascular risk factors.
  • General measures for aPL positive individuals should include screening for and strict control of cardiovascular risk factors (smoking cessation; management of hypertension, dyslipidemia and diabetes, and regular physical activity) in all individuals; and particularly those with a high-risk aPL profile, screening for and management of venous thrombosis risk factors, and use of low molecular weight heparin in high-risk situations such as surgery, hospitalisation, prolonged immobilisation and the puerperium.
  • Patient education and counselling on treatment adherence, international normalised ratio (INR) monitoring in patients treated with vitamin K antagonists, use of perioperative bridging therapy with low molecular weight heparin for patients on oral anticoagulants, oral contraceptive use, pregnancy and postpartum period, postmenopausal hormone therapy, and lifestyle recommendations (diet, exercise) are important in the management of APS.
The twelve recommendations address the following areas:
  • Asymptomatic aPL carriers (not fulfilling any vascular or obstetric APS classification criteria) with a high-risk aPL profile with or without traditional risk factors
  • Patients with SLE and no history of thrombosis or pregnancy complications
  • Non-pregnant women with a history of obstetric APS
  • Patients with definite APS and first venous thrombosis
  • Patients with definite APS and recurrent venous thrombosis despite treatment with vitamin K antagonists with target INR 2-3
  • Patients with definite APS and first arterial thrombosis
  • Patients with recurrent arterial thrombosis despite adequate treatment with vitamin K antagonists (VKA)
  • Women with a high-risk aPL profile but no history of thrombosis or pregnancy complications
  • Women with a history of obstetric APS only
  • Women with ‘criteria’ obstetric APS with recurrent pregnancy complications despite combination treatment with low disease activity (LDA) and heparin at prophylactic dosage
  • Women with a history of thrombotic APS
  • Prevention and first-line treatment of patients with Catastrophic Antiphospholipid Syndrome (CAPS); treatment of patients with refractory catastrophic APS.

The level of evidence, grade of recommendation and level of agreement were allocated to each statement.

Patients with Sjögren’s Syndrome gather to take their destiny into their own hands

31st May 2019

Sjögren Europe is a European Federation of national patient associations for Sjögren’s Syndrome and rheumatic diseases created in February 2019 by the patient organisations of Finland, France, Greece, Italy, Netherlands, Portugal, Spain, Switzerland, United Kingdom and the support of the informal association of Belgium.
 
The headquarters of Sjögren Europe are in Switzerland and the first General Assembly will be held in Madrid in June 2019 during the EULAR congress where Sjögren Europe will be officially introduced to the rheumatology community.
 
The main objectives of Sjögren Europe:
  • Empower national organisations
  • Assist, promote and encourage the improvement of knowledge about Sjögren’s
  • Syndrome and raise awareness about the disease and all its aspects among national Sjögren’s Syndrome and health-related organisations, patients, members of the health, welfare and medical professions, governmental bodies, pharmaceutical companies and the public
  • Work to achieve an optimal care system, medical treatment and follow-up, psychosocial support and quality of life for all the Sjögren’s Syndrome patients in Europe
  • Be involved in decisions, programs, strategies etc. which affect patients with Sjögren’s Syndrome in Europe
  • Foster and/or undertake surveys and research projects related to the disease and the publication of the results of any such research
Sjögren’s Syndrome
Sjögren’s Syndrome is a complex systemic autoimmune rheumatic disease that specifically targets exocrine glands. Patients typically experience dry eyes and dry mouth. In addition to extensive dryness, other serious complications include profound fatigue, chronic pain, major organ involvement, neuropathies and lymphomas.
 
Despite its considerable prevalence among connective tissue diseases, Sjögren’s has been devoted less research, interest, time and effort compared with other close conditions.
 
Active and synergistic involvement of patients, clinicians and scientists in the definition of unmet needs and areas of future research is crucial.
In this context, “we decided to set up Sjögren Europe to address the lack of visibility and the unmet needs, foster patient training and involvement in research, raise awareness and articulate patient voices throughout Europe. Sjögren Europe would like this condition to be better considered, to speed up the discovery of the different mechanisms of the disease and of new treatments, enhance the global understanding of Sjögren’s Syndrome and want patients who so wish to have access to real and appropriate psycho- social support” pointed out Alice Grosjean.
 
About Sjögren Europe
The idea of Sjögren Europe emerged in April 2018 in Washington DC during the International Sjögren’s Syndrome Symposium (ISSS) and the decision to materialise it was launched during the EULAR congress in Amsterdam in June 2018. This new and great adventure is a wonderful opportunity to merge the voices, perspectives and needs of patient communities from different countries at European level and to bring a ray of hope to patients with Sjögren’s Syndrome. This is Sjögren Europe’s mission: working together and be a partner to all stakeholders of the sector in order to build a better future for patients with Sjögren’s Syndrome.
 
Sjögren Europe Board
  • • Alice Grosjean (Switzerland), president
  • Association Romande du Syndrome de Sjögren (ARSYS)
  • • Mascha Oosterbaan (Netherlands), vice-president Nationale Vereniging Sjögrenpatiënten (NVSP)
  • • Coralie Bouillot (France), secretary Association Française du Gougerot Sjögren et des Syndromes Secs (AFGS)
  • •Katy Antonopoulou (Greece), treasurer, Hellenic League Against Rheumatism (EL.E.AN.A.)
  • Ana Vieira (Portugal), member, Liga Portuguesa contra as Doenças Reumáticas (LPCDR)
  • • Joyce Koelewijn-Tukker (Netherlands), member Nationale Vereniging Sjögrenpatiënten (NVSP)
  • • Isabelle Lesuisse (Belgium), member Association de patients informelle Sjögren.be

Sjögren Europe Medical Board

  • Prof Hendrika Bootsma (Netherlands)
  • Prof Xavier Mariette (France)
  • Prof Athanasios Tzioufas (Greece)
  • Prof Chiara Baldini (Italy)
  • Prof Wan-Fai Ng (United Kingdom)
  • Dr Juan Ovalles (Spain)
  

New findings reveal how microbiome is disrupted during IBD

A new study led by researchers from Harvard T.H. Chan School of Public Health and the Broad Institute of MIT and Harvard is the first to have observed the complex set of chemical and molecular events that disrupt the microbiome and trigger immune responses during flare-ups of inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis.1
 
While previous studies have catalogued microbial changes during IBD, the researchers in this study developed a unique biotechnology toolbox to understand why microbiomes change during IBD and how this provokes an unhealthy inflammatory reaction. These tools allowed them to measure microbial chemical changes and human gene regulatory shifts, potentially allowing for new therapies in the future.
 
The study, which included dozens of collaborators, was part of the second phase of the Human Microbiome Project (HMP). The project, the first phase of which was launched in 2007 by the National Institutes of Health (NIH) Common Fund, aimed to characterise the microbiome in healthy adults and in people with specific microbiome-associated diseases. The most recent phase of work began in 2013 with support from across the NIH, and with the mandate to tease apart the molecular mechanisms underlying the microbiome’s roles in disease.
 
“The Human Microbiome Project overall has been a flagship effort in understanding the microbiome’s contributions to health, and in creating a community of researchers who can study the microbiome to discover new diagnostics and therapies for disease,” said Curtis Huttenhower, professor of computational biology and bioinformatics at Harvard Chan School and associate member at the Broad Institute and senior author of the study. “Our results from this study pave the way for early detection of upcoming flares in disease activity – which can then be aggressively treated – or potentially for new biochemical therapeutic opportunities to encourage complete remission of IBD.”
 
For this study, the most comprehensive analysis to date of human microbiome interactions during IBD, researchers followed 132 participants for one year and compared Crohn’s disease and ulcerative colitis patients to a control group of participants that did not have IBD. Participants provided stool samples every two weeks, blood samples approximately once a quarter, and a set of colon biopsies at the start of the study for analysis. In total, 2965 stool, biopsy, and blood samples were analysed with an unprecedented suite of molecular, cellular, and clinical tools to understand the detailed biochemistry of the disease.
 
First, these detailed measurements made it easy to observe and confirm findings from previous studies, such as a reduction in overall gut ecological diversity and the gain and loss of specific “pro-” and “anti-inflammatory” microbes during disease.
 
More importantly, the suite of tools deployed for this study allowed researchers to determine the reasons for the changes. The results showed that during periods of disease activity, people with IBD had fewer microbially-derived chemicals, which they speculated could be due to a combination of factors, including less beneficial microbial metabolism, poorer nutrient absorption, greater water or blood levels in the bowels, and more urgent bowel movements. These factors decreased the overall stability of the gut microbial ecosystem, leading to more episodes of improper immune responses and overreaction to the normal gut microbiome among IBD patients.
 
Specifically, during periods of disease activity people with IBD had higher levels of polyunsaturated fatty acids, including adrenate and arachidonate. The researchers also discovered that nicotinuric acid was found almost exclusively in the stool of patients with IBD and that levels of vitamins B5 and B3 were particularly depleted in the gut of people with IBD.
 
The team also found that bile acids were disrupted during IBD as well, in tandem with molecular regulation in groups of microbes. These included a group of bacteria related to the genus Subdoligranulum that are carried by almost everyone, but are depleted during inflammation, and which have not been previously isolated or characterised.
 
Overall, the findings provide the most detailed snapshot to date of the microbiome in people with IBD, during active and non-active disease states. The findings showed that different forms of IBD – Crohn’s disease compared with ulcerative colitis, for instance – had different effects on the activity and composition of the microbiome. The researchers said the findings provide promising new targets for potential IBD treatments, including polyunsaturated fatty acids, bile acid derivatives, and human immune response pathways, as well as new data, tools, and protocols that will enable future research on IBD and the microbiome.
 
“Given how tightly connected the microbiome is with our health and wellbeing, these results shed some light on how we might avoid the problems that arise when this relationship goes awry, and how we might be better stewards of these life-long companions,” said Jason Lloyd-Price, who worked on the study while a research scientist at Harvard Chan School and the Broad Institute and was lead author of the paper.
 
Reference
  1. Lloyd-Price J et al. Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases. Nature 2019;569(7758):655 DOI: 10.1038/s41586-019-1237-9

New regulator of immune responses discovered

30th May 2019

Scientists have identified a new internal regulator that helps control the body’s response to fight infection.
The discovery could be a target for new drugs to tackle autoimmune diseases, such as lupus and scleroderma, where healthy tissues are attacked by the body’s own immune system.
“We want to put a brake on the body’s own immune system to stop it turning on itself,” said Dr Elton Zeqiraj from the University of Leeds.
“Our discovery has the potential to help us find a new drug to target this regulator, to suppress the immune system and stop the body destroying its own cells, even when there is no infection present.
“We’re a long way off being able to find a new effective treatment for autoimmune disease, but we’re excited because this discovery could open the door to a new class of drugs.”
Autoimmune diseases include a wide range of difficult-to-treat conditions, including Type 1 diabetes and rheumatoid arthritis.
The scientists used powerful cryo-electron microscopes at the University of Leeds’ Astbury Centre to reveal the structure of the regulator, comprised of two proteins in the body called BRISC and SHMT2, to understand for the first time how they work together in a cell.
The protein complex acts to increase the immune response of cells, which occurs when they detect an invading pathogen.
Dr Elton Zeqiraj continued: “The microscopes have allowed us to understand the structure of this protein complex in superb detail, and by building an accurate 3D model, we discovered that it plays a completely unexpected role in regulating our immune response.
“The next step is to find a way of targeting this protein to inhibit the process, to prevent our immune system from attacking healthy cells.”
The international collaboration of scientists and clinicians included co-first authors Dr Miriam Walden from Leeds and Dr Lei Tian from Pennsylvania, as well as researchers from the University of Liverpool, The Wistar Institute (Philadelphia), UbiQ Bio BV (Amsterdam), Warsaw University of Life Sciences and Lund University.
The research was primarily funded by the Wellcome Trust, The Royal Society, the National Cancer Institute, the Lupus Research Alliance, and Scleroderma and Raynaud’s UK.
Sue Farrington, Chief Executive of Scleroderma and Raynaud’s UK, said: “Thousands of people in the UK are suffering from autoimmune diseases like scleroderma, which can cause serious skin problems that can greatly reduce quality of life.
“We are very proud to have helped fund this important scientific breakthrough, and we hope this can open up a new avenue for drug discovery so that we can create more effective treatments for autoimmune conditions.”

Phase III QUARTZ study meets primary and key secondary endpoints

Novartis has announced the first study results from the Phase III PLATINUM clinical development program assessing the safety and efficacy of QMF149, an investigational, once-daily, fixed dose combination asthma treatment containing indacaterol acetate (IND – a long-acting beta agonist [LABA]) and mometasone furoate (MF – an anti-inflammatory (ICS)).
 
In this multicentre, randomised, double-blind Phase III QUARTZ study (ClinicalTrials.gov Identifier: NCT02892344), once-daily, low dose IND/MF (QMF149) 150/80μg met the primary and key secondary endpoints (trough FEV1 and ACQ-7 score at Week 12, respectively) when compared to once-daily mometasone furoate (MF), an ICS, delivered via the Twisthaler® device (200μg) in both adult and adolescent patients with asthma1. 
 
Patients included in the QUARTZ study were inadequately controlled (symptomatic as defined by Asthma Control Questionnaire, ACQ-7>1.5) on low dose ICS (with or without an additional maintenance treatment).1
 
“Despite the number of available treatments, many patients’ lives remain impacted by their asthma,” said Linda Armstrong, MD, Respiratory Development Unit Head. “The QMF149 results of the QUARTZ study complement the recently presented Phase II data of QVM149 at the 2019 American Thoracic Society Congress, showing superiority of QVM149 to the current standard of care. We look forward to seeing the rest of the data from the PLATINUM clinical trial program.”
 
IND/MF demonstrated statistically significant improvements in lung function as measured by trough FEV1 (volume of air that can be forced out in one second after taking a deep breath, which is measured approximately 24 hours after the last administration of study drug) compared to MF after 12 weeks of treatment in adult and adolescent patients with inadequately controlled asthma (Least squares (LS) mean treatment difference: 0.182l, 95% CI: 0.148, 0.217; p<0.001).1 In addition, clinically meaningful lung function benefit for IND/MF is supported by improvements in evening PEF of 26.1l/min compared to MF alone (95% CI, 21.0, 31.2).
 
IND/MF also demonstrated statistically significant improvements in asthma control compared with MF, as measured by ACQ-7 after 12 weeks of treatment (LS mean treatment difference: −0.218, 95% CI: −0.293, −0.143; p<0.001)1. In addition, clinically meaningful improvement in ACQ-7 is supported by a responder analysis, in which the QMF149 group had a greater proportion of responders (improvement in ACQ-7 ≥0.5) compared to the MF group (74.7% vs 64.9%, respectively (odd ratio: 1.69, 95% CI: 1.23, 2.33).
 
Both treatments (IND/MF and MF) were generally well tolerated. The overall incidence of adverse events (AEs) was lower in the IND/MF group compared with the MF group (32.3% vs. 38.3%, respectively). The majority of AEs in both treatment groups were mild to moderate (>90% AEs) in severity, and were comparable between the treatment groups. The incidence of severe AEs was low and were reported in 7 (1.8%) patients in the QMF149 group compared with 14 (3.5%) patients in the MF group.1
 
“I am very pleased with the results of the QUARTZ study looking at the efficacy and safety of the fixed dose combination of indacaterol and mometasone furoate,” Dr Oliver Kornmann, Pulmonary Department, Internal Medicine, University Hospital Mainz, Germany. “Fixed-dose combination inhalers may offer advantages to people with asthma by simplifying complex inhaler regimens, especially when they can be dosed once daily which can therefore further reduce the burden of the disease.”
 
Reference
  1. Clinicaltrial.gov (Identifier: NCT02892344)   https://clinicaltrials.gov/ct2/show/NCT02892344?term=NCT02892344&rank=1

Key link discovered between tissue cell type and different forms of arthritis

Pioneering research by scientists at the Universities of Oxford and Birmingham published in Nature brings us a step closer to developing targeted therapies for inflammatory diseases.1
 
The research team shows, for the first time, that different types of fibroblasts – the most common cells of connective tissue in animals – are organised in different layers in the joint and are responsible for two very different forms of arthritis; osteoarthritis and rheumatoid arthritis.
 
Targeted therapies could alter the behaviour of fibroblasts to reduce inflammation and tissue destruction in these two diseases without the need for long-term immunosuppression or joint replacements, say the scientists.
 
The research is part of the Arthritis Therapy Acceleration Programme (A-TAP), a joint alliance between the Universities of Birmingham and Oxford, which aims to ensure that world-class basic science observations are accelerated into early-phase experimental therapy for patients. A-TAP is funded by the Kennedy Trust for Rheumatology Research at the University of Oxford.
 
Chief investigator Professor Chris Buckley, of the University of Birmingham’s Institute of Inflammation and Ageing and Director of Clinical Research at the Kennedy Institute at the University of Oxford, said: “If we compare fibroblasts to soil, this research has shown for the first time that not all soil is the same.
 
“Just as there are different layers of soil in our gardens – top soil and subsoil – there are different types of fibroblasts in our joints – and each layer seems to be associated with a different type of arthritis.
 
“From a research perspective this is exciting, but the clinical implications are also very important too. For the first time, we have identified two different types of fibroblasts in the joint, which, just like the different types of soil, lead to different types of arthritis.
 
“The top soil is what goes wrong in osteoarthritis, whereas in rheumatoid arthritis it’s the subsoil that is at fault.
 
“When patients are seen in clinic and we can’t help them, it motivates us to think creatively about how we conduct our research and classify disease.
 
“We have now discovered a new way to classify, and therefore treat, arthritis based on the underlying cell, rather than just the clinical features and genes involved.
 
“Current therapies work like weed killer – they kill the weeds but the weeds come back if you don’t continue to apply the weed killer. Our research will facilitate research aimed at changing the top soil, subsoil – or both – to treat arthritis.
 
“To know we are getting closer to offering patients new solutions is very exciting and we are doing it because we are finally looking at diseases using a process-driven cell based approach through the A-TAP project.”
 
Two recent technical and clinical advances have helped lead to the researchers’ discovery: minimally invasive biopsies and single-cell sequencing. These two developments have allowed the research team to investigate fibroblast cells and their location in the joint as never before, ultimately identifying and describing the biology of distinct subsets of fibroblasts responsible for mediating either inflammation or cartilage/bone damage in arthritis.
 
First author Dr Adam Croft, currently NIHR Academic Clinical Lecturer in Rheumatology at the University of Birmingham and previously funded by a Wellcome Trust Clinical Career Development Fellowship, adds: “Rheumatoid arthritis is challenging to treat. It causes chronic inflammation in joints, leading to pain, swelling and, over time, damage to the joint. This is due to the body’s own immune system attacking the joints, which leads to an influx of immune cells in the lining of the joint.
 
“Current treatments target these immune cells either directly or by trying to disrupt the signals that attract the cells to the joint. No treatments directly target fibroblasts, key effector cells in the pathology of this disease.
 
“Thanks to advances in technology we have now, for the first time, been able to identify which fibroblasts are pathogenic in arthritis and how they contribute to disease.
 
Importantly, we found that by getting rid of these fibroblasts from the joint we could reduce the influx of immune cells to the joint, leading to less inflammation and destruction.
 
“These findings mean we now have a clear rationale for developing drugs that can target joint fibroblasts directly and provide more effective treatment for persistent disease.”
 
Reference
  1. Croft A et al. Distinct fibroblast subsets drive inflammation and damage in arthritis. Nature 2019; May 29

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