hheadmin, Author at Hospital Healthcare Europe

Press Releases

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

No-deal Brexit could disrupt medicines supply by ‘at least’ six months, health minister warns

21st February 2019

Manufacturers may have to rethink the way they transport stock to avoid ‘at least’ six months of border delays in a no-deal Brexit, a letter from a UK health minister has warned.

A letter from the MP Stephen Hammond, sent this month (8 February), was written in response to concerns raised by the House of Lords EU Home Affairs Sub-Committee about access to medical supplies in a no-deal Brexit scenario and outlined the Department of Health and Social Care’s (DHSC) “detailed contingency plans”.

The short straits crossings via Dover and Folkestone, through which 90% of medicines enter the UK, “may be subject to a significantly reduced flow of goods for at least six months rather than the previous estimate of six weeks of disruption”, according to the letter.

‘Critical’ medicines affected

Mr Hammond said disruption to supplies would affect “critical” prescription-only and pharmacy medicines and would also affect UK manufacturers.

He said: “The possible border delays indicated in the updated planning assumptions would impact any import of medicines, including prescription-only and pharmacy medicines, critical to the continuity of patient care.

‘It would also impact UK manufacturers of medicines that may rely on the import of raw materials from or via the EU. Therefore, we have asked all suppliers to consider their supply routes and whether any re-routing to avoid the short straits is necessary.”

Flying medicines to UK?

In December, the Government predicted disruption could cause “up to six months” of reduced access across the channel and announced plans for stockpiling and began discussions to arrange the transportation of medicines with short shelf lives via air freight.

This month’s update saw suppliers instructed to ensure that these plans are in place for those medicines that cannot “reasonably” be stockpiled. However, Mr Hammond refused to give the committee further information about which medicines would be prioritised and the cost of flying them in for a six-week period, citing commercial sensitivities.

He said: “The Department is still reviewing what support it may provide to companies flying medicines to the UK. The cost of flying in medicines is a confidential commercial decision made between air-freight companies and the manufacturer.”

No-deal Brexit could disrupt medicines supply by ‘at least’ six months

Study shows that lupus is strongly linked to imbalances in gut microbiome

20th February 2019

Systemic lupus erythematosus (SLE) is linked to an abnormal mix of bacteria in the gut according to a new study led by scientists at NYU School of Medicine.

The study, published in the Annals of Rheumatic Diseasesshowed that 61 women diagnosed with SLE had roughly five times more Ruminococcus gnavusgut bacteria than 17 women of similar ages and racial backgrounds who did not have the disease and were healthy.¹ Lupus is more common in women than in men.

Moreover, study results showed that disease ‘flares’, which can range from instances of skin rash and joint pain to severe kidney dysfunction requiring dialysis, closely tracked major increases in R. gnavus bacterial growth in the gut, alongside the presence in blood samples of immune proteins called antibodies, specifically shaped to attach to the bacteria. Study participants with kidney flares had especially high levels of antibodies to R. gnavus.

The authors say the specific causes of lupus, which affects as many as 1.5 million Americans, are unknown, although many suspect that genetic factors are partly responsible.

“Our study strongly suggests that in some patients bacterial imbalances may be driving lupus and its associated disease flares,” says study senior investigator and immunologist Gregg Silverman, MD. “Our results also point to leakages of bacteria from the gut as a possible immune system trigger of the disease, and suggest that the internal gut environment may therefore play a more critical role than genetics in renal flares of this all too often fatal disease,” says Silverman, a professor in the departments of Medicine and Pathology at NYU Langone Health. He also suspects that antibodies to R. gnavus provoke a “continuous and unrelenting” immune attack on organs involved in flares.

Among the more practical consequences of the new research, Silverman says, could be the development of relatively simple blood tests to detect antibodies to leaked bacteria, which in turn could also be used to diagnose and track lupus progression and therapy, even in the disease’s earliest stages. Current tests, he says, are often inconclusive and rely on signs and symptoms that only appear after the disease has already advanced.

Silverman cautions that larger studies are needed to confirm how these bacteria may cause lupus. But if future experiments show similarly positive results, then it could result in shifts from current approaches to treating the disease, which focus on immune-suppressing anticancer medications to relieve symptoms and injury to the kidneys.

If the study team’s results are validated, then some current treatments may actually be causing harm if they impair overall immune defences against infection.

Instead, Silverman says future treatments could include inexpensive probiotics or dietary regimens that impede R. gnavus growth and prevent flares. Faecal transplants from healthy individuals would also be a possibility.

Alternatively, Silverman says new treatments could also be used to promote growth of Bacteroides uniformis, bacteria thought to hinder growth of R. gnavus in the gut and whose numbers decreased by as much as fourfold in study participants with lupus when compared to those without the disease. Experts say that over a 1000 different types of bacteria make up the human gut microbiome.

For the study, researchers analysed blood and stool samples from participants. Researchers were surprised to find strong immune antibody reactions to R. gnavus in the blood because the gut lining prevents the bacterium from escaping to other parts of the body. Researchers say this suggests that small pieces of the bacteria, known as antigens, must have ‘leaked’ into the gut to trigger the immune reaction.

Reference

Azzouz D et al. Lupus nephritis is linked to disease-activity associated expansions and immunity to a gut commensal. Ann Rheum Dis epub ahead of print: [19 February 2019]. doi:10.1136/ annrheumdis-2018-214856

Study shows that lupus is strongly linked to imbalances in gut microbiome

Allergen immunotherapy shows positive effects in the nasal membrane

According to a study by researchers at the University of Helsinki, pollen allergen immunotherapy has favourable effects on the molecular events and microbiome profile in the nasal membrane.

Birch pollen allergic rhinitis is the most common chronic disorder in the Northern part of the globe, and it attributes to significant morbidity and economic burden.

The researchers studied five healthy, non-smoking adult subjects and six allergic rhinitis patients longitudinally during two springs and two winters in 2011 and 2012. Half of the allergy patients started subcutaneous birch allergen immunotherapy after the first winter.

In total, 44 nasal brushings were subjected to RNA-sequencing analysis to find gene expression and microbial community changes driven by allergic rhinitis and allergen immunotherapy.

According to the results, the group who started allergen immunotherapy showed decreased symptom score and reprogramming of nasal epithelial transcriptome, set of RNA molecules, during the pollen season.

“The immunotherapy affected asthma-, chemokine signaling-, and toll like receptor signaling pathways in the spring. No major differential expression was found between the two winters in any group,” said researcher Sanna Toppila-Salmi from the University of Helsinki and Helsinki University Hospital, Finland.

The results also indicated that microbial community diversity of the group that underwent allergen immunotherapy approached that of the healthy controls.

According to the researchers, the study shows that RNA sequencing is a promising method to monitor allergen immunotherapy response.

Allergen immunotherapy shows positive effects in the nasal membrane

Immunological scarring from coeliac disease

18th February 2019

Immune cells in the bowel of people who suffer with coeliac disease are permanently replaced by a new subset of cells that promote inflammation, suggests a new study involving researchers at Cardiff University.¹

This permanent ‘immunological scarring’ lays the foundation for the disease to progress and could have long-term implications for gut health in affected patients.

The results also suggest that the same process could be contributing to other chronic intestinal disorders, such as ulcerative colitis.

Dr James McLaren, from Cardiff University’s School of Medicine, said: “In coeliac disease, T cells found in the bowel react to gluten and cause inflammation, which damages the lining of the bowel.

“Under normal circumstances, T cells have a protective role in the bowel and form a stable population. However, in coeliac disease, they contribute to the inflammatory process, causing short-term symptoms and increasing the risk of developing certain types of bowel cancer.

“Our new study suggests that even though short-term symptoms, such as diarrhoea and abdominal pain, can be alleviated by removing gluten from the diet, long-term implications may remain, because ’tissue-healing’ T cells in the bowel are permanently replaced by ‘pro-inflammatory’ T cells.”

Source: Cardiff University.

Reference

Mayassi T et al. Chronic inflammation permanently reshapes tissue-resident immunity in celiac disease. Cell 2019; DOI: 10.1016/j.cell.2018.12.039

Immunological scarring from coeliac disease

Patients’ own cells could be the key to treating Crohn’s disease

Researchers at the NIHR Guy’s and St Thomas’ Biomedical Research Centre (BRC) developed the technique by studying white blood cells taken from patients who have Crohn’s disease, and comparing them to cells of healthy people. Their findings allowed cell therapy specialists in the BRC to develop a treatment involving taking patients’ cells, and culturing them so that they behave more like cells from healthy people.

The research, published in the journal Gastroenterology, shows that this technique is effective in human cells.¹ The proposed Tribute Trial will test whether the treatment is safe and effective for treating Crohn’s disease.

Professor Graham Lord, previously Director of the NIHR Guy’s and St Thomas’ BRC, led the research. He recently took up a role as Vice-President and Dean of the Faculty of Biology, Medicine and Health at the University of Manchester. He said: “This is the next frontier in cell therapy, as we’re going beyond treating the symptoms of Crohn’s disease, and trying to reset the immune system to address the condition.

“It’s a real home-grown treatment in the sense that we started with observing cells and tissues donated by patients at Guy’s and St Thomas’, have developed a treatment, and are now starting to undertake trials, all at the Trust. It shows how central patients are to research, helping to create a treatment that might help thousands more people.”

Rachel Sawyer, a communications manager who is 50 and lives in Anerley in south east London, was diagnosed with Crohn’s disease in 2000 and treated at Guy’s and St Thomas’.

She said: “One of the worst things for me was the unpredictability, particularly around needing the toilet in a hurry. Having Crohn’s completely re-routes your daily life and makes it hard to do the normal things most of us take for granted like going out socially or taking public transport. Even now, the fear of it is never really far from my mind.

“Another difficult thing is the stigma associated with bowel disease. It’s difficult to talk and be open about it, even with family and friends. I found life very isolating and challenging at times — and that’s something so many people with Crohn’s experience, regardless of whether they were diagnosed years ago or last month. For people diagnosed young, it can impact on the formative years of their life.

“Anything that could help people with Crohn’s have the confidence to go out and get back to being the people they were destined to be would be a game-changer.”

The researchers found that specialised white blood cells called regulatory T cells from Crohn’s patients produced less of a gut-specific protein called integrin α4β7 than regulatory T cells from healthy people. Working with the specialists at the NIHR Guy’s and St Thomas’ BRC’s Advanced Therapies Manufacturing Platform, they developed a cell therapy technique based on these findings.

This technique involves developing cells from the Crohn’s disease patients with a molecule called RAR568, which restores healthy levels of integrin α4β7. The cells are then given back to patients by intravenous infusion.

Dr Peter Irving, a Consultant Gastroenterologist and co-author on the paper, said: “While the treatments available for Crohn’s disease have increased over recent years, they only work in some patients. In addition, the treatments have potentially serious side effects in some patients. This research paves the way for a trial of using patients’ own cells to treat their Crohn’s disease and we look forward to offering people the chance to take part in the very near future.”

Source: NIHR Biomedical Research Centre at Guy’s and St Thomas’ and King’s College London.

Reference

Goldberg R. Correction of defective T-regulatory cells from patients with Crohn’s disease by ex vivo ligation of retinoic acid receptor alpha. Gastroenterology,2019; DOI: 10.1053/j.gastro.2019.01.025

Patients' own cells could be the key to treating Crohn's disease

A position statement from the Global Interventional IBD Group

A report from the panel, Role of interventional inflammatory bowel disease in the era of biologic therapy; a position statement for the Global Interventional IBD Group, was published in the February issue of GIE: Gastrointestinal Endoscopy.¹

Endoscopic therapy has been explored and used in the management of numerous conditions and situations related to IBD, including strictures, fistulas/abscesses, colitis-associated neoplasia, postsurgical acute or chronic leaks, and obstructions. The endoscopic therapeutic modalities include balloon dilation, stricturotomy, stent placement, fistulotomy, fistula injection and clipping, sinusotomy, endoscopic mucosal resection, and endoscopic submucosal dissection.

With a better understanding of the disease process and course of IBD, improved long-term impact of medical therapy, and advances in endoscopic technology, the panel foresees interventional IBD becoming an integrated part of the multidisciplinary approach to patients with complex IBD.

In recent decades, rapid advances have taken place in medical and surgical therapy for both Crohn’s disease (CD) and ulcerative colitis (UC). For example, the availability and growing use of anti-tumour necrosis factor (TNF), anti-integrin, and anti-interleukin biologics have been shown to result in deep clinical remission beyond improvement of symptoms. These medical treatments also reduce the risk for adverse events associated with IBD, thereby avoiding hospitalisation and surgery for some patients. Additional agents are being investigated.

However, the long-term impact of the appropriate use of these newer agents on the natural history of IBD is not clear. In addition, the long-term use of these immunosuppressive agents can be associated with various adverse events, ranging from infection and increased risk for certain malignancies to a paradoxic autoimmune response. Furthermore, a significant number of patients with CD or UC still require surgical intervention for medically refractory disease or disease-associated adverse events such as strictures, fistulas, abscesses, and colitis-associated neoplasia (CAN).

The common surgical treatment modalities for CD or ulcerative colitis include bowel resection, anastomosis, stoma construction, strictureplasty, and restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA). Although the surgical approach offers an immediate resolution of symptoms and relief of mechanical or neoplastic adverse events, it is often associated with postoperative adverse events and postoperative disease recurrence. Current unmet needs in IBD management include the availability of therapeutic approaches to mechanical adverse events that can reach beyond the limits of pharmacologic agents and are less invasive than surgery.

Therapeutic endoscopy can offer a unique bridge between medical and surgical treatments. Endoscopic management of mechanical and neoplastic adverse events may help reduce or postpone the need for surgical resection and help treat postoperative adverse events, if surgery is performed. Currently, four main areas of IBD are amenable to endoscopic treatment: strictures, fistulas or abscesses, CAN, and IBD surgery-associated adverse events.

To meet the growing need for endoscopic treatment in complex IBD, a panel of national and international experts in gastroenterology, IBD, advanced endoscopy, GI radiology, GI pathology, GI education, and colorectal surgery voluntarily formed a subspecialty group in 2018, the Global Interventional IBD Group, to coordinate clinical, educational, and investigational activities. This self-appointed group includes a mixture of IBD specialists with expertise in endoscopy and endoscopists with expertise in IBD. In addition, the group also consists of IBD pathologists and IBD specialists with expertise in abdominal imaging. The current article is a position statement from the group, based on currently available literature and the combined expertise of its members. This work is expected to continue and expand.

Reference

Shen B et al. Role of interventional inflammatory bowel disease in the era of biologic therapy: a position statement from the Global Interventional IBD Group. Gastrointest Endosc 2019;89(2):215-37.

A position statement from the Global Interventional IBD Group

More needs to be done to raise awareness of lung cancer risk in people with COPD

During a unique study, led by the University of Glasgow and University of Surrey, researchers have investigated how the experience of COPD influences how individuals understand new or changing chest symptoms and their decision to seek help from medical professionals.

Incidence of lung cancer is four-times higher in those with COPD compared with the general population and patients often confuse early signs of the devastating disease with a deterioration of their existing condition and do not seek medical advice.

Interviewing 40 participants with COPD, researchers discovered that none of the participants were aware that having the condition put them at increased risk of developing lung cancer. Due to a lack of knowledge and support, participants often attributed chest symptoms to external factors such as the weather or illness.

Researchers found that some participants did not seek medical advice following the development of symptoms as they were keen to ‘not make a fuss’ and believed that poor health was something to be accepted when diagnosed with the condition. A stigma associated with continued smoking was also identified by researchers, as participants were found to be reluctant in seeking help as they felt the doctor would blame their symptoms on smoking.

Participants also spoke about barriers in accessing care, which included scheduling appointments outside of usual working hours and difficulties in getting to the GP’s surgery, when symptoms present themselves.

Early diagnosis of lung cancer is vital to improving survival. Figures from Cancer Research UK reveal that when diagnosed at its earliest stage, almost 6 in 10 people with lung cancer will survive their disease for five years or more, compared with almost 5 in 100 people when diagnosed at a later stage.

Dr Katie Robb, Senior Lecturer at the University of Glasgow, said: “Healthcare professionals need to do more to educate those with COPD about their increased risk of developing lung cancer and be more vigilant when a patient with the illness presents changing symptoms.”

Dr Katriina Whitaker, Reader in Cancer Care at the University of Surrey, said: “Early diagnosis of lung cancer is vital in improving survival rates, we need those with COPD to go to the doctor as a matter of course when they notice a change in their symptoms and not be concerned about wasting the doctor’s time.”

Jodie Moffat, Head of Early Diagnosis at Cancer Research UK, said: “It’s vital patients and their doctors stay alert to signs of cancer to ensure that any potential cancer is diagnosed as soon as possible. Symptoms of other diseases can mask cancer signs, so it’s important patients know what to look out for. Changes to existing conditions, as well as new symptoms, should be checked out by a GP, and GPs need to be ready to consider cancer as an option.”

More needs to be done to raise awareness of lung cancer risk in people with COPD

Expert view: Immunosenescence vs autoimmunity

11th February 2019

Frailty is a syndrome characterised by reduced strength and endurance, accelerated decline in multiple physiologic functions and failure to restore homeostasis, particularly in senior subjects. In fact, frailty is a hallmark of ageing and predisposes subjects to health risks, such as fractures and falls, leading to further disability and morbidity and frequent adverse outcomes. Osteoporosis and immunosenescence (for example, ageing of the immune function) are paradigmatic components of this condition.

Immunosenescence or the decline of the immune function and a chronic inflammatory state are well illustrated by the reduced response to vaccines, and ultimately add to the musculoskeletal decay, resulting in a global public health problem, due to the expansion of the elder population caused by prolonged life expectancy and to the associated huge social and health care costs. The increasing prevalence of serum autoantibodies with age and the different manifestations of rheumatic diseases in the ageing population well represent these aspects. The ultimate goal of modern medicine is a personalised approach being tailored on the single patient, that is, tailored, based on a finely tuned definition of the immunogenetics, epigenetics, microbiome, and biomarkers, to maximise results and minimise risks. While this might appear an overambitious goal, we should 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 and the paradigm of anti-nuclear and anti-citrullinated peptide antibodies should be discussed. Among individual factors around which to tailor the patient management are sex and age, with gender-medicine finally becoming central to the research agenda.

Frailty progression can be delayed and partial reversion can be achieved if adequate interventions are undertaken. A wider understanding of the pathogenesis of frailty and the identification of possible biomarkers to measure its severity in routine clinical practice will help address this health challenge.

Expert view: Immunosenescence vs autoimmunity

Identical twins light the way for new genetic cause of inflammatory arthritis

Identical twin toddlers who presented with severe arthritis helped scientists to identify the first gene mutation that can single-handedly cause a juvenile form of this inflammatory joint disease.

By investigating the DNA of individual blood cells of both children and then modelling the genetic defect in a mouse model, the research team led by Adrian Liston (VIB-KU Leuven) was able to unravel the disease mechanism. The findings may help to develop an appropriate treatment as well.

Juvenile idiopathic arthritis is the most common form of all childhood rheumatic diseases. Patients present with a highly variable clinical picture, and scientists have long suspected that different combinations of specific genetic susceptibilities and environmental triggers drive the disease.

A single gene mutation

In a new study by researchers at VIB, KU Leuven and UZ Leuven, the cause of juvenile arthritis in a young pair of identical twins was traced back to a single genetic mutation.¹

“Single-cell sequencing let us track what was going wrong in every cell type in the twin’s blood, creating a link from genetic mutation to disease onset,” explains D. Stephanie Humblet-Baron (VIB-KU Leuven), one of the researchers involved in the study. “It was the combination of next generation genetics and immunology approaches that allowed us to find out why these patients were developing arthritis at such a young age.”

Modelling a human disease in mice

Parallel studies in mice confirmed that the gene defect found in the patients’ blood cells indeed led to an enhanced susceptibility to arthritis. Prof Susan Schlenner (VIB-KU Leuven), first author of the study, stresses the relevance of this approach: “New genetic editing approaches bring mouse research much closer to the patient. We can now rapidly produce new mouse models that reproduce human mutations in mice, allowing us to model the disease of individual patients.”

From cause to cure

Liston’s team collaborated closely with Prof Carine Wouters (UZ Leuven), who coordinated the clinical aspect of the research: “The identification of a single gene that can cause juvenile idiopathic arthritis is an important milestone. A parallel mouse model with the same genetic mutation is a great tool to dissect the disease mechanism in more detail and to develop more effective targeted therapies for this condition.”

And the young patients? They are relieved to know that scientists found the cause of their symptoms: “We are delighted to know that an explanation has been found for our illness and more so because we are sure it will help other children.”

Reference

Schlenner S et al. NFIL3 mutations alter immune homeostasis and sensitise for arthritis pathology. Ann Rheum Dis 2018; annrheumdis-2018-213764 DOI: 10.1136/annrheumdis-2018-213764

Source: VIB (the Flanders Institute for Biotechnology)

Identical twins light the way for new genetic cause of inflammatory arthritis

Manufacturer advises caution when dispensing some batches of amoxicillin

6th February 2019

Pharmacists in the UK have been urged caution when dispensing the drug Amoxicillin by manufacturer Accord.

The class 4 drug alert has been issued by the Medicines and Healthcare products Regulatory Agency (MHRA) for Amoxicillin 500mg capsules. The relevant batch numbers are MP18062, MP18063, and MP18064, distributed in October last year.

Accord Healthcare Limited said important information about potentially life-threatening side effects was not added to the patient information leaflet for some batches.

Pharmacy teams dispensing this drug have been asked to remove the patient information leaflet and provide a copy of the correct version which can be downloaded here.

They have also been advised to check the Marketing Authorisation Holder and batch number.

Any patients who have noticed any symptoms have been asked to seek immediate medical advice.

Manufacturer advises caution when dispensing some batches of amoxicillin

Press Releases

No-deal Brexit could disrupt medicines supply by ‘at least’ six months, health minister warns

Study shows that lupus is strongly linked to imbalances in gut microbiome

Allergen immunotherapy shows positive effects in the nasal membrane

Immunological scarring from coeliac disease

Patients’ own cells could be the key to treating Crohn’s disease

A position statement from the Global Interventional IBD Group

More needs to be done to raise awareness of lung cancer risk in people with COPD

Expert view: Immunosenescence vs autoimmunity

Identical twins light the way for new genetic cause of inflammatory arthritis

Manufacturer advises caution when dispensing some batches of amoxicillin

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