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24th January 2020
The event, co- hosted by Tanja Fajon MEP (S&D, Slovenia) and Ewa Kopacz MEP (EPP, Poland), featured presentations on the growing importance of radioligand therapy as part of cancer care, led by patient representatives and experts in oncology, nuclear medicine and European health policy. Speakers considered the political and practical actions needed to create an enabling environment for radioligand therapy in the EU to better integrate it into current oncology approaches.
Radioligand therapy delivers radiation directly to cancer cells, using structural differences to target these specific cells anywhere in the body while leaving healthy cells largely unaffected. It is an increasingly promising element of cancer care and its use has expanded significantly in recent years – but uptake and availability remain highly variable across Europe. Radioligand therapy is currently approved for use in neuroendocrine cancers and metastatic castrate-resistant prostate cancer that has spread to bones, and may have applications for many different types of cancer and even other diseases.
Discussions at the launch event centred around the barriers and recommendations for radioligand therapy identified in the new report. Barriers include low awareness and understanding within the health community and unclear models of care. The proposed recommendations to address these challenges range from increasing use of multidisciplinary care in oncology to boosting investment in real-world data collection.
Suzanne Wait, Managing Director, The Health Policy Partnership says: ‘The challenges to integrating radioligand therapy into cancer care are not unique to this form of treatment – and reflecting on them from all perspectives (that of clinicians, patients, regulatory agencies, hospitals and policymakers) may help progress towards more personalised and integrated models of cancer care.’
Radioligand therapy can be personalised to individual patients and relies on strong multidisciplinary teamwork among expert clinicians. Cancer is the second highest cause of death in Europe and its prevalence is set to increase in the coming years. As more people are living with cancer, and living longer with the disease, quality of life is increasingly being prioritised in treatment and care planning. With fewer side effects than conventional cancer treatments, radioligand therapy can help cancer patients live with improved quality of life.
17th January 2020
According to Cancer Research UK, “using sunbeds can increase your risk of melanoma skin cancer by 16-20%”.1
In support of this statement, a meta-analysis of observational studies in 2014 of those with melanoma who had used indoor tanning beds (sunbeds), found that the odds ratio for melanoma associated with “ever use” of sunbeds was 1.16.2 In other words, there was a 16% increase in the odds of getting a melanoma with sunbed use compared to not using a sunbed. However, the authors conceded that the quality of the evidence contributing to their analysis ranged from poor to mediocre and the acknowledged a recognised limitation of observational studies, namely recall bias.
In contrast, a meta-analysis of observational studies in 2018 was less circumspect and concluded that scientific knowledge [on the link between indoor tanning and melanoma] is mainly based on poor quality data and that there is currently no convincing evidence that moderate/responsible use of solarium (indoor tanning) increases melanoma risk.3
The problem with analysing observational studies is that they can only demonstrate that the two factors, in this case sunbed use and melanoma, are associated: it is impossible to prove causality, that is, that sunbed use leads to melanoma. The fallacy of relying upon observational studies to “prove” that associations are causally related was most clearly highlighted with the use of hormone replacement therapy (HRT). Meta-analysis of observational studies clearly showed that HRT had cardio-protective effects,4 yet when randomised controlled trials (that is, the gold standard) were undertaken, there were no cardiovascular benefits from HRT.5
In the most recent review on sunbed use and the association with melanoma, published in January 2020, yet another article was critical of the available evidence.6 A key argument made in the latest analysis is that individuals who use sunbeds are effectively “sun-worshippers” that indulge in sun risk behaviours and that trying to untangle the effects of over-exposure to sunlight and the use of sunbeds is extremely difficult.
In support of their argument, a recent study of the characteristics of sunbed users described a typical user as a young adult female, who also smoked and engaged in sun-seeking behaviours (e.g. sunny holidays and sunburn).7 Further support for the notion that it is over-exposure to sunlight rather than sunbed use that leads to melanoma comes from a recent French study.
The authors found that 83% of melanomas were due to exposure to UV radiation and only 1.5 % (for men) and 4.6% (for women) are due to use of sunbeds.8 Furthermore, in an analysis of the factors associated with the development of a second melanoma, Austrian researchers found that both outdoor occupation and solarium (sunbed) use did not increase the risk of a subsequent melanoma.9
Although meta-analyses generally report an odds ratio of around 1.2 for the relationship between sunbed use and melanoma, is this something to be worried about? In order to provide some context, it has been suggested that an odds ratio of 1.68 represents a “weak association” between two factors, whereas an odds ratio of 6.71 represents a strong association10 hence an odds ratio of 1.2 is a very weak association.
Furthermore, public health campaigns to warn about the dangers of sunbed use would appear to go unheeded. In a recent European study in 30 countries including over 227,000 individuals, the overall prevalence of sunbed use was found to be 10.6% with a higher prevalence in younger females.11 Fortunately, other work has shown that the introduction of regulations on the use of sunbed has been found to lead to a 70% drop in teenage use of sunbeds.12
While legislation can help to regulate who uses a sunbed, public health campaigns warning of the dangers are being potentially undermined when bodies such as the World Health Organization (WHO) say that “few studies have been undertaken to systematically assess the dangers of sunbed use, and the picture remains equivocal … due to the long latency period for skin cancer and eye damage it has been difficult so far to demonstrate any long-term health effects.”13
With research describing how use of sunbeds is driven by aesthetic needs,7 getting a pre-holiday tan and modelling parental behaviours, it would seem that public health campaigns need to focus not solely on the harms associated with sunbed use but to emphasise that the short-term cosmetic benefits from a sunbed may result in a higher price in later life. With the absence of definitive proof that sunbed use increases the risk of developing a melanoma, it would still be folly to suggest otherwise.
References
1 Cancer Research UK. How do sunbeds cause skin cancer? www.cancerresearchuk.org/about-cancer/causes-of-cancer/sun-uv-and-cancer/how-do-sunbeds-cause-skin-cancer (accessed January 2020).
2 Colantonio S, Bracken MB, Beecker J. The association of indoor tanning and melanoma in adults: systemic review and meta-analysis. J Am Acad Dermatol 2014;70:847–57.
3 Burgard B et al. Solarium use and risk of malignant melanoma: meta-analysis and evidence-based medicine systematic review. Anticancer Res 2018;38(2):1187–99.
4 Stampfer MJ, Colditz GA. Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiological evidence. 2004;33:445–53.
5 Hulley S et al. Randomised trial of oestrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progesin replacement study (HERS) research group. JAMA 1998;280(7):605–13.
6 Reichrath J et al. Sunbeds and melanoma risk: many questions open questions, not yet time to close the debate. Anticancer Res 2020;40(1):501–9.
7 Suppa M et al. Who, why where: an overview of determinants of sunbed use in Europe. J Eur Acad Dermatol Venereol 2019;33(Suppl 2):6–12.
8 Arnold M et al. Cutaneous melanomas in France in 2015 attributable to solar ultraviolet radiation and the use of sunbeds. J Eur Acad Dermatol Venereol 2018;32(10):1681–6.
9 Miller C et al. Risk factors of subsequent primary melanomas in Austria. JAMA Dermatol 2019;155(2):188–95.
10 Chen H, Cohen P, Chen S. How big is a big odds ratio? Interpreting the magnitude of odds ratios in epidemiological studies. Commun Stat-simul C 2010;39(4):860–4.
11 Suppa M et al. Prevalence and determinants of sunbed use in thirty European countries: data from the Euromelanoma skin cancer prevention campaign. J Eur Acad Dermatol Venereol 2019;33(Suppl 2):13–27.
12 Rodriguez-Acevedo AJ et al. Indoor tanning prevalence after the international agency for research on cancer statement on carcinogenicity of artificial tanning devices: a systematic review and meta-analysis. Br J Dermatol 2019; 5 Aug [Epub ahead of print].
13 World Health Organisation. What are the risks from sunbed use? www.who.int/uv/faq/sunbeds/en/index4.html (accessed January 2020).
10th January 2020
This is according to a new study published in The Lancet by a team of Swedish and Danish researchers.
Previous research has shown that patients with ulcerative colitis have an increased risk of colorectal cancer. Screening recommendations are therefore in place for this patient group. But to what extent have new therapeutic methods helped to reduce this risk? This much-debated question has now found new answers. A large study involving 96,000 patients diagnosed with ulcerative colitis between the years 1969 and 2017 has now shown that these patients run a higher risk of developing and dying of colorectal cancer.
“The risk of colorectal cancer has dropped substantially over the past 30 years, but in spite of this patients who have had access to modern treatments for ulcerative colitis and screening for colorectal cancer still have a significantly elevated risk,” says Ola Olen, senior researcher at the Department of Medicine in Solna at Karolinska Institutet in Sweden.
Seen over the entire study period (1969 – 2017) the chances of a patient with ulcerative colitis being diagnosed with colorectal cancer were 66% higher than the control group, with the corresponding mortality rate 59% higher. For the latest five-year period only, however, these figures were, respectively, 38% and 25%.
This study differs from previous ones in that it factored in both the tumour stage when the cancer risk was assessed and the mortality rates, which the researchers included to ensure that the risks were not being over-estimated. The reason for examining mortality from colorectal cancer and not only incidence for this cancer is that regular endoscopic screening might detect relatively early forms of colorectal cancer that would otherwise go undetected.
“An important result of the study is that the risks are indeed elevated but there are major differences from one patient group to another,” says Olen.
At particularly high risk of developing colorectal cancer are the patients with extensive colitis, primary sclerosing cholangitis (a liver complication sometimes seen in ulcerative colitis), heredity for colorectal cancer susceptibility or childhood onset ulcerative colitis.
According to co-author and Professor Jonas F Ludvigsson, the study indicates a need to develop the care provided for these patients even further.
“Our study shows that screening and treatment of these patients can likely be further improved, since patients with ulcerative colitis are still more likely to die of colon cancer,” he says.
9th January 2020
Biological therapy with monoclonal antibodies (biologics) has revolutionised the treatment landscape of several therapeutic areas including gastroenterology, rheumatology, immunology and chemotherapy.
Biologics have also had a significant impact in the treatment of patients with skin disorders and in particular psoriasis, which affects up to 3% of the population in the UK.
Since 2017, a biologic, dupilumab, has been introduced for the treatment of patients with moderate to severe atopic eczema (AE), a long-term and pruritic, inflammatory skin disorder that affects up to 20% of children and roughly 3% of adults.
Prior to the introduction of dupilumab, treatment options for those with moderate to severe AE involved the use of systemic agents and while these are generally effective, all caused side-effects that limited their use.
Dupilumab has been approved by NICE for the management of patients with moderate to severe atopic eczema who failed to respond to at least one systemic therapy or if such treatments cannot be used because of either patient intolerance or contra-indications.
The drug blocks the interleukin (IL)-4 receptor subunit, which is the site of action for the cytokines IL-4 and IL-13, produced by T-helper 2 cells, both of which appear to have an important role in the initiation of the symptoms of atopic eczema.
The efficacy of dupilumab has sparked much interest in the potential of other biologics for the management of moderate to severe AE and both nemolizumab (Galderma) and lebrikizumab (Dermira) are showing great promise as additional therapies and fast approaching FDA approval.1
It has also clear that IL-4 and IL-13 signalling is an important inflammatory pathway in asthma and based on the results of several studies, dupilumab has recently been granted approval by the EMA as an add-on therapy for patients with severe asthma.2
But is it possible that blockage of the IL-4,13 pathway is important in other inflammatory dermatological conditions? A recent retrospective analysis observed that dupilumab produced improvements in hand dermatitis3 and alopecia areata.4
Additionally, a case report suggested that the drug may be of value in chronic urticaria,5 as witnessed by a patient whose condition was recalcitrant to treatment with omalizumab but successfully resolved with dupilumab.
The potential role for dupilumab in the management of skin problems other than atopic eczema was the subject of a recent systematic review.6 It identified several case studies where dupilumab had been successfully used off-license, to manage a wide range of skin problems including chronic pruritus, prurigo nodularis, allergic contact dermatitis and bullous pemphigoid.
The authors concluded that dupilumab appeared to be an effective treatment for these other conditions. It was also apparent from a review of the case studies, that dupilumab had been used as a last resort following the failure of multiple conventional treatments for the condition in question.
Furthermore, and somewhat interestingly, all of the case reports had used the dosing schedule of dupilumab that was approved for atopic eczema.
These case reports have provided the impetus for several Phase II trials examining the effectiveness of dupilumab in hand eczema, alopecia areata and chronic urticaria, all of which can be difficult to manage.
The favourable results from the diverse case studies make it increasingly apparent that the IL-4 and IL-13 inflammatory pathways are likely to predominate in a much wider range of skin conditions it is also clear that we still have some distance to travel on our journey of understanding with regard to the significance of IL-4 and IL-13 signalling.
Publication of the Phase II trials will serve to offer greater clarity into the importance of these pathways in a variety of inflammatory dermatoses. But perhaps most importantly, if the results of the trials can substantiate the observations in case studies, it will offer clinicians an effective therapy to manage a broader range of skin conditions and ultimately improve disease outcomes for a larger number of patients.
The results of an international, three-year, Phase III trial of a potential new drug that treats systemic lupus erythematosus (SLE) have been published in the New England Journal of Medicine.
Lupus is an autoimmune disease in which the immune system attacks healthy parts of the body. It is particularly insidious disease as it has a 10-year mortality of 10%, “which if you are diagnosed in your early twenties is a terrible outcome,” according to Professor Eric Morand of Monash University, Australia, who oversaw the global trial in over 360 people with SLE.
The trial, called TULIP 2, evaluated AstraZeneca’s anifrolumab and achieved a statistically-significant and clinically-meaningful reduction in disease activity versus placebo, with both arms receiving standard of care.
Professor Morand has also been key in developing new lupus assessment criteria.
According to Professor Morand, there has only been one new treatment approved for the disease in the last 60 years, which is not available on the Pharmaceutical Benefits Scheme in Australia.
Between 60% and 80% of adults with SLE show increased interferon-induced genes, which reflect overproduction of the immune protein Type 1 interferon. While previous attempts to block this protein in lupus have failed, the potential new treatment, anifrolumab, works by blocking the receptor on all cells in the body, aiming to reverse the triggering of lupus symptoms.
Professor Morand said that interferon is associated with other autoimmune diseases such as Scleroderma and Sjögren‘s disease “so there may be potential for using anifrolumab in the treatment of other interferon related diseases as well.”
In the TULIP 2 trial, eligible patients received a fixed-dose intravenous infusion of anifrolumab or placebo every four weeks. TULIP 2 assessed the effect of anifrolumab in reducing disease activity – noting a significant effect in global disease activity measures.
The trial, from 2015 to 2018, involved 362 patients receiving either 300mg of the drug or placebo intravenously once every four weeks for 48 weeks. Benefit was measured using a defined clinical assessment of improvement in all organs as well as the number of flare ups (which see the patient experiencing fever, painful or swollen joints, fatigue, rashes or sores or ulcers in the mouth or nose). The volunteers were aged between 18 and 70 and had moderate to severe disease despite standard treatments. Patients with SLE typically die of organ failure.
The study found that 52 weeks after the trial started, significantly more patients on the drug than the placebo had:
The TULIP 2 trial followed on from the TULIP 1 trial which failed to meet its primary outcome. The second trial, published in the New England Journal of Medicine, used a different endpoint.
“Measurement of treatment response in SLE has been very problematic and this represents a kind of second breakthrough of this trial,” Professor Morand said.
The study was done in collaboration with colleagues in Japan, the UK, the US, France and South Korea.
7th January 2020
The results from the longitudinal study, believed to be the first to characterise growth patterns from early childhood to adolescence in children with persistent food allergies, was published online in The Journal of Allergy and Clinical Immunology.
“Published data about growth trajectories for kids with ongoing food allergies is scarce,” says Karen A. Robbins, MD, lead study author and an allergist in the Division of Allergy and Immunology at Children’s National Hospital when the study was conducted. “It remains unclear how these growth trends ultimately influence how tall these children will become and how much they’ll weigh as adults. However, our findings align with recent research that suggests young adults with persistent cow’s milk allergy may not reach their full growth potential,” Dr. Robbins says.
The multi-institutional research team reviewed the charts of paediatric patients diagnosed with persistent immunoglobulin E-mediated allergy to cow’s milk, peanuts or tree nuts based on their clinical symptoms, food-specific immunoglobulin levels, skin prick tests and food challenges. To be included in the study, the children had to have at least one clinical visit during three defined time frames from the time they were age 2 to age 12. During those visits, their height and weight had to be measured with complete data from their visit available to the research team. The children allergic to cow’s milk had to eliminate it completely from their diets, even extensively heated milk.
From November 1994 to March 2015, 191 children were enrolled in the study, 111 with cow’s milk allergies and 80 with nut allergies. All told, they had 1186 clinical visits between the ages of 2 to 12. Sixty-one per cent of children with cow’s milk allergies were boys, while 51.3% of children with peanut/tree nut allergies were boys.
In addition to children allergic to cow’s milk being shorter, the height discrepancy was more pronounced by ages 5 to 8 and ages 9 to 12. And, for the 53 teenagers who had clinical data gathered after age 13, differences in their weight and height were even more notable.
“As these children often have multiple food allergies and other conditions, such as asthma, there are likely factors besides simply avoiding cow’s milk that may contribute to these findings. These children also tend to restrict foods beyond cow’s milk,” she adds.
12th December 2019
Their study, which was done in collaboration with Professor Suresh Awale from the University of Toyama, Japan, shows that all three molecules kill pancreatic cancer cells in a petri dish. Two of these killed the cells more effectively than the original Grandifloracin molecule.
Whilst this research is more than five years away from trialling new drugs in humans, the researchers say these molecules could become a promising new class of drugs for treating pancreatic cancer.
The research is published in the journal ChemMedChem.
Dr Simon Lewis, Senior Lecturer in Chemistry from the University of Bath, said: “Pancreatic cancers are especially aggressive and fast-growing, so the tumours develop faster than the blood vessels can supply nutrients to them.
“This leads to a lack of nutrients, to an extent that would kill ordinary cells, but the pancreatic cancer cells can survive these ‘austere’ conditions and keep on growing.
“The molecules we have identified are so-called ‘anti-austerity’ agents that can remove the ability of the cancer cells to tolerate these starvation conditions, so they will die, whereas ordinary cells with a normal supply of nutrients remain unaffected.”
Dr Lorenzo Caggiano, Senior Lecturer in the Medicinal Chemistry group at the University’s Department of Pharmacy & Pharmacology, said: “Through evolution, nature has developed a huge variety of active compounds to help it survive and thrive under a wide range of environmental conditions.
“These so-called natural products are of great interest in the development of new drugs and as such approximately a quarter of all medicines are derived from plants.
“As part of our ongoing research into the development of new treatments for brain cancers based on compounds found in daffodils, the research published in collaboration with Dr Lewis describes a compound also found in flowering plants that is able to selectively kill pancreatic cancer cells in a new way.
“This exciting approach could potentially lead to a new drug to treat pancreatic cancers that is more effective yet less toxic than current treatments.”
Now Yale scientists have essentially flipped this script and found that when impaired a molecularly similar regulator can cause the damaging immune system attacks on skin and organs that are the hallmark of the autoimmune disease lupus, as reported in Science Translational Medicine.
The study results help explain the origins of lupus and suggest novel ways researchers might be able to restore function of this inhibitor and provide much needed new therapy to treat the disease, the scientists said.
Yale researchers found that mice lacking an immune system inhibitor called programmed death-1 homolog, or PD-1H, spontaneously developed symptoms that resemble two forms of lupus — systemic, in which the immune system attacks multiple organs; and cutaneous, which is marked by pronounced skin deformities.
“This molecule is clearly involved in inhibiting lupus, but it seems to be selective because it does not have the same effect in several other autoimmune diseases,” said senior author Lieping Chen, the United Technologies Corporation Professor in Cancer Research, and professor of immunobiology, dermatology, and medicine.
PD-1H is molecularly similar to the more commonly known PD-1 molecule, which also helps suppress immune system response. Chen was a pioneer in identifying and developing inhibitors to PD-1, which freed T cells to attack several forms of cancer. Several labs have also tried to use PD-1H as a cancer treatment but so far have been unsuccessful.
Chen said his findings suggest that in people with lupus the function of PD-1H is critical. When it is impaired, they are vulnerable to the immune system attacks on skin and multiple organs that are the hallmark of the disease.
Lupus patients currently have very limited options for treatment, but the new findings suggest a novel approach called protein fusion might mimic PD-1H and help control the immune system and combat the disease, Chen said.
5th December 2019
The study is the first to show the drug, tofacitinib (Xeljanz) has a direct effect on cells lining the gut by correcting defects that occur in inflammation. Until now, the effects of tofacitinib on intestinal epithelial cell functions were largely unknown.
“Our work increases our understanding of how this drug is useful for treating ulcerative colitis,” said Declan McCole, a professor of biomedical sciences in the UCR School of Medicine, and the lead author of the study that appears in the journal Inflammatory Bowel Diseases. “We now better understand where in the gut the drug is working, and how.”
McCole explained that increased intestinal permeability — or leakiness — is a feature of ulcerative colitis and plays a critical role in promoting inflammation. His team tested tofacitinib in human intestinal epithelial cell lines, as well as in organoids, or colonoids, that were derived from primary human colonic stem cells isolated from human subjects — primarily patients undergoing elective colonoscopy for colon cancer screening — and found tofacitinib repaired inflammation-induced permeability defects in both.
The epithelium is a thin layer that lines the alimentary canal. The gastrointestinal epithelium is comprised of cells that have gaps between them, making them selectively permeable and providing a barrier that keeps out pathogens, toxins, and antigens from entering the gut, while allowing the absorption of nutrients. In ulcerative colitis, this epithelial permeability becomes leaky, allowing bacterial products to cross into the gut and nutrients and water to leak out. This, in turn, triggers immune responses, resulting in fluid loss and diarrhea.
“We found tofacitinib fixes the leakiness in the intestinal barrier,” McCole said. “Specifically, it fixes intestinal epithelial permeability defects caused by ‘interferon-gamma,’ an inflammatory cytokine involved in autoimmune diseases such as ulcerative colitis and rheumatoid arthritis.”
“By targeting specific molecules, the drug inhibits a pathway that is activated by inflammation,” said Anica Sayoc-Becerra, a graduate student in the Biomedical Sciences Graduate Program, a member of McCole’s lab, and the first author of the research paper. “Our study shows tofacitinib is not just acting on immune cells, as was first thought, but can have a direct effect on the epithelial cells that are the key factor in maintaining gut barrier function.”
In the first study of its kind, researchers analysed almost 2700 IBD patients in a Paris referral centre to understand the respective roles of IBD activity and drugs in promoting systemic serious viral infection (SVI). The study identified clinically active IBD and thiopurines (a class of immunomodulators used to treat an estimated 60% of IBD patients2) as the main drivers of infection. Despite the highest risk of infection being seen in young patients between the ages of 18 and 35, a three-fold increased incidence of severe viral infections was observed in IBD patients of all ages.
The study also uncovered a concerning link between thiopurine use and a number of harmful infections. Whilst IBD patients receiving no treatment were at a similar risk level to the general population, patients treated with immunomodulators were found to be six times more likely to develop an SVI. The most common SVIs developed by IBD patients were identified as Epstein-Barr virus (EBV), which is associated with a range of diseases such as glandular fever and Hodgkin’s Lymphoma, and cytomegalovirus (CMV), an infection which can pose a risk to unborn babies.
A correlation was also found between thiopurine use and EBV-induced hemophagocytic lymphohistiocytosis (HLH), an aggressive disease associated with high mortality rates.3 With a third of patients estimated to be stopping thiopurine use due to adverse side effects, these new findings underline the need to find novel therapeutic approaches to tackle IBD.2
Lead researcher Professor Laurent Beaugerie, from the Department of Gastroenterology at Saint-Antoine Hospital, commented, “Clinicians need to be aware of the substantially increased risk of SVI in patients with IBD, which had previously remained unclear. Young IBD patients are the most vulnerable to the development of SVIs, as they are less likely to have been exposed to viruses such as EBV or CMV before. They will therefore mount a less effective immune response. Their risk is further elevated by the inhibiting effect of the immunosuppressive drugs they are treated with.”
The number of individual IBD cases, which encompasses both Crohn’s disease and ulcerative colitis, has shown a marked increase since 1990, rising from 3.6 million cases globally to over 6.8 million in 2017.4 Commenting on the increasingly heavy burden of IBD, Professor Beaugerie added, “The relation between IBD drugs and SVIs is especially concerning, as presently, hospitalisation due to the serious complications that accompany the disease is the main cost associated with the management of IBD. The growing prevalence of IBD across the globe will only add further to the pressure placed on healthcare structures.”
New treatment pathways such as nutritional therapies in Crohn’s disease and faecal microbiota transplantations (FMT), which are not evidenced to be associated with an increased risk of SVI, could potentially alleviate the strain placed on healthcare systems. Therapies such as these could transform the course of treatment and confer significant benefits to patients.
The study, which has cast new light on the strong association between IBD drugs and SVI, emphasises the need for further research and funding into the area to improve patient outcomes. An investigation into promising new treatments should become the next course of action if the risk of SVI in IBD patients is to be brought closer that of the general population.
References
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