Category: Respiratory Diseases

Bronchodilators Don’t Ease Smoking-related Respiratory Symptoms in non-COPD Patients

Anatomical model of lungs
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A study published in the New England Journal of Medicine have found that dual bronchodilators do little to help people who do not have chronic obstructive pulmonary disease (COPD), but who do have respiratory symptoms and a history of smoking.

Millions of people who smoke or used to smoke and have some symptoms of COPD have been prescribed bronchodilators.

“We’ve assumed these medications worked in patients who don’t meet lung function criteria for COPD, but we never checked,” said MeiLan K. Han, MD, a principal investigator and first author of the study. “We now know these existing medications don’t work for these patients.”

According to scientists, the implications are significant. First, they show the importance of diagnosing lung conditions through spirometry, a lung function test Dr Han noted is underutilised in clinical practice. Second, they show the need for new, effective therapies for patients without COPD.

Inhalers have long been the primary go-to treatment for these patients, she explained, because doctors either assume a patient has COPD, or else that their smoking-related symptoms could be helped by the inhalers. But while tobacco smoking causes a large spectrum of lung damage, the study showed bronchodilator therapy only helps patients with enough lung damage that would result in abnormal spirometry readings.

In the 12-week, randomised, double-blinded study, which was part of the Redefining Therapy in Early COPD for the Pulmonary Trials Cooperative (RETHINC), researchers enrolled 535 adults with symptoms of COPD, ages 40–80. Participants used an inhaler twice daily that contained either medication or a placebo.

By the end of the trial, some adults in the medication and placebo groups saw slight respiratory improvements, eg coughed less, produced less phlegm, or felt less winded, which was assessed through the St. George’s Respiratory Questionnaire. However, the researchers found no significant differences between those receiving medication or placebo. They reported 56% (128 of 227) of participants who received the medication saw respiratory symptom improvements, compared to 59% (144 of 244) of those who took the placebo.

According to Dr Han, these data underscore the need to change the standard practice, which is not doing spirometry and just treating patients with the same COPD medications and expecting to see improvement.

Antonello Punturieri, MD, PhD, program director of NHLBI’s Chronic Obstructive Pulmonary Disease/Environment Program, said spirometry testing should be used for any patient who shows signs of COPD, airflow obstruction, or who has a history of cigarette smoking. Though spirometry readings are used during about one-third of medical visits related to COPD, roughly half of patients who would meet criteria for COPD go undiagnosed.

Promoting smoking cessation a primary way to prevent COPD or COPD-like symptoms, the study noted. About one in four current or former smokers without COPD have reported having shortness of breath. In addition to encouraging smoking cessation, doctors can help patients who do not meet lung-function criteria of COPD by working with them to address any other underlying issues, such as overweight and obesity, heart failure, or other lung issues.

“In the meantime, research should be focused on finding new treatments for them,” Dr Han explained. “The next question is, can we develop more targeted therapies for these patients who are on the milder end of the spectrum?”

“Because cough and mucus production show up prominently among these patients, we believe therapies that target mucus production in the airways may be effective,” said Prescott G. Woodruff, MD, a principal investigator and senior author of the study.

Some of these therapies are already in development, and data from other studies may offer insight into the biological causes of excessive airway mucus, which could help point to additional therapies.

Source: NIH/National Heart, Lung and Blood Institute

Hospital Readmissions for Children with Asthma on The Increase

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Hospital readmissions for asthma are increasing among children, likely stemming from COVID lockdowns reducing immunity to common respiratory viruses. These are the findings of a new study published in the Journal of Asthma. The finding highlights the gaps in health care for this most common of chronic paediatric illnesses.

The Australian study, led by the Murdoch Children’s Research Institute, found about one in three children, mostly pre-schoolers, are readmitted to hospital for asthma compared to one in five a decade ago.

Most asthma hospital presentations were preventable, Murdoch Children’s Dr Katherine Chen said, which emphasises the need for a holistic evaluation of each child’s asthma management to prevent future readmissions.

The study involved 767 children, aged three to 18 years, who were admitted to three hospitals in Victoria state between 2017-2018 with a diagnosis of asthma. It found that 34.3% were readmitted to hospital for asthma, with those aged three to five years accounting for 69.2%. Of the 767 participants, 20.6% were readmitted once, and 13.7% had two or more readmissions in 12 months. 

“Our study highlighted gaps in the children’s asthma care,” Dr Chen said. Over a third of children hadn’t had a review of their inhaler technique, and only about a quarter were prescribed a preventer or asked to continue using it.

“Almost three quarters were discharged without a preventer medication, and over 80 per cent did not have a follow-up clinic booked at the hospital, often reserved for children with difficult-to-control asthma. Most families, therefore, need to navigate their child’s asthma follow-up with their GP.”

Recently, said Dr Chen, asthma admissions had spiked due to the rise in respiratory infections and children lacking immunity to common viruses as a result of COVID lockdowns.

Professor Harriet Hiscock at MCRI said that the findings confirmed the important role of GPs in paediatric asthma management and how targeted interventions at each hospital could reduce readmissions.

“Less than 10 per cent were readmitted within 30 days suggesting the importance of ongoing community care and longer-term asthma control,” she said. The need to regularly review overall asthma management, minimise risk factors, arrange follow-up, and support optimum care in the community are key.

“Interactive digital symptom monitoring with specialist nurse support, home-based education and a culturally tailored education program could also help.”

Prof Hiscock said linked datasets were important to objectively measure the burden of asthma cases on health services.

“Our current dataset cannot verify whether the follow-up appointment was attended, whether caregivers had arranged follow-up post-discharge and if the medications were used as prescribed,” she said. “Integrating datasets such as health services and medication use into clinical care will improve the clinician’s understanding of the child’s asthma control and medication adherence and would assist in providing targeted treatments.”

Asthma is the most common chronic paediatric illness in industrialised countries, affecting 8–10% of children.

Source: Murdoch Children’s Research Institute

Urine Metabolites Yield Clues on Severe Asthma

Asthma inhaler
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A study published in the European Respiratory Journal found severe asthmatics have a distinct metabolite profile detectable in their urine, compared to healthy individuals and those with milder asthma.

Researchers analysed urine samples from more than 600 participants as part of the U-BIOPRED study, a Europe-wide initiative to identify and better understand different sub-types of severe asthma.

The research team discovered a specific type of metabolite, called carnitines, decreased in severe asthmatics. Carnitines play an important role in cellular energy generation and immune responses. Further analyses found carnitine metabolism was lower in severe asthmatics.

These new findings will help enable researchers work towards new, more effective therapies for asthmatics.

Study leader Dr Stacey Reinke said it is vital that asthma treatment is improved.

“To identify and develop new treatment options, we first need to better understand the underlying mechanisms of the disease,” she said.

Examining the body’s chemical profile, or ‘metabolome’, provides a snapshot of a person’s current physiological state and gives useful insight into disease processes.

“In this case, we were able to use the urinary metabolome of asthmatics to identify fundamental differences in energy metabolism that may represent a target for new interventions in asthma control,” Dr Reinke said.

Dr Reinke said it can be difficult and invasive to investigate the lungs directly – but fortunately they contain a lot of blood vessels.

“Therefore, any biochemical changes in the lungs can enter the blood stream, and then be excreted through the urine,” she said.

“These are preliminary results, but we will continue to investigate carnitine metabolism to evaluate its potential as a new asthma treatment target.”

‘Urinary metabotype of severe asthma evidences decreased carnitine metabolism independent of oral corticosteroid treatment in the U-BIOPRED study’ was published in the .

Source: Edith Cowan University

Mucus Hydration Approach Could Help Treat Cystic Fibrosis

Anatomical model of lungs
Photo by Robina Weermeijer on Unsplash

Using a model reproducing a respiratory epithelium, researchers have discovered that a simple film of liquid is sufficient to restore the airways’ seal and reduce the risk of bacterial infection. Their findings, published in the journal Cells, may enable new therapies based on mucus hydration – a promising alternative to current therapies which often lack efficacy.

Despite recent therapeutic advances, people with cystic fibrosis (one in every 2500 births in Europe) have a life expectancy of no more than 46 years and altered quality of life. The disease is caused by one or more mutations in the CFTR gene, which affects the proper functioning of an essential protective barrier. The epithelial cells that line the airways are usually sealed together and thus protect the airways from bacterial colonisation. They are also lined with a fluid, a slippery mucus that traps unwanted germs and carries them away. When the CFTR protein is altered, the junctions between the cells loosen and the dehydrated mucus tends to stagnate, both of which promote the development of respiratory infections.

“While it was already known that mucus hydration and the presence of sufficiently tight junctions preserved the integrity of the airways, the mechanisms involved and the links between these two mechanisms remained mysterious, which hindered the development of new therapies,” explained Professor Marc Chanson, who led the reasearch.

Hydrating to restore tightness

The scientists first developed an in vitro model using human lung cells. This model reproduces airways epithelium of healthy and cystic fibrosis patients in a way that is both accurate and close to clinical reality. The researchers compared the response of epithelial cells invalidated for CFTR to bacterial infection, to which either hydrated, healthy mucus or physiological saline solution had been added.

“We observed a similar response in both cases: the presence of liquid, whatever its composition, restored the airways and protected them from infection,” explained Juliette Simonin, post-doctoral fellow in Prof Chanson’s laboratory and first author of the study. “Surface hydration is sufficient to tighten the junctions between cells and protects the epithelium integrity from bacterial colonisation, even when CFTR is not functioning.”

One treatment for all mutations?

A triple therapy pharmacologically targeting the CFTR protein has recently become available on the market. However, it only targets certain mutations of the CFTR gene and is only prescribed for a specific population of people with cystic fibrosis. More widely effective and safe treatments are still sorely lacking.

“Our results provide evidence that rehydration of the airway surface is beneficial. The challenge now is to find a simple way of doing this in all people with the disease, whatever the mutation involved,” concluded Prof Chanson.

Source: Université de Genève

Two-drug Combination Inhaler Looks Good for Asthma ‘Rescue’ Therapy

Asthma inhaler
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An analysis published in the NEJM testing a two-drug combination inhaler shows promising results for helping asthma patients get their condition back under control when standard medication isn’t working for them. The phase III trial found that users of the product PT027, (90μg albuterol combined with 80μg budesonide), were 26% less likely to experience severe exacerbations than those using albuterol alone.

A version with a lower steroid dose (40 μg) also appeared to reduce severe exacerbation risk, but the 16% advantage over conventional albuterol-only treatment narrowly missed by statistically significant with a P value of 0.052.

The study authors explain that the approach is based on the notion that short-acting beta agonist (SABA) drugs, eg albuterol, are quite effective in reducing acute symptoms, but do not address the underlying inflammation causing the symptoms. The product’s developers reasoned that addition of a steroid should help prevent symptoms recurrence.

In the MANDALA trial, 3132 patients were randomised to one of three regimens: two actuations each of the 90/80 μg or 90/40 μg versions, or two actuations of 90 μg albuterol. Patients were all instructed to use the device when they experienced acute symptoms, and remained on their normal maintenance treatment, which consisted of long-acting beta agonists and inhaled corticosteroids, either individually or in combination and in a variety of doses.

Severe exacerbation was the primary endpoint, defined as any of the following:

  • Inpatient admission for asthma symptoms
  • Emergency department or urgent care visit
  • A minimum og three days of systemic steroid therapy for worsening symptoms

The researchers also tracked a variety of secondary outcomes, such as time to first exacerbation, and safety parameters.

Annualised severe exacerbation rates were 0.43 for the high-dose product versus 0.58 for albuterol alone, for a rate ratio of 0.75. As the low-dose group included all of the child participants, it was compared to a slightly different set of albuterol-only controls, giving annualised exacerbation rates in that comparison of 0.48 and 0.60, respectively. That rate ratio of 0.81 was significant.

Systemic steroids was another secondary outcome, with the combination inhaler proving superior again, with averages of 83.6 mg (prednisone equivalent) for the high-dose version, 94.7mg with the lower dose, and 130.0/127.6 mg for the respective albuterol-only control groups. Adverse effects were similar in either arm (46–47%).

Source: MedPage Today

WHO Announces Guidance Updates to Treatment of Drug-resistant TB

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The World Health Organization (WHO) Global Tuberculosis Programme has announced upcoming updates to the guidance on the treatment of drug-resistant tuberculosis (DR-TB). These updates are announced in a Rapid Communication and include shorter novel 6-month all-oral regimens for the treatment of multidrug- and rifampicin-resistant TB (MDR/RR-TB), with or without additional resistance to fluoroquinolones (pre-XDR-TB), and also an alternative 9-month all-oral regimen for the treatment of MDR/RR-TB.

The Rapid Communication is released ahead of updated WHO consolidated guidelines to come later in the year which will inform national programmes and stakeholders.

Dr Tereza Kasaeva, Director of WHO’s Global TB Programme said: “We now have more and much better treatment options for people with drug-resistant TB thanks to research generating new evidence. This is major progress compared to what was available even a few years ago, and will be of great benefit for people struggling with TB and drug-resistant TB, resulting in better outcomes, saving lives and reducing suffering.”

All patients with MDR/RR-TB, including those with additional resistance to fluoroquinolones, stand to benefit from effective all-oral treatment regimens, either shorter or longer, implemented under programmatic conditions.

The summary of the updates are as follows:

The 6-month BPaLM regimen, comprising bedaquiline, pretomanid, linezolid (600 mg) and moxifloxacin, may be used programmatically in place of 9-month or longer (>18 months) regimens, in patients (aged ≥ 15 years) with MDR/RR-TB who have not had previous exposure to bedaquiline, pretomanid and linezolid (defined as > 1 month exposure). This regimen may be used without moxifloxacin (BPaL) in the case of documented resistance to fluoroquinolones (in patients with pre-XDR-TB). Drug susceptibility testing (DST) to fluoroquinolones is strongly encouraged, but DST should not delay treatment initiation.

The 9-month, all-oral, bedaquiline-containing regimens are preferred over the longer (>18 months) regimen in adults and children with MDR/RR-TB, without previous exposure to second-line treatment (including bedaquiline), without fluoroquinolone resistance and with no extensive pulmonary TB disease or severe extrapulmonary TB. In these regimens, 2 months of linezolid (600 mg) can be used as an alternative to 4 months of ethionamide. Access to rapid DST for ruling out fluoroquinolone resistance is required before starting a patient on one of these regimens.

Patients with extensive forms of DR-TB (eg XDR-TB4) or those who are not eligible for or have failed shorter treatment regimens will benefit from an individualised longer regimen designed using the priority grouping of medicines recommended in current WHO guidelines.6

Decisions on appropriate regimens should be made according to clinical judgement and patient preference, considering results of DST, patient treatment history, risk of adverse events, and severity and site of the disease.

All treatment should be delivered under WHO-recommended standards, including patient-centred care and support, informed consent where necessary, principles of good clinical practice, active drug safety monitoring and management, and regular monitoring of patients and of drug resistance to assess regimen effectiveness.

The full details of the regimens included in the review are available in the Rapid Communication.

Source: World Health Organization

Why People with Asthma are Less Vulnerable to COVID

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Researchers have revealed biological reasons for how disease progression happens and why a certain population of asthma patients are less susceptible to severe COVID.

This research, published in PNAS, shows the importance of the well-known cytokine interleukin-13 (IL-13) in protecting cells against SARS-CoV-2, something which helps explain why people with allergic asthma fare better than the general population despite having a chronic lung condition. However, the same cannot be said for individuals with other diseases, such as chronic obstructive pulmonary disease (COPD) or emphysema, who are at very high risk of severe COVID.

“We knew there had to be a bio-mechanistic reason why people with allergic asthma seemed more protected from severe disease,” said Assistant Professor Camille Ehre, PhD, senior author of the paper. “Our research team discovered a number of significant cellular changes, particularly due to IL-13, leading us to conclude that IL-13 plays a unique role in defence against SARS-CoV-2 infection in certain patient populations.”

Although cytokines like IL-13 cannot be used as therapies because they trigger inflammation, it is important to understand natural molecular pathways that cells use to protect themselves from pathogen invasion, as these studies have the potential to reveal new therapeutic targets.

Many health factors increase a person’s risk of severe COVID, but during the pandemic, epidemiologists found that people with allergic asthma were less susceptible to severe disease.

“These are patients with asthma caused by allergens, such as mould, pollen, and dander,” said A/Prof Ehre. “To find out why they are less susceptible, we investigated specific cellular mechanisms in primary human airway epithelial cell cultures.”

Genetic analysis human airway cell cultures infected with SARS-CoV-2 revealed that the expression of ACE2 governed which cell types were infected and their viral load.

Electron microscopy (EM) identified an intense exodus of virus from infected ciliated cells, which move mucus along the airway surface. EM also revealed severe cytopathogenesis – changes inside human cells due to viral infection. And these changes culminating in ciliated cells (packed with virions) shedding away from the airway surface.

“This shedding is what provides a large viral reservoir for spread and transmission of SARS-CoV-2,” A/Prof Ehre said. “It also seems to increase the potential for infected cells to relocate to deeper lung tissue.”

Further experiments on infected airway cells revealed that a major mucus protein called MUC5AC was depleted inside cells, likely because the proteins were secreted to try to trap invading viruses. But the virus load kept increasing because the cells tasked with producing MUC5AC were overwhelmed in the face of a rampant viral infection.

The researchers knew from epidemiological studies that allergic asthma patients—known to overproduce MUC5AC—were less susceptible to severe COVID. A/Prof Ehre and colleagues also knew the cytokine IL-13 increased MUC5AC secretion in the lungs when asthma patients faced an allergen.

The scientists decided to mimic asthmatic airways by treating human airway cells with IL-13. They then measured viral titres, viral mRNA, the rate of infected cell shedding, and the overall number of infected cells. Each one was significantly decreased. They found this remained true even when mucus was removed from the cultures, suggesting other factors were involved in the protective effects of IL-13 against SARS-CoV-2.

Bulk RNA-sequencing analyses revealed that IL-13 upregulated genes that control glycoprotein synthesis, ion transport, and antiviral processes – all of which are important in airway immune defence. They also showed that IL-13 reduced the expression of the viral receptor, ACE2, as well as reducing the amount of virus inside cells and cell-to-cell viral transmission.

Taken together, these findings indicate that IL-13 significantly affected viral entry into cells, replication inside cells, and spread of virus, thus limiting the virus’s ability to find its way deeper into the airways to trigger severe disease.

“We think this research further shows how important it is to treat SARS-CoV-2 infection as early as possible,” A/Prof Ehre said. “And it shows just how important specific mechanisms involving ACE2 and IL-13 are, as we try our best to protect patients from developing severe infections.”

Source: University of North Carolina Health Care

Mepolizumab Weans Severe Asthma Patients off Steroids

Asthma inhaler
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In a real world study, patients taking oral corticosteroids for severe asthma, taking mepolizumab reduced the need for those steroids by 75%. These findings were presented at the annual meeting of the American Academy of Allergy, Asthma & Immunology.

By the end study, patients on a median 10 mg maintenance dose of oral corticosteroids at baseline reduced their intake to 2.5 mg, reported Mark Liu, MD, of Johns Hopkins Medicine, who presented the findings.

And those on a median 5 mg maintenance dose at the start of the trial reduced their use to 0.4 mg by study end, Dr Liu said.

In the high steroid dose group, 36% were able to be weaned off the drugs by the end of the study, he reported. In the lower dose group, 49% were able to discontinue steroid use.

Treatment with the interleukin-5 (IL-5) antagonist mepolizumab reduced clinically significant annual exacerbations from a mean of 4.3 in the 12 months prior to the trial to 1.5 with mepolizumab use. This reduction from baseline was seen across all patient groups, said Dr Liu, including those with high and low steroid use and those who were not taking steroids at baseline to control symptoms.

Dr Liu suggested that despite the limitation of being a single-arm study, the “clinically important real-world findings indicate that patients with severe asthma treated with mepolizumab can reduce their oral corticosteroid use, potentially reducing the risk of side effects associated with their use, while improving their asthma control.”

The co-moderator of the presentation session, William Anderson, MD, of Children’s Hospital Colorado, said the study was important – “especially for our adult patients who are on chronic steroids, because the side effects of chronic steroids are so profound and oftentimes can lead to equal if not worse effects than the underlying asthma itself.”

“The ability to use a biologic agent to decrease the dose of an oral steroid for our patients is certainly extraordinarily promising,” Dr Anderson said to MedPage Today. “Our ultimate goal is to get patients off oral steroids.”

For the year-long study, Dr Liu and colleagues enrolled 822 adults with asthma and a new prescription for mepolizumab with at least 12 months of previous medical records. Mepolizumab was given at the standard 100mg subcutaneous dose.

“Patients with severe asthma often rely on oral corticosteroids to control their symptoms despite a well-recognized risk of complications even at low daily doses,” Dr Liu explained. The goal of the study, he said, was to determine what happened in a real-world setting when these patients were treated with mepolizumab, stratified by steroid use. The researchers enrolled patients from December 2016 through October 2019.

About 10% of patients experienced adverse events, but serious adverse events occurred in less than 1%, Dr Liu noted.

Source: MedPage Today

Year Round Asthma Relief With Tezepelumab

asthma inhaler
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The biologic tezepelumab provided year-round relief for patients with severe, uncontrolled asthma, according to findings from the year-long phase III NAVIGATOR study.

Tezepelumab was shown to significantly reduce the annualised asthma exacerbation rate by 56% in the overall study population, and by 41% in those with baseline blood eosinophil counts below 300 cells/µL, according to Andrew Lindsley, MD, PhD, medical director at Amgen in Thousand Oaks, California, presenting at the American Academy of Allergy, Asthma & Immunology (AAAAI) annual meeting.

When stratified by season, the annualised asthma exacerbation rate was consistently reduced with tezepelumab:

  • Winter: 2.62 with placebo versus 0.96 with tezepelumab (63% reduction)
  • Spring: 1.71 versus 0.92 (46% reduction)
  • Summer: 1.93 versus 0.73 (62% reduction)
  • Autumn: 2.28 versus 1.05 (54% reduction)

Tezepelumab, recently approved for severe asthma by the FDA in 2021, inhibits thymic stromal lymphopoietin. It is a key component of airway inflammation and is thought to be released in response to airborne asthma triggers, such as pollen and viruses. Tezepelumab has been shown to reduce exacerbations when compared with placebo.

Dupilumab was shown to have similar results in the 52-week QUEST study, which established the effectiveness of dupilumab as an add-on treatment for asthma. This was also true of the 96-week TRAVERSE open-label extension trial, in which researchers found that asthma exacerbations were reduced to below 7% all year long, and staying mostly under 5%.

The seasonal studies were performed during NAVIGATOR because asthma exacerbation has a number of environmental, seasonal factors.

“We know that allergies are seasonal, but depend on the trigger for asthma – early spring is the tree pollen season, late spring is grass pollen, in the fall it is ragweed” Roxana Siles, MD, co-director of the asthma centre at the Cleveland Clinic, told MedPage Today. Dust mites and animal dander are year-round, but may affect people more in the winter when they spend more time indoors, she added.

There was a question of how biologics were affected by the seasons, she said, and as it turned out, they work on all types of asthma, year round.

Tezepelumab decreased the proportion of patients with at least one exacerbation during all seasons, from 33.4% to 18.3% in winter, 23.7% to 15.7% in spring, 26.9% to 13.2% in summer, and 33.4% to 20.6% in autumn.

Additionally, the average number of days with an exacerbation per patient in each season fell between:

  • 4.9 to 1.9 days in winter
  • 3.6 to 1.7 days in spring
  • 3.6 to 1.5 days in summer
  • 4.3 to 2.1 days in autumn

Source: MedPage Today

Nintedanib Slows Autoimmune-related Lung Disease

Anatomical model of lungs
Photo by Robina Weermeijer on Unsplash

Findings from a new clinical trial published in Arthritis & Rheumatology reveal that nintedanib,  an intracellular inhibitor of tyrosine kinases, may help patients with fibrosing from autoimmune disease-related interstitial lung diseases (ILDs).

ILDs are a common manifestation of systemic autoimmune diseases such as rheumatoid arthritis. Connective tissue diseases and vasculitides affect all areas of the lungs (bronchioles, parenchyma, alveoles) which is why ILD is a common feature of rheumatology diseases.

The trial enrolled 170 subjects with a fibrosing ILD other than idiopathic pulmonary fibrosis, with diffuse fibrosing lung disease of > 10% extent on high-resolution CT imagery, forced vital capacity (FVC) ≥ 45% predicted and diffusing capacity of the lungs for carbon monoxide ≥ 30% –< 80% predicted. FVC is a predictor of mortality in patients with autoimmune disease-associated ILDs.

Patients were randomised to receive nintedanib or placebo. Investigators assessed patients’ forced vital capacity (FVC). The trial found that the rate of decline in FVC over one year was -75.9 mL/year with nintedanib versus -178.6 mL/year with placebo.

“Until now, therapies that can significantly reduce the rate of decline in lung function in connective tissue disease–related ILDs characterised by progressive fibrosis have been lacking. We now have a therapeutic approach that offers a strategy for reducing the morbidity associated with these diseases,” said lead author Eric L. Matteson, MD, MPH, of the Mayo Clinic College of Medicine and Science.

Source: Wiley