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BARNEY CALMAN: Cystic fibrosis sufferers get drug after endless talks

BARNEY CALMAN: After cystic fibrosis sufferers finally get a ‘wonder drug’ after endless talks, it’s time to ask – did it really have to be this difficult?

Dare we dream? Amid the flurry of tweets in response to our articles over the past fortnight that predicted the Government would soon strike a deal for a lifesaving cystic fibrosis drug, this simple sentence stood out. 

It summed up the hopes – and fears – of thousands of British families blighted by this horrible illness, which kills many sufferers before they reach their 40s. 

Last Tuesday, the drug, Kaftrio, was approved – and the dream finally became a reality, just as we had said it would. It was a watershed moment, and an end to many months of uncertainty. And the relief last week among both campaigners and those involved in the negotiations was palpable. 

The deal is, we can reveal, the biggest of its kind in NHS history – potentially amounting to £1billion over the next four years. 

But thousands of patients can now plan a future – one that’s not defined by pain, infections, hospital visits and gradually failing lungs. For those who are severely ill, the drug isn’t simply a lifeline, but a chance to live normally again. 

Over the past six months, in the run-up to last week’s announcement, the MoS has published a series of reports, lifting the lid on the secretive negotiations between NHS England and drug company Vertex on access to cystic fibrosis drugs. 

BARNEY CALMAN: The deal is, we can reveal, the biggest of its kind in NHS history – potentially amounting to £1billion over the next four years 

What was discussed during these talks is ‘commercially sensitive’, hence their shadowy nature – and patients were increasingly surprised that we knew so much. 

There are limits to what I can say, in order to protect the identity of our sources, but I’d like to take this opportunity to clarify a few points. We ran our first report last November, revealing that the Government had just signed a £100million deal for the now pretty much ‘obsolete’ cystic fibrosis drug Orkambi. 

It followed a row over cost for the tablets that began in 2017 – a dispute that dragged on so long that by the time an agreement was reached at the end of October 2019, the newer and vastly more effective Kaftrio was already being given to patients in America (where it’s known as Trikafta). 

When Orkambi was introduced in July 2015, it was the best drug on offer. Patients, of course, wanted access – the drug would, and has, made a difference. 

But overall the health improvements were often modest, many didn’t benefit, and many suffered intolerable side effects. Alone, it wasn’t worth the money. 

However, the drug’s maker, Vertex, was asking the NHS to invest in the future: buy Orkambi now, at the high price being asked for, and you can have Kaftrio when it comes out in a few years for no extra cost. A so-called pipeline deal. 

NHS England and its financial advisers, the National Institute for Health and Care Excellence (NICE), refused. Things became acrimonious. 

Vertex was repeatedly and publicly accused by our politicians and health chiefs of ‘poor practice’ for not ‘complying’ with their wishes and told they ‘ought to know better’. But by mid-2018 it was apparent from clinical trial results that Kaftrio was ‘the one’ everyone had been waiting for – ‘almost a cure’. 


 

BARNEY CALMAN: Over the past six months, in the run-up to last week’s announcement, the MoS has published a series of reports, lifting the lid on the secretive negotiations between NHS England and drug company Vertex on access to cystic fibrosis drugs

The company, really, held all the aces. And then, in May 2019 came a shocking decision that still makes little sense: the NHS agreed to take the triple therapy ‘off the table’ in talks, in order to get Orkambi at a lower price. 

In the run-up to the General Election, health chiefs had been under increasing pressure from Ministers to close the deal. But this ultimately meant three days after Kaftrio was approved in America, Orkambi – by then a five-year-old medicine that had been superseded – was given to UK patients. 

We were approached with the story by a group of whistleblowers, who told us how the NHS had not only ‘bought the wrong drug’ – but also that there was little hope of a resolution over Kaftrio. These were not the kind of people who normally talk to the press. But with a progressive condition such as cystic fibrosis, every single day counts – and they felt they could not afford further delay or deadlock. 

By making public what had been going on, they hoped to heap pressure on dealmakers to come to an agreement swiftly. And it worked. 

After our report, both parties returned to the negotiating table. Talks faltered again in May, but then came a breakthrough. Again, we ran stories to let them know that the world was watching. And finally, last week, came the result everyone had longed for. But did it have to be so difficult? 

The main lobbyists, the CF Trust, are a focal point in the cystic fibrosis community, providing ground-level support to families, giving advice and funding research. To say they are an integral part of thousands of patients lives is no understatement. 

But, as contentious as it is, there are some who say the Trust should not have campaigned for Orkambi, when the superior Kaftrio was on the near horizon. 

As far back as 2018, Kaftrio was already transforming the health of patients in trials. But when the drug was ‘taken off the table’ in talks, prior to the Orkambi deal last year, there appeared to be no public objection from them. 

It was common knowledge in the medical world by that time just how important Kaftrio was, so even some of those inside the Trust felt this was a missed opportunity. By the time the Kaftrio agreement was being thrashed out this year, the Trust appeared to have neither the ear of the Government, nor the drug company. 

Indeed, just a few weeks ago staff were reportedly told by boss David Ramsden that access to Kaftrio was ‘a long way off’ – at the very point that Ministers and Vertex were moving to close the deal. 

On Twitter, where cystic fibrosis campaigners are highly active, the Trust dismissed our reports that an agreement was close, saying it would be ‘months’ before anything happened. 

Given there was such urgency for the medicine during the Covid-19 pandemic – those with cystic fibrosis are at high risk – the mixed messages caused anxiety and upset. And, of course, the Trust was wrong in this instance. 

A CF Trust spokesman said: ‘We are incredibly proud to have worked alongside the cystic fibrosis community in the long campaign for life-saving medicines. The four-year battle to secure Orkambi was a critical step and it remains the only medicine suitable for many children. We have and will always fight for those with cystic fibrosis.’ 

And, to their credit, the Government and health chiefs have listened, and delivered. They did the deal they should have done almost a year ago – and, some feel they would have, if they’d been better advised by the CF Trust. 

In the end, the patients, parents, and concerned supporters who fought for Kaftrio dared to dream, and they won.  

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Popular chemotherapy drug may be less effective in overweight and obese women

Breast cancer patients who are overweight or obese might benefit less from treatment with docetaxel, a common chemotherapy drug, than lean patients. An international team of researchers based this conclusion on a retrospective analysis of data from a large clinical trial. Their study was published in the Journal of Clinical Oncology.

In most European countries, more than 50% of women are overweight or obese (with a body mass index (BMI) above 25 kg/m2, as defined by the WHO). In the United States this is the case for over 63% of women and this proportion is expected to further increase in the coming years. It is not widely known, but obese women have a higher risk of getting breast cancer and obese breast cancer patients have a higher risk of relapsing. Moreover, while many cancer patients are overweight or obese, the efficacy of anticancer drugs according to their BMI is generally not known.

Analysis of 2,800 patients

For the study, a team led by researchers from KU Leuven and the Institut Jules Bordet (Belgium), the University of Milan and National Cancer Institute (Italy) analyzed data from a clinical trial with over 2800 breast cancer patients that started around the turn of the millennium. Patient data were collected over the course of more than ten years. The patients in the trial were treated with a combination of chemotherapy drugs with or without docetaxel, one of the most widely used chemotherapy drugs in the world.

The researchers then looked at how many patients relapsed and how many had passed away. Their statistical analysis of the data shows that overweight and obese patients who received docetaxel as part of their treatment had poorer outcomes than lean patients (BMI between 18.5 and 25 kg/m2). This difference was not observed in patients who received the chemotherapy regimen that did not include docetaxel. “Docetaxel is a lipophilic drug, suggesting that fat present in the body could absorb part of the drug before it can reach the tumor,” explains Professor Christine Desmedt from the KU Leuven Laboratory for Translational Breast Cancer Research.

Raising public awareness

The results raise concerns about treating overweight and obese cancer patients with docetaxel.

“If follow-up research confirms that this finding is solely related to the pharmacological characteristics of docetaxel, this might also apply to patients with other cancer types that are treated with docetaxel, such as prostate or lung cancer. These results also make us wonder whether other chemotherapy drugs from the same family, like paclitaxel, will show the same effect. More research is needed before changes in treatment can be implemented. Patients who have concerns about docetaxel can discuss these with their doctor,” explains Professor Desmedt.

“In general, the public needs to be better informed about the link between BMI and breast cancer.”

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Study finds drug beneficial for shrinking mesothelioma tumors

A drug that is designed to boost the immune system against mesothelioma, when combined with immunotherapy, was found to be beneficial in a small study involving ten patients. The results, which appeared July 1, 2020, in Science Translational Medicine, suggest that the drug LMB-100 could prolong the life of some patients with advanced disease.

Mesothelioma is a rare and hard to treat form of cancer and affects the cells that make up a thin membrane around organs, such as the lungs and heart. To treat this cancer, some drugs have been created that bind to a protein on the surface of these cells, called mesothelin. The hope is to train a patient’s immune system to identify the protein and thus to attack the cancerous cells.

Raffit Hassan, M.D., Chief of the Thoracic and GI Malignancies Branch, and his colleagues decided to study one of these mesothelin-targeting drugs, called LMB-100, which was developed by Ira Pastan, M.D., Co-Chief of the Laboratory of Molecular Biology. His team conducted a phase I trial to explore the safety of the drug, and ten of these patients subsequently received an immune checkpoint inhibitor, pembrolizumab or nivolumab, which helps boost the immune system’s ability to attack cancer cells.

“In some of the patients, receiving pembrolizumab after LMB-100 resulted in greater efficacy than what would be expected from pembrolizumab alone,” says Hassan.

“Four out of the 10 patients responded to the treatment including one complete response and three partial responses.”

Based on these positive results in humans, Qun Jiang, Ph.D., a staff scientist in Hassan’s lab, conducted further studies in mice who were implanted, or grafted, with human mesotheliomas. These experiments yielded similar results whereby tumor shrinkage was greater in mice who received both LMB-100 and pembrolizumab compared to mice who received just one of therapies.

Hassan cautions that since this involved a small number of patients, it is possible that the patients may have simply been responding to the immunotherapy agent pembrolizumab rather than the combination of drugs.

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Study shows asthma drug salbutamol’s potential as Alzheimer’s treatment

A new study reveals that the common asthma drug salbutamol may offer potential as a treatment for Alzheimer’s disease.

Alzheimer’s disease is the most common form of dementia, affecting 47 million people worldwide and its prevalence is expected to triple to more than 130 million cases by 2050.

No effective treatments that cure the disease or slow down its progression have been discovered. However, this new early-stage study has revealed that repurposing an existing drug, salbutamol, offers significant potential as a low cost and rapid response option.

Extensive analytical in-vitro experiments conducted by the research team show that salbutamol is effective at reducing the accumulation of insoluble fibers of the tau protein—which is found in the brains of people with Alzheimer’s disease. These microscopic fibers accumulate into neurofibrillary tangles and can cause neuron destabilization, brain cell death, and are a key characteristic of the disease’s progression.

Much Alzheimer’s disease research has focused on the build-up of amyloid plaques, caused by misfolding of the amyloid-β protein. However, because of disappointing results from numerous therapies targeting Aβ aggregation, more attention is shifting towards tau.

This study, led by researchers at Lancaster University, used a new automated ‘high throughput’ screening approach to study the structure of the misfolding tau protein with a special analytical technique called ‘Synchrotron Radiation Circular Dichroism’ (SRCD) at Diamond Light Source, the UK national synchrotron light source in Oxfordshire. With this powerful technique they were able to look at a selection of more than 80 existing compounds and drugs simultaneously to determine their effectiveness at preventing the formation of tau fibrils.

This method confirmed the compound epinephrine, more commonly known as adrenaline, was effective at stabilizing the tau proteins and preventing the formation of tau tangles. However, our bodies do not easily absorb epinephrine and it rapidly gets metabolized, so the scientists then looked at a range of readily available compounds with similar chemical structures. This search revealed four current drugs as possible candidates—etamivan, fenoterol, dobutamine and salbutamol.

Etaminvan and fenoterol were found to have little effect on the assembly of tau tangles. Dobutamine, which is used for the rapid treatment of heart attacks and heart failure, was found to have some benefit. However, because its effects are very short-lived, and because it needs to be administered intravenously, it is not ideal as a basis for treatment of Alzheimer’s disease.

Further tests using a range of analytical techniques all revealed salbutamol could inhibit tau aggregation in vitro. Tests where salbutamol was added to solutions containing tau resulted in drastically reduced density of fibrous tau structures responsible for the tau neurofibrillary tangles.

The researchers believe that salbutamol interacts with an early stage of tau fibril formation, reducing their ability to form an initial nucleus which drives the aggregation process.

Because it is easily ingested, absorbed into the brain, and remains in the body for several hours, salbutamol has attractive properties as a research avenue for potential new treatment for Alzheimer’s.

Dr. David Townsend, of Lancaster University and lead author of the research, said: “Our work highlights the potential impact of repurposing drugs for secondary medical uses, by discovering a novel therapeutic strategy that impedes the molecular pathology of Alzheimer’s disease, and which may have otherwise gone unstudied.

“Salbutamol has already undergone extensive human safety reviews, and if follow up research reveals an ability to impede Alzheimer’s disease progression in cellular and animal models, this drug could offer a step forward, whilst drastically reducing the cost and time associated with typical drug development.”

Professor David Middleton, co-author of the research, said: “This work is in the very early stages and we are some way from knowing whether or not salbutamol will be effective at treating Alzheimer’s disease in human patients. However, our results justify further testing of salbutamol, and similar drugs, in animal models of the disease and eventually, if successful, in clinical trials.”

Dr. Rohanah Hussain, of Diamond Light Source, Senior Beamline Scientist and co-author said: “Diamond B23 beamline unique micro-collimated beam has made high throughput CD possible allowing the screening of many compounds through structural activity correlation crucial in drug discovery.”

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Health experts slam US hoarding of only licensed virus drug

Health experts on Wednesday slammed the U.S. decision to hog nearly the entire global supply of remdesivir, the only drug licensed so far to treat COVID-19, warning that type of selfish behavior sets a dangerous precedent for attempts to share scarce treatments amid the pandemic.

The U.S. government announced Tuesday that President Donald Trump had struck “an amazing deal” to buy the drug for Americans, made by Gilead Sciences. The Department of Health and Human Services said Trump has secured 500,000 treatments of the drug through September, representing 100% of Gilead’s July production capacity and 90% of its capacity in August and September.

“The Trump administration is doing everything in our power to learn more about lifesaving therapeutics for COVID-19 and secure access to these options for the American people,” HHS said in a statement.

Early trials testing remdesivir in patients hospitalized with COVID-19 found that those who received the drug recovered quicker than those who didn’t. It is the only drug licensed by both the U.S. and the European Union as a treatment for those with severe illness from the coronavirus.

Ohid Yaqub, a senior lecturer at the University of Sussex. called the move “disappointing news.”

“It so clearly signals an unwillingness to cooperate with other countries and the chilling effect this has on international agreements about intellectual property rights,” Yaqub said in a statement.

Dr. Peter Horby, who is running a large clinical trial testing several treatments for COVID-19, told the BBC that “a stronger framework” was needed to ensure fair prices and access to key medicines for people and nations around the world. He said that as an American company, Gilead was likely under “certain political pressures locally.”

British Prime Minister Boris Johnson’s spokesman, James Slack, declined to criticize the United States for the move, but said the U.K. had a stockpile of remdesivir.

“The U.K. has been using remdesivir for some time, first in trials and now in the ‘Early Access to Medicines Scheme,'” he said.

He added that Britain had a “sufficient stock” of remdesivir for patients who need it, but didn’t specify how much that was.

Thomas Senderovitz, head of the Danish Medicines Agency, told Danish broadcaster DR that the move could endanger Europeans and others down the road.

“I have never seen anything like that. That a company chooses to sell their stock to only one country. It’s very strange and quite inappropriate,” he said. “Right now we have enough to make it through the summer if the intake of patients is as it is now. If a second wave comes, we may be challenged.”

In earlier stages of the pandemic, the U.S. refused to export pre-ordered masks to other countries, including neighboring Canada, and reportedly paid off planes delivering ventilators that were originally destined for other countries.

To date, COVID-19 has sickened more than 10.5 million people worldwide, killing around 512,000, according to a tally by Johns Hopkins University. Experts say the true toll of the pandemic is much higher due to limited testing and other issues.

The U.S. has the worst outbreak in the world, with 2.6 million reported infected and 127,000 confirmed virus-related deaths, according to Johns Hopkins.

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Designing anew: Radical COVID-19 drug development approach shows promise

Nearly every drug that is, or has ever been, used was derived from nature—harnessing compounds created by organisms over eons to fight diseases. But decades ago, biochemists postulated that it might be possible to design a new drug from scratch by linking up amino acids in precise ways.

The tricky part, as it turned out, was predicting in advance how the amino acids in a protein would fold. The folded form determines the three-dimensional shape of the protein, as well as its electrostatic potential, and hydrophobicity (the degree to which a molecule is repelled from a mass of water)—factors that are critical when it comes to designing an effective drug.

David Baker, professor of Biochemistry at the University of Washington and head of the Institute for Protein Design there, pioneered methods for using computers to predict how proteins fold. Based on that knowledge, he and his team have designed new, never-before-seen proteins for use as drugs, sensors, or even biological logic gates.

This approach is known as de novo protein design. There are currently only a few drugs in trial that have used this approach, but it holds incredible potential—and at no time has such an approach been more critical than now.

The platform that the Institute for Protein Design developed allows for the rapid design of protein binders to target proteins of interest. Computer (in silico) simulations generate a library of candidate protein sequences that are then tested at their in-house testing facility. Promising candidates are evolved both in silico and in the wet lab until a final binding protein is created.

Starting in January, researchers in the Baker Lab began have been using their methodology to design a drug or vaccine to treat COVID-19. Their studies involve calculating the three-dimensional shape of millions of possible proteins, and then computationally testing how such proteins would fit into, and dock with, parts of the SARS-CoV-2 virus.

To assist in this effort, they are using the Stampede2 supercomputer at the Texas Advanced Computing Center (TACC)—one of the fastest in the world—as well as the network of volunteer computers known as [email protected] (Rosetta is the name of the software developed in the Baker Lab to predict protein folding and to design new proteins.)

“In just a two-month span, our team has been able to computationally design millions of protein therapeutics that target the seven major proteins related to COVID-19,” Baker reported in March.

To date, 733,000 proteins have been ordered, 323,000 of these protein therapeutics have been tested in the laboratory, and more than 2,000 have shown binding signals to their respective targets.

From Scaffolds to Protein Structures

The team began by testing its collection of 20,000 scaffold proteins that form the starting point for future drugs or vaccines. Each can be docked in over 1,000 orientations; and each dock is subsampled 1,000 times with slight perturbations—leading to 20 billion potential interactions to compute.

“In the scaffold phase, we’re looking for signs these are going to be atomically accurate,” said Brian Coventry, a Ph.D. student in the group working on the project. “If we’re off by 0.1 nanometers, there’s no way it will work. These things have to be perfect.”

The top 1 million of these docks then move forward to sequence design where each position on the scaffold backbone must be assigned an amino acid. With 20 amino acid choices at each position, and a variety of conformations for each, the computer must solve the combinatorial explosion to assign the best combination of amino acids to each scaffold.

From the 1 million designed proteins, they determine the most promising subset—roughly 100,000 proteins. The team sends a text file containing DNA sequences for these candidates to Agilent, a company that can create synthetic DNA molecules on demand. Agilent returns test tubes with physical DNA, which is then inserted into yeast genomes in such a way that the various synthetic proteins are made and displayed on tethers from the cell membrane of yeast, allowing them to be tested against the virus.

Based on the initial computational and experimental results, the team then engages in site saturation mutagenesis, where each individual amino acid on the chain is mutated at every location and re-tested to see how it behaves.

“We get data back and look at what made a given protein better or worse. And we ask the question: ‘Does this protein look like it’s working for the right reasons?'” Coventry said.

Based on the results and insights from the mutagenesis, they go one step further and develop a combo library that includes degenerate codons, where alternate nucleotides replace the typical ones in a given amino acid.

The best combination of mutations and replacements undergo further experimental testing including bacterial expression and thermodynamic analysis. Using this method, they derived 50 highly promising leads for the spike protein binder from an initial screening of 100,000 proteins.

“The spike protein binder is the most likely to result in a drug because of its mechanism of action,” Coventry said.

But the ability to create designer proteins is not the lab’s only innovation, nor is a single binder their final goal. They are also pioneering a new approach to drugs called mini-protein binders that combine the specificity of antibodies with the high stability and manufacturability of small molecule drugs.

Mini-protein binders have been shown to have much greater stability at elevated temperatures and better neutralization than comparable antibodies and natural protein derivatives. They are also approximately 1/30th of the molecular weight of typical proteins, and can be synthesized chemically, which enables the introduction of a wide variety of functionalities. Probably as a result of their small size and very high stability, they elicit little immune response.

“We aim to connect four to six of the most potent neutralizers in a single chain by flexible linkers to achieve highly avid binding with little potential for escape,” Baker said in a presentation to the Defense Advanced Research Projects Agency (DARPA), one of the funders of the research.

“We try to get many binders and connect them with linkers,” Coventry explained further. “The idea is that you get an avidity effect”—the accumulated strength of multiple affinities. “At least one of those proteins will be binding at any given time and the virus particle won’t be able to escape the chain. Since the binders block the viral binding epitope, the virus will not be able to enter our cells.”

Building on Collaborations

TACC is currently supporting more than 40 COVID-19 research projects. The one from the Baker Lab has been among the largest users of compute time on Stampede2 since it began in March.

“TACC has a lot of computing power and that has been really helpful for us,” Coventry said. “Everything we do is purely parallel. We’re able to rapidly test 20 million different designs and the calculations don’t need to talk to each other.” This type of approach, known as high-throughput screening, is a good fit for Stampede2’s architecture.

Baker and his team were able to ramp up quickly on TACC resources in part because of their involvement in an ongoing DARPA-funded program known as the Synergistic Discovery and Design (SD2), a multi-institution collaboration whose goal is to develop data-driven methods to accelerate scientific discovery.

Since 2017, the SD2 program has been developing pipelines to “design-test-learn” faster, using a combination of high-performance computing, advanced data management practices, automated laboratory testing, and machine learning. The collaboration between the Baker Lab and TACC is emblematic of that methodology and is helping to accelerate their research from idea to reality.

According to Dr. Matthew Vaughn, Director of Life Sciences Computing at TACC, the protein design project appears poised to yield powerful new therapeutic molecules for the fight against COVID-19 due in part to the remarkable synergy between computational simulation and experimentation.

“The rapid pace at which the Baker lab has been able to onboard and become productive on a leadership-class resource like Stampede 2 reinforces just how critical our national investments in advanced computing capability and methodology have been and will continue to be in the future,” Vaughn said.

The team’s next milestone will be to develop multiple inhibitors that can reduce the response by half and that can be linked those together into a big molecule, or construct, that is well behaved.

Further testing to establish whether the mini-binder provokes an immune response would follow, and then the construct would be tested for efficacy in a petri dish, then in animals and humans.

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Drug used to slow kidney disease found to be ineffective

Following a major clinical trial, clinicians find the drug allopurinol does not prevent worsening of kidney disease.

The Australasian Kidney Trials Network led a large, two-year study, known as CKD-FIX, to assess the effectiveness of allopurinol, in slowing the rate of decline in kidney function.

They found the drug is ineffective in treating the condition, despite up to 20 per cent of kidney disease patients being prescribed the medication.

Queensland Renal Transplant Service Medical Director and University of Queensland Professor of Medicine based at the Translational Research Institute, David Johnson, said until now there had been little robust evidence to demonstrate allopurinol’s benefit in slowing the rate of decline in kidney function.

“We felt it was important to gather evidence of allopurinol’s impact on patients with kidney disease who have never had gout,” said Professor Johnson.

“In the CKD-FIX study, we compared the use of allopurinol to a placebo and found, to our surprise, that it made no difference to the rate of kidney function decline,” he said.

“Based on these results we believe there is no benefit in prescribing this medication, unless there is an additional specific medical reason, such as gout. This much awaited, high-quality evidence will inform global clinical guidelines for patient treatment.

“It is important, though, that people with kidney disease who are already taking a medication like allopurinol to lower blood urate levels don’t abruptly stop this treatment. They should discuss their kidney care management with their doctor first.”

Lead Investigator-New Zealand, Dr. Janak de Zoysa from the University of Auckland and Waitemata District Health Board said trials like CKD-FIX were very important as they allowed doctors to optimise clinical practice.

“Trials which show existing treatments to be not as effective as anticipated, allow for those medications to be stopped or not started in the first place, reducing unnecessary healthcare costs,” said Dr. de Zoysa.

Commercially available since the late 1960s, allopurinol helps the body reduce urate in the blood. High levels of the chemical are common among patients with chronic kidney disease, where it is associated with a higher risk of developing chronic kidney disease and its progression.

The George Institute for Global Health Senior Research Fellow and St George Hospital nephrologist, Associate Professor Sunil Badve said the widely held view that elevated blood urate levels were responsible for rapid decline of kidney function was probably wrong.

“Based on our study results, it appears that elevated blood urate levels are most likely an indicator of reduced kidney function rather than a cause of reduced kidney function,” said A/Prof Badve.

The CKD-FIX study ran across 31 hospitals in Australia and New Zealand, with more than 369 patients -with stage 3 or 4 chronic kidney disease who were at increased risk of further progression—taking part in the trial.

The results from the study were published in The New England Journal of Medicine.

In the paper, the study authors reported a 35% reduction in blood urate levels, which was maintained throughout the two-year study period for patients prescribed allopurinol. Kidney function, however, declined at similar rates for two treatment groups; allopurinol -3.33 mL/min/1.73 m2/year (95% CI -4·11 to -2·55) and control -3.23 mL/min/1.73 m2/year (95% CI -3·98 to -2·47). There was no difference in the quantity of protein in the urine and blood pressure between the groups.

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Gout drug may improve survival odds for COVID-19 patients, study says

Could an old gout drug help treat coronavirus? Study suggests colchicine can fight inflammation and improve survival odds for COVID-19 patients by nearly 10-FOLD

  • Researchers gave half a group of coronavirus patients colchicine, a drug commonly used to treat gout, and the other half a placebo
  • Patients receiving colchicine had lower levels of proteins that are a sign of heart injury and inflammation
  • About 14% of those in the control group died, living an average of 18.6 days, while the 1.8% in the drug group died, living an average of 20.7 days
  • Scientists theorize the anti-inflammatory effects of colchicine may prevent cytokine storms, which occur when the body attacks its own tissues
  • Here’s how to help people impacted by Covid-19

A common anti-inflammatory drug can prevent serious complications caused by the novel coronavirus and improve survival odds in patients, a new study suggests.

Researchers found that those given colchicine had lower levels of proteins in the blood that are a sign of heart injury and of a protein made by the liver as a marker of inflammation.

What’s more, patients who received the medication increased the chance of surviving by nearly 10-fold.

The team, from the University of Athens in Greece, says colchicine could help the most severely ill patients eventually be discharged from the hospital.

Researchers gave half a group of coronavirus patients colchicine (pictured), a drug commonly used to treat gout, and the other half a placebo

Patients receiving colchicine had lower levels of proteins that are a sign of heart injury and inflammation. Pictured: Medical staff members are seen at the Northwestern Memorial Hospital in Chicago, Illinois, May 2020

About 14% of those in the control group died, living an average of 18.6 days, while the 1.8% in the drug group died, living an average of 20.7 days (above)

Colchicine is most often used to treat gout, a complex form of arthritis that causes pain, swelling, redness and tenderness in the joints, most often in the big toe. 

Scientists theorize the anti-inflammatory effects of the drug may prevent cytokine storms, which occur when the body doesn’t just fight off the virus but also attacks its own cells and tissues.

For the study, published in JAMA Network Open, the team looked at 105 coronavirus patients across 16 tertiary hospitals in Greece. 

Between April 3 and April 27, half the group were given two doses of colchicine per day and the other half were given a placebo. 

Researchers compared levels of cardiac troponin and C-reactive proteins in the two groups.

Cardiac troponins are a group of proteins found in skeletal and heart muscle fibers that help detect heart injury.  

Levels were 0.0112 nanograms per milliliter (ng/mL) in the control group and 0.008 in the colchicine group.

Meanwhile, C-reactive proteins are made by the liver and levels in the blood increase when there is a condition causing inflammation somewhere in the body.

Normal levels are typically below 3.0 milligrams per deciliter (mg/dL).

Median maximum C-reactive protein levels were 4.5 mg/dL in the control group and 3.1 mg/dL in the colchicine group. 

Patients were also more likely to die in the control group with 14 percent dying who didn’t receive colchicine compared to 1.8 percent who did.

And, of those who did pass away, people in the control group lived for an average of 18.6 days and those in the colchicine group lived an average of 20.7 days.

‘In this randomized clinical trial, participants who received colchicine had statistically significant improved time to clinical deterioration compared with a control group that did not receive colchicine,’ the authors wrote.

‘The hypothesis-generating findings of this study suggest a role for colchicine in the treatment of patients with coronavirus disease 2019.’

In the US, there are more than 2.3 million confirmed cases of the virus and more than 121,000 deaths. 

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