Experimental Drugs Reverse Arthritis in Rats Study

The science shows potential results in treating a debilitating condition.

People with osteoarthritis, or “wear and tear” arthritis, have limited treatment options: pain relievers or joint replacement surgery. Now, Salk researchers have discovered that a powerful combination of two experimental drugs reverses the cellular and molecular signs of osteoarthritis in rats as well as in isolated human cartilage cells. Their results were published in the journal Protein & Cell on January 16, 2020.

“What’s really exciting is that this is potentially a therapy that can be translated to the clinic quite easily,” says Juan Carlos Izpisua Belmonte, lead author and a professor in Salk’s Gene Expression Laboratory. “We are excited to continue refining this promising combination therapy for human use.”

Affecting 30 million adults, osteoarthritis is the most common joint disorder in the United States and its prevalence is expected to rise in coming years due to the aging population and increasing rate of obesity. The disease is caused by gradual changes to cartilage that cushions bones and joints. During aging and repetitive stress, molecules and genes in the cells of this articular cartilage change, eventually leading to the breakdown of the cartilage and the overgrowth of underlying bone, causing chronic pain and stiffness.

Previous research had pinpointed two molecules, alpha-KLOTHO and TGF beta receptor 2 (TGFβR2), as potential drugs to treat osteoarthritis. αKLOTHO acts on the mesh of molecules surrounding articular cartilage cells, keeping this extra-cellular matrix from degrading. TGFβR2 acts more directly on cartilage cells, stimulating their proliferation and preventing their breakdown.

While each drug alone had only moderately curbed osteoarthritis in animal models of the disease, Izpisua Belmonte and his colleagues wondered if the two drugs would act more effectively in concert.

“We thought that by mixing these two molecules that work in different ways, maybe we could make something better,” says Paloma Martinez-Redondo, a Salk postdoctoral fellow and co-first author of the new study.

The researchers treated young, otherwise healthy rats with osteoarthritis with viral particles containing the DNA instructions for making αKLOTHO and TGFβR2.

Six weeks after the treatment, rats that had received control particles had more severe osteoarthritis in their knees, with the disease progressing from stage 2 to stage 4. However, rats that had received particles containing αKLOTHO and TGFβR2 DNA showed recovery of their cartilage: the cartilage was thicker, fewer cells were dying, and actively proliferating cells were present. These animals’ disease improved from stage 2 to stage 1, a mild form of osteoarthritis, and no negative side effects were observed.

“From the very first time we tested this drug combination on just a few animals, we saw a huge improvement,” says Isabel Guillen-Guillen, the paper’s co-first author. “We kept checking more animals and seeing the same encouraging results.”

Further experiments revealed 136 genes that were more active and 18 genes that were less active in the cartilage cells of treated rats compared to control rats. Among those were genes involved in inflammation and immune responses, suggesting some pathways by which the combination treatment works.

To test the applicability of the drug combination to humans, the team treated isolated human articular cartilage cells with αKLOTHO and TGFβR2. Levels of molecules involved in cell proliferation, extra-cellular matrix formation and cartilage cell identity all increased.

“That’s not the same as showing how these drugs affect the knee joint in humans, but we think it’s a good sign that this could potentially work for patients,” says Martinez-Redondo.

The research team plans to develop the treatment further, including investigating whether soluble molecules of the αKLOTHO and TGFβR2 proteins can be taken directly, rather than administered through viral particles. They also will study whether the combination of drugs can prevent the development of osteoarthritis before symptoms develop.

“We think that this could be a viable treatment for osteoarthritis in humans,” says Pedro Guillen, director of the Clinica CEMTRO and co-corresponding author.

Reducing the Very Overpriced Cost of Healthcare

As is known to many people, American healthcare is far more expensive than necessary.

One of most enduring, economically and socially damaging, downright frustrating facts about life in the United States is how expensive health care is here. Not only does U.S. health care cost far more than in other advanced economies, but compared with the nations that spend less, we have worse or equivalent health outcomes. In fact, U.S. life expectancy now lags behind that of all the advanced economies.

An MRI scan that cost $1,400 here went for $450 in Britain and $190 in Holland. Thirty tablets of a drug to reduce the risk of blood clots (Xarelto) cost $380 here, $70 in Britain, $80 in Switzerland and $60 in Holland. Hospital admission for angioplasty is $32,000 here, $15,000 in Australia, $12,000 in Britain, $7,000 in Switzerland, $6,000 in the Netherlands.

Add to those differences the latest outrage in health-care costs: surprise medical billing, when even well-insured patients can wake up from surgery finding that they owe thousands of dollars, because someone treating them while they were unconscious was out of their insurance network.

Princeton economists Anne Case and Angus Deaton (a Nobel winner) recently summarized the problem by labeling it an $8,000-a-year annual health-care tax paid by U.S. families. This is the difference in costs between what we pay for health care and what people in other countries pay. As Case put it: “We can brag we have the most expensive health care. We can also now brag that it delivers the worst health of any rich country.”

Why call this expense a tax? Well, for one, if you want health coverage, you can’t escape it. But even if you don’t — and good luck with that — you still can’t escape the tax, as both employer- and government-provided health care extract payments through lower paychecks and public financing.

Case and Deaton may be erring on the low side in their $8,000-per-family figure. The Organization for Economic Cooperation and Development puts per-person spending in the United States at $8,950 a year. That compares with $5,060 in Germany, $3,470 in Canada and just $3,140 in Britain. If we assume a family of three, we would get an annual health-care tax of $11,670 compared with Germany and more than $17,000 compared with the cost of health care in Britain.

How can such differences persist, especially in a service where consumption is so essential to well-being? If ice cream were that much more expensive here, we’d have a lot to squawk about, for sure. But it wouldn’t be a matter of life and death.

An obvious, and correct, answer as to why U.S. health care is so expensive is because we do so little, relative to other systems, to control costs. But it’s worse than that. We do a fair amount to make health care more expensive.

First, our system of private insurance costs far more than single-payer systems like Canada’s, and also more than countries with private but heavily regulated insurers like Germany. OECD data show that as a share of health spending, our administrative costs are three times that of Canada’s and twice that of Germany’s. Getting our administrative costs closer to those in other countries would require regulating private insurers and expanding public coverage, but it could save us at least 10 percent of our total health-care bill.

Next, we pay twice as much to our health-care providers and for prescription drugs as everyone else. The latter costs us more than $3,000 per family per year. We pay more than twice as much for medical equipment, costing us a bit less than $1,500 per family per year. Doctors and dentists cost us close to an extra $750 per family per year.

One reason for the outsize costs of these inputs to U.S. health care is that government policy protects our providers. When it comes to manufactured goods, like cars and clothes and almost everything on the shelves of Walmart, economists and policymakers push for “free trade” and more competition. But when it comes to health-care providers, these same authorities turn protectionist.

In areas like prescription drugs and medical equipment, this protection is explicit: Manufacturers are granted patent monopolies. The government will arrest anyone who sells protected items in competition with a patent holder.

In the case of doctors, we have maintained or increased barriers that make it difficult for qualified foreign physicians to practice in the United States. We also prevent other health-care professionals, such as physicians’ assistants and nurse practitioners, from doing many tasks for which they are entirely competent. There is a similar story with dentists and dental hygienists.

Other countries directly control drug prices. In France, the government determines whether a new drug is an improvement or a copycat, and, if the drug is deemed useful, the government negotiates drug prices with the manufacturers and caps their revenue. When sales exceed the cap, the manufacturer must rebate most of the difference back to the government.

Here in the United States, we give drug companies and medical equipment manufacturers’ patent monopolies and allow them to charge whatever they want. We don’t even let the government use its massive leverage to negotiate lower drug prices for Medicare beneficiaries. That’s what makes these goods expensive; they’re almost always relatively cheap to produce.

This is fixable. It would take regulating costs, reducing reimbursements to providers and increasing competition.

The pharmaceutical industry’s rationale for cost-exploding medical patents is that it helps incentivize research and innovation. Without them, it’s likely that pharmaceuticals and medical equipment companies would do less speculative research. But it would take a fraction of the savings from reducing such protectionism to replace patent-support research with publicly supported research (for which we already spend $40 billion a year).

In terms of boosting competition, allowing foreign doctors whose training meets our standards to more easily practice medicine here would bring U.S. physicians’ pay in line with international standards. Of course, our doctors pay much more for their education than doctors trained elsewhere, so part of this new structure would also require reducing the domestic cost of medical education and alleviating some of the educational debt burden that U.S.-trained doctors have acquired.

Increasing competition would also require using antitrust measures to push back on the pricing power engendered by the consolidation of both hospital groups and medical practices. An analysis by the New York Times of 25 metro areas found that hospital mergers “have essentially banished competition and raised prices for hospital admissions.”

Even if we succeed in raising competition and reducing protectionism, health care will still be too expensive for many low- and moderate-income families, many of whom have suffered stagnant incomes in recent decades. Like every other wealthy country, we will need to get on a path to universal coverage. But whatever form that takes, if we can significantly reduce our current health-care tax, the savings will easily be large enough to extend quality, affordable coverage to every American.

USA Memory Champion on Improving One’s Memory

The American memory champion’s results give credence to the notion that (as with other things in life) you can get good at anything you practice at — including memory.

In 2009, after Nelson Dellis’s grandmother Josephine passed away from Alzheimer’s disease (which may have a hereditary component), he was inspired to find ways to keep his own brain healthy and sharp.

“I was a good student, but my memory was average,” Dellis, 35, tells CNBC Make It.

Dellis scoured the internet looking for tips to improve his memory and joined a few forums where professional “memory athletes” (people who train their memory skills for high performance) chatted about different memory techniques. Then he listened to “Quantum Memory: Learn to Improve Your Memory with The World Memory Champion,” an audiobook by Dominic O’Brien, a seven-time world memory champion.

“After that, I went off and, through trial and error, figured out what [techniques] worked well for me,” Dellis says.

Today Dellis, author of the book “Remember It” and a four-time USA Memory Champion (an annual competition for elite mental athletes), is a full-time memory coach based in Miami, Florida. He charges $250 an hour for private lessons to the likes CEOs and billionaires, including Mark Cuban and Sara Blakely.

Here are Dellis’ top three tips on improving your memory and staying sharp.

1. Go offline

Dellis says one the easiest memory tips that he’s learned over the years is to take time to totally disconnect from technology — including your smartphone — for at least an hour a day.

That’s because presence is important for memory, says Dellis.

“Your brain is a processing unit,” he says. “If your brain isn’t present to receive [information] (i.e., you’re distracted and not paying attention), how on earth do you think it’s going to be able to remember it? You’ll be surprised how powerful your natural memory is if you just try and pay attention.”

Dellis’s advice is supported by research: According to a 2017 study from the McCombs School of Business at The University of Texas at Austin, researchers found the mere presence of a smartphone reduces cognitive capacity, affecting one’s brain to hold and process data.

2. Think in pictures

“My goal whenever I memorize something is to turn it into a mental picture in my mind,” he says, which is “any mental representation of what you’re trying to memorize, using as many of your senses as possible.” It could be an association, a sound, a feeling — anything that’s “meaningful” to you, Dellis says.

That’s because it’s much easier to remember a picture of something that you are familiar with than words relating to something new and difficult, he says. (Studies in older adults have shown that pictures can help with memory.)

Dellis uses the example of remembering the name chervil (an herb) to buy at the grocery store.

“Most people might not even know what that is. So I might break that word down into what it sounds like: ‘sure-vill.’ So maybe my meaningful image could be, me saying ‘sure!’ enthusiastically to a ’vill’ain. The more context the better. Maybe I’m agreeing with this villain, because if I don’t, he’ll take all the chervil in the world and secretly garnish all the food in the world and ruin the taste of everything,” Dellis says.

The “more over-the-top and bizarre you make the image, the better.”

To practice, Dellis suggests that when you meet someone for the first time, turn their name into mental images, as he did with chervil.

“You’ll have a higher chance of remembering the person’s name, and you’ll be training your brain to get better/quicker at thinking in pictures,” he says.

3. Explore your ‘memory palace’

When you’re thinking in pictures, you need a place to store those images. So most memory athletes use a technique called the “memory palace,” according to Dellis. The technique (which dates back to the ancient Greeks) has to do with remembering things based on location

According to Dellis, a memory palace works like this: Think of a familiar place (like your house, apartment, office, etc.) and imagine a mental pathway through it. To store your images, simply imagine or “stick” each image on a location along the path in your mind. The idea is that later on when you want to retrieve the information, all you have to do is think of your memory palace, walk back through it in your mind and pick up the images you left there.

It sounds a bit crazy, but it works, according to Dellis and it allows top memory athletes to memorize thousands of pieces of information, he says.

“It’s an effective way of stringing together sets of memories because it uses more and various parts of the brain than simply short term recall (visual, emotional, language, imagination and short term memory),” neuroscientist Tara Swart tells CNBC Make It.

To practice, Dellis suggests choosing three familiar places and selecting 10 locations along your mental path through each. Start by storing daily to-do lists and grocery lists there as practice.

Drinking Tea Regularly Linked to a Longer Life

Scientists found that there really is merit to drinking green tea.

Drinking tea at least three times a week could be linked with a longer and healthier life, scientists say.

According to new research “habitual” consumption of the hot drink is associated with lower risks of cardiovascular disease and all-cause death.

But whether the tea being consumed is green or black may make a difference.

The analysis included 100,902 participants of the China-PAR project2 with no history of heart attack, stroke, or cancer.

Participants were categorised into two groups – habitual tea drinkers, those drinking three or more times a week, and never or non-habitual tea drinkers  – those drinking less than three times a week.

They were followed-up for a median of 7.3 years, in the study published in the European Journal of Preventative Cardiology.

The research suggests a 50-year-old habitual tea drinker would develop coronary heart disease and stroke 1.41 years later, and live 1.26 years, longer than someone who never or seldom drank tea.

Compared with never or non-habitual tea drinkers, habitual tea consumers had a 20% lower risk of incident heart disease and stroke, and a 22% lower risk of fatal heart disease and stroke.

They also had a 15% decreased risk of all-cause death, the study suggests.

First author Dr Xinyan Wang, of the Chinese Academy of Medical Science in Beijing, said: “Habitual tea consumption is associated with lower risks of cardiovascular disease and all-cause death.

“The favourable health effects are the most robust for green tea and for long-term habitual tea drinkers.”

Researchers analysed the potential influence of changes in tea drinking behaviour in a subset of 14,081 participants with assessments at two time points.

The average duration between the two surveys was 8.2 years, and the median follow-up after the second survey was 5.3 years.

Habitual drinkers who maintained their habit in both surveys had a 39% lower risk of incident heart disease and stroke, 56% lower risk of fatal heart disease and stroke, and 29% decreased risk of all-cause death compared to consistent never or non-habitual tea drinkers, the study suggests.

In a sub-analysis by tea type, drinking green tea was linked with around 25% lower risks for incident heart disease and stroke, fatal heart disease and stroke, and all-cause death.

However, no significant associations were observed for black tea.

Scientists found 49% of habitual tea drinkers in the study consumed green tea most frequently, while only 8% preferred black tea.

They noted a preference for green tea in East Asia, and said the small proportion of habitual black tea drinkers might make it more difficult to observe robust associations, but that the findings hint at a differential effect between tea types.

The researchers suggest a number of reasons for this.

They indicate that green tea is a rich source of polyphenols which protect against cardiovascular disease.

While black tea is fully fermented and during this process may lose antioxidant effects.

Gunter Kuhnle, professor of nutrition and food science at the University of Reading, said: “This study is an observational study and can therefore only establish an association – not a causal relationship.”

He added that the two cups per week as cut-off point was very little when compared to the average consumption of three to four cups per day in the UK.

Prof Kuhnle said: “It is not clear from the study whether there is any benefit from higher tea intake – and therefore there is no likely benefit from increasing tea intake by the majority of the British public.”

AI Becomes Very Good at Diagnosing Breast Cancer

Artificial intelligence is becoming more of a hot topic, and people should remember more that AI can be used both to hurt humans and (as in this case) help humans.

A computer programme can identify breast cancer from routine scans with greater accuracy than human experts, researchers said in what they hoped could prove a breakthrough in the fight against the global killer.

Breast cancer is one of the most common cancers in women, with more than 2 million new diagnoses last year alone.

Regular screening is vital in detecting the earliest signs of the disease in patients who show no obvious symptoms.

In Britain, women over 50 are advised to get a mammogram every three years, the results of which are analysed by two independent experts.

But interpreting the scans leaves room for error, and a small percentage of all mammograms either return a false positive – misdiagnosing a healthy patient as having cancer – or false negative – missing the disease as it spreads.

Now researchers at Google Health have trained an artificial intelligence model to detect cancer in breast scans from thousands of women in Britain and the United States.

The images had already been reviewed by doctors in real life but unlike in a clinical setting, the machine had no patient history to inform its diagnoses.

The team found that their AI model could predict breast cancer from the scans with a similar accuracy level to expert radiographers.

Further, the AI showed a reduction in the proportion of cases where cancer was incorrectly identified – 5.7 percent in the US and 1.2 percent in Britain, respectively.

It also reduced the percentage of missed diagnoses by 9.4 percent among US patients and by 2.7 percent in Britain.

“The earlier you identify a breast cancer the better it is for the patient,” Dominic King, UK lead at Google Health, told AFP.

“We think about this technology in a way that supports and enables an expert, or a patient ultimately, to get the best outcome from whatever diagnostics they’ve had.”

Computer ‘second opinion’

In Britain all mammograms are reviewed by two radiologists, a necessary but labour-intensive process.

The team at Google Health also conducted experiments comparing the computer’s decision with that of the first human scan reader.​

If the two diagnoses agreed, the case was marked as resolved. Only with discordant outcomes was the machine then asked to compare with the second reader’s decision.

The study by King and his team, published in Nature, showed that using AI to verify the first human expert reviewer’s diagnosis could save up to 88 percent of the workload for the second clinician.

“Find me a country where you can find a nurse or doctor that isn’t busy,” said King.

“There’s the opportunity for this technology to support the existing excellent service of the (human) reviewers.”

Ken Young, a doctor who manages mammogram collection for Cancer Research UK, contributed to the study.

He said it was unique for its use of real-life diagnosis scenarios from nearly 30,000 scans.

“We have a sample that is representative of all the women that might come through breast screening,” he said.

“It includes easy cases, difficult cases and everything in between.”

The team said further research was needed but they hoped that the technology could one day act as a “second opinion” for cancer diagnoses.

Abortion Reversal — The Dangerous Practice You’ve Probably Never Heard Of

In the United States, many more laws have been implemented that restrict or ban a woman’s ability to have an abortion. Abortion reversal is a new technique that hasn’t undergone much medical testing since the one test on it showed significant harm to the women.

Several states now require women who seek medication abortions to be provided with dubious information that the procedure could be stopped, allowing a pregnancy to continue.

But when researchers attempted to carry out a legitimate study of whether these “abortion reversal” treatments were effective and safe, they had to stop almost immediately – because some of the women who participated in the study experienced dangerous hemorrhaging that sent them to the hospital.

By passing these abortion reversal laws, “states are encouraging women to participate in an unmonitored experiment,” Creinin said.

Creinin and his colleagues detailed their concerns in a commentary in the journal Contraception, and they will publish their study in January’s edition of Obstetrics and Gynecology.

Medication abortions, which are used up to 10 weeks into a pregnancy, consist of taking two pills in sequence. The first pill in the regimen, mifepristone, loosens the pregnancy’s attachment to the uterus. The second pill, misoprostol, forces the uterus to contract to push out the pregnancy. The pills must be taken consecutively to complete the abortion, and there’s a chance the pregnancy will continue if the second pill is not taken.

A total of 862,320 abortions were provided in clinical settings in 2017, according to the Guttmacher Institute, about 39 percent of which were medication abortions. Research has shown that using these drugs is a safe way to end a pregnancy.

Some antiabortion activists and legislators claim that not taking the second pill, or giving a woman high doses of the hormone progesterone after taking mifepristone, can help stop, or “reverse,” a medical abortion.

The American College of Obstetricians and Gynecologists firmly states that “claims regarding abortion ‘reversal’ treatment are not based on science and do not meet clinical standards” and say the purported studies that underpin these antiabortion arguments lack scientific rigor and ethics.

Despite this, the claims made in these discredited studies have worked their way to antiabortion lawmakers, who in turn have put them into abortion reversal legislation that was signed by governors in North Dakota, Idaho, Utah, South Dakota, Kentucky, NebraskaOklahoma and Arkansas. The laws are currently blocked or enjoined in Oklahoma and North Dakota.

Because reliable research on these treatments is nonexistent, earlier this year, Creinin and his colleagues designed a legitimate double-blind, placebo-controlled, randomized trial that aimed to observe 40 volunteers who had already elected to have a surgical abortion.

Their goal was to see if giving progesterone to women who took the first pill in the prescribed regimen would effectively and safely halt an abortion.

After the women took the first pill in the abortion protocol, mifepristone, rather than take the second pill, misoprostol, they were either given a placebo or a dose of progesterone.

Researchers only enrolled 12 women before they had to stop the study.

Bleeding is normal during a medication abortion. But three of the women who enrolled in the UC-Davis study experienced far more serious bleeding than anyone could have anticipated when the second pill was not administered.

One woman “was so scared she called an ambulance,” while another woman startled by the amount of blood “called 911 and crawled into her bathtub”, Creinin said. A third woman who went to the emergency room needed a transfusion. One of the women had received a placebo, while two others had taken the progesterone.

Creinin and his colleagues halted the study as soon as it became clear that they could not proceed safely.

“I feel really horrible that I couldn’t finish the study. I feel really horrible that the women … had to go through all this,” Creinin said. Because the study ended prematurely, the researchers could not establish any evidence that progesterone was an effective way to stop a medication abortion.

“What the results do show, though, is that there’s a very significant safety signal” when it comes to disrupting the approved medication abortion protocol, Creinin said.

In their upcoming paper in Obstetrics and Gynecology, the researchers warn that “patients in early pregnancy who use only mifepristone may be at high risk of significant hemorrhage.”

Medical experts are so concerned about abortion reversal laws that the American Medical Association joined a lawsuit against North Dakota’s abortion reversal law, which was blocked by a federal judge in September.

The North Dakota abortion reversal law, signed by Gov. Doug Burgum (R) in March, instructed health-care providers to tell a woman “that it may be possible to reverse the effects of an abortion-inducing drug if she changes her mind, but time is of the essence” and to provide a woman with literature on how to do this. The law fails to specify what that literature would include, or what such a treatment might entail.

Clinical Trial on Lupus Shows Significant Promise on Better Treating It

Lupus is surprisingly prevalent and is in many respects a uniquely terrible disorder, and this experimental trial shows statistically significant results in treating it. The long-term side effects of using this new medicine (anifrolumab) on lupus patients aren’t known, but the progress on lupus is still important.

Lupus is a potentially fatal autoimmune disorder that impacts roughly 5 million people worldwide, and yet it still has no known cause or cure.

Today, most treatments come with a whole bunch of adverse side effects, and given how little we know, finding new avenues for medicine has proved extremely difficult.

In the past six decades, only one drug for lupus has been approved by the United States Food and Drug Association and it’s still unavailable to many. Now, an international three-year clinical trial offers the first real hope for patients in half a century.

The Phase 3 trial, called TULIP-2, tested a drug called anifrolumab on a randomised selection of 180 people with lupus, giving them 300 mg every four weeks for 48 weeks.

Compared to the placebo, which was given to a further 182 participants who also had lupus, the authors say anifrolumab produced a statistically significant and clinically-meaningful reduction in the disease.

After 52 weeks, not only only did this drug reduce autoimmune activity in the relevant organs of many of the treated patients, it also reduced the rate of flare-ups – which include fever, painful joints, fatigue and rashes – and lessened the need for steroids.

“There is now a strong body of evidence demonstrating the benefit of anifrolumab, and we look forward to bringing this potential new medicine to patients with systemic lupus erythematosus as soon as possible,” says Mene Pangalos, the executive vice president of BioPharmaceutical R&D.

Even when no virus infection can be found, recent studies show the vast majority of lupus patients produce excess Type 1 interferon, which is an immune protein linked to the development of white blood cells.

Previous attempts to block this protein have failed, but anifrolumab blocks the receptors for this protein instead and not the molecule itself.

Another clinical trial that tested this drug, called TULIP-1, couldn’t support any particular benefits based on its specific method, although there were signs that it might help improve the health of certain organs.

The smaller second trial has now explored this second outcome further – known as the British Isles Lupus Assessment Group–based Composite Lupus Assessment (BICLA) – and the results look much more promising.

Unlike TULIP-1, TULIP-2 showed benefits on both the BICLA and SRI index.

“Measurement of treatment response in [systemic lupus erythematosus] has been very problematic and this represents a kind of second breakthrough of this trial,” says rheumatologist and lead researcher Eric Morand from Monash University.

It’s still unclear why TULIP-1 and TULIP-2 produced different results, especially since they were nearly identical. But an accompanying editorial explains they might have differed because various elements of lupus were weighted differently. One of the assessments, for example, only captures partial responses while another only captures complete responses.

“Therefore, the effect of a drug on particular disease features may produce superior results with one end point and not another,” the editorial reads.

So far, three clinical trials in total have tested anifrolumab, and the results for five of the six outcomes favoured the drug over the placebo. Given the desperate need for treatment, many in the lupus community are urging regulators to consider trials that allow greater flexibility in defining success.

“For example,” the authors of the editorial write, “perhaps a benefit with respect to just one of two end points — the SRI or the BCLA — needs to be observed to declare a drug effective in this complex disease.”

This could accelerate drug development until we know better what response measures and biomarkers are most useful when trialling lupus medication.

More research is needed for anifrolumab before we can say for sure whether its benefits outweigh its side-effects in the long run. Some patients taking the drug were more at risk of bronchitis and upper respiratory infection and the risks beyond 52 weeks are still unclear.

“As clinicians we need new medicines for this complex and difficult-to-treat disease,” says Morand.

“These exciting results from the TULIP 2 trial demonstrate that, by targeting the type I interferon receptor, anifrolumab reduced disease activity in patients with systemic lupus erythematosus.”

The study was published in NEJM.