Cardiac arrests in young people — what causes them and can they be prevented or treated? A heart expert explains


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Jessica Orchard, University of SydneyOn June 12, 16,000 spectators at Copenhagen’s Parken Stadium and millions of viewers around the world watched in shock as Danish midfielder Christian Eriksen’s heart stopped.

Late in the first half of Denmark’s opening game of the Euro 2020 soccer tournament against Finland, the 29 year-old was running just after a throw-in and suddenly collapsed. It appears he suffered a sudden cardiac arrest.

Fortunately, he was quickly attended to by a medical team with full resuscitation equipment, who administered CPR and successfully used a defibrillator. Erikson survived and has been fitted with an implantable cardiac defibrillator. This is a small device which is connected to the heart and fitted under the skin. If a dangerously abnormal rhythm is detected, it will deliver an electric shock to the heart to try to restore a normal rhythm.

So how often do cardiac arrests happen in young people? What are the risk factors, and can they be prevented?

Cardiac arrests during sport are extremely rare. If you’re playing sport next weekend, you should go ahead in the knowledge it’s almost certain not to happen. The benefits of exercise far outweigh the risks.

But because events like this do happen, albeit very rarely, we need public venues to have good emergency plans to improve survival, including the widespread availability of defibrillators.

There have been some recent improvements in this regard in Australia. For example, defibrillators are now installed in all Coles and Woolworths stores nationally, and there are several programs to support rollout of defibrillators and emergency action plans to community sports clubs. But there’s still room for improvement.

Am I at risk? How often does this happen?

Sudden death from cardiac arrest in a young person is a very rare but tragic outcome. The baseline risk in Australia for people under 35 is 1.3 per 100,000 people per year, with 15% occurring either during or immediately after exercise.

Across all ages, there are 20,000 sudden cardiac arrests in Australia that occur out of hospital every year, and sadly only 10% of people survive.

It’s also worth remembering a cardiac arrest isn’t exactly the same thing as a heart attack. A heart attack occurs when one of the coronary arteries is blocked, stopping blood supply to part of the heart. A cardiac arrest is when the heart stops pumping blood around the body, and can occur due to a heart attack or another cause.

The major causes of cardiac arrest depend on age. In people over 35, the vast majority are caused by coronary artery disease, where arteries supplying blood to the heart are blocked or damaged.

In people aged under 35, there’s no single major cause of cardiac arrest. Some of the conditions that can cause cardiac arrest in young people include:

However, 40% of sudden cardiac deaths in young people remain unexplained even after autopsy.

Is cardiac screening the answer?

Cardiac screening in young people looks for certain heart abnormalities that haven’t yet been detected. It’s common for elite and professional athletes in Australia and internationally, and is mandatory for young athletes in some countries, for example Italy and Israel.

This screening usually includes a “12-lead electrocardiogram” or ECG, which is a painless test that involves putting some sticky dots on the body and recording the electrical activity of the heart over a ten second period.

However, ECG screening cannot detect all of the conditions which can cause sudden cardiac arrests. This is because some conditions don’t show ECG abnormalities before a cardiac arrest.

Eriksen’s condition was likely in that category, because we know he had regular heart screenings while at Tottenham and these hadn’t shown any problems.

Medicare in Australia funds heart health checks for people who are middle aged or older, but not in younger people. This is similar to most countries. Other than in professional athletes and those with a family history, most professional bodies don’t recommend widespread screening of younger people because the risk of cardiac arrests is so low overall.

How else can we prevent sudden cardiac death? Defibrillators and data

The best strategy for preventing sudden cardiac death at any age is having defibrillators widely available. A defibrillator is a device that can analyse the heart’s rhythm and deliver an electric shock if needed. This can shock the heart back into a normal rhythm.

While they obviously can’t stop the cardiac arrest happening in the first place, they are crucial to survival once they do happen. Early access to a defibrillator can improve survival to almost 90%.

However, access needs to be very quick, ideally within 2-5 minutes, as we know the chances of survival drop by 10% for every minute of delay before defibrillation.

We also need as many as people as possible to be regularly trained to provide CPR.

Fabrice Muamba, a former midfielder for the Bolton Wanderers soccer team in the UK, was lucky to survive after he collapsed and his heart stopped on the field during a 2012 FA cup quarter-final.

Muamba, who recovered after he received CPR and 26 defibrillator shocks, last week voiced his support for defibrillators to be a legal requirement in public places in the UK. Ideally, Australia could also introduce a similar requirement to have defibrillators in public venues, supported by widespread CPR training (including how to use a defibrillator) to improve survival rates from out of hospital cardiac arrests.

In addition to defibrillators and CPR training, venues such as schools and sporting stadiums need to have good cardiac emergency plans so they can respond efficiently and effectively if someone’s heart stops.

Some of the conditions that are diagnosable prior to a cardiac arrest run in families, such as “Long QT syndrome”. So, it’s important to seek medical advice for anyone with a family member who has had cardiac arrest under the age of 40.




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Importantly, anyone who has any worrying symptoms should seek medical advice, especially fainting or collapse during exercise.

Finally, research projects such as the Australian End Unexplained Cardiac Death (EndUCD) registry are urgently needed to identify the underlying causes of cardiac death in young people so we can prevent deaths from sudden cardiac arrest.The Conversation

Jessica Orchard, Postdoctoral Fellow, Centenary Institute; and Adjunct Senior Lecturer, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Could a simple pill beat COVID-19? Pfizer is giving it a go


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Peter Wark, University of NewcastleWhile the focus has been largely on vaccines, you might have also heard Pfizer is trialling a pill to treat COVID-19.

It almost sounds too good to be true. Indeed, the results are very preliminary — but it’s a promising approach.

Where most antiviral agents we’ve tried to treat COVID-19 target the inflammatory and immune response resulting from infection, Pfizer’s pill directly targets SARS-CoV-2 — the virus itself.

Mounting our defence against the virus

Much of the illness associated with COVID-19 is due to the intense inflammatory and immune response that can occur with an infection. The most successful treatments so far have targeted this overzealous immune response.

Taken early in the disease, the inhaled corticosteroid budesonide has been shown to reduce the development of more severe disease.

In people hospitalised with COVID-19 requiring oxygen, the oral corticosteroid dexamethasone reduces the likelihood of death.

In the most severe cases — COVID patients admitted to ICU — the anti-inflammatory tocilizumab administered intravenously gives a person a better chance of survival.

But these treatments don’t target SARS-CoV-2 itself; just the consequences of infection. Directly targeting the virus has proven to be more difficult.




Read more:
Have Australian researchers developed an effective COVID-19 treatment? Potentially, but we need to wait for human trials


Targeting SARS-CoV-2

A virus like SARS-CoV-2 must enter a host cell to reproduce. It does this using its spike protein (a protein on the virus’ surface) to attach to the cell, and then it uses the cell’s own proteins to gain entry.

Once inside the cell, SARS-CoV-2 removes its outer coat and releases its viral RNA (ribonucleic acid, a type of genetic material). This acts as a template, allowing the virus to replicate, and then infect other cells. At any point of this life cycle the virus could be vulnerable to an intervention.

SARS-CoV-2 carries an enzyme, 3C-like protease (3CLpro), which plays a crucial role in the replication process. This protease is almost identical to the protease used by the SARS-CoV-1 (SARS) virus, and similar to the protease used by the Middle Eastern Respiratory Virus (MERS).

So a drug that could effectively target 3CLpro and prevent virus replication could be beneficial against multiple known coronaviruses, and possibly any that emerge in the future.

An illustration of SARS-CoV-2.
SARS-CoV-2 uses its spike protein to attatch to a host cell.
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Protease inhibitors have been successfully used to treat other viral infections, especially chronic infections such as HIV and hepatitis C.

They were put forward early in the pandemic as a possible treatment for COVID-19. But the HIV drug lopinavir-ritonavir was shown in two clinical trials to be ineffective, with drug levels probably too low to work against SARS-CoV-2. While a higher dose might be effective, it would also likely produce more side effects.

Scientists also proposed a repurposed antiviral drug, remdesevir, originally developed to treat Ebola. Remdesivir delays the ability of the virus to replicate its RNA.

Initial case reports appeared promising and saw the US Food and Drugs Administration approve the drug for emergency use. But the results of randomised controlled trials in hospitalised patients with severe COVID-19 were disappointing.

Although there was a reduction in duration of illness for patients who survived, it didn’t significantly reduce a person’s chance of dying.




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Of course, neither of these agents were designed specifically to target SARS-CoV-2. But in 2020, Pfizer/BioNtech identified a small molecule — PF-00835231 — that blocks the SARS-CoV-2 3CLpro protease. It was originally designed against SARS-CoV-1, but the enzyme in the two viruses is almost identical.

PF-00835231, both alone and in conjunction with remdesevir, appears to reduce the replication of a range of coronaviruses including SARS-CoV-2 in cells in the lab. It also reduced viral replication in a number of animal models, with no adverse safety signals. But it’s important to note this research hasn’t yet been peer reviewed.

What now?

Pfizer/BioNtech are taking two drugs to clinical trials for COVID-19: PF-07304814, an intravenous injection for use in patients hospitalised with severe COVID-19 and PF-07321332, an oral agent, or pill, that could potentially be used earlier in the disease. Both are formulations of a 3CLpro inhibitor.

These phase 1 trials, which began in March, represent the earliest stage of drug development. These trials select healthy volunteers and use different doses of the drugs to establish their safety. They also look at whether the drugs elicit sufficient responses in the body to indicate they could be effective against SARS-CoV-2.

The next step would be phase 2 or 3 trials to see if they improve outcomes in COVID-19. Usually this process takes years, but as the pandemic continues to rage globally, Pfizer says it will do this in a matter of months, if phase 1 trials are successful.




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The application of antiviral agents in acute COVID-19 has been difficult and unrewarding. Though results are at this stage preliminary, these agents by Pfizer/BioNtech are promising. They could be used early in disease, especially in people poorly protected by vaccination or in those who haven’t been vaccinated.

They could also be used as a means of prevention, to contain outbreaks in exposed people. They should be effective against all the SARS-CoV-2 variants of concern, as well as against other known and possibly emergent coronaviruses.

The Pfizer CEO’s recent suggestion the pill could be available by the end of the year is probably a long shot. But the pandemic has shown us what’s possible in the realm of swift scientific advances, and we’ll watch this space with interest.The Conversation

Peter Wark, Conjoint Professor, School of Medicine and Public Health, University of Newcastle

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Why the TGA should reschedule MDMA and psilocybin for the treatment of mental illness


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Sarah-Catherine Rodan, University of Sydney and Samuel Banister, University of SydneyThe Therapeutic Goods Administration (TGA) is considering rescheduling psilocybin and MDMA from their current classification as Schedule 9 prohibited substances to Schedule 8 controlled substances.

This would allow psychiatrists to use these drugs in combination with psychotherapy for the treatment of conditions such as depression and post-traumatic stress disorder (PTSD).

Here’s why we believe that would be a good idea.




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Mind molding psychedelic drugs could treat depression, and other mental illnesses


A bit of background

On February 3, the TGA announced an interim decision to retain psilocybin and MDMA as Schedule 9 drugs.

The TGA cited limited evidence of therapeutic benefit, safety concerns, potential for abuse, and lack of suitably trained psychiatrists.

But the final ruling, which was expected on April 22, has now been delayed while the TGA seek independent expert advice on the “therapeutic value, risks, and benefits to public health” of the change.

A man sits on the couch during a therapy session.
If MDMA and psilocybin are reclassified, they would be administered in a supervised environment.
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The case for MDMA and psilocybin

Research on psychedelic substances such as LSD and psilocybin first began in the 1960s.

The number of clinical trials involving psilocybin or MDMA has increased steadily in the past decade, with more than 70 studies completed since 2010.

Around 60 trials are underway in Europe and the United States involving MDMA or psilocybin.




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The results of completed studies are very promising.

For example, last month, a study of 59 patients with major depression showed just two sessions of psilocybin-assisted therapy was as effective as a six-week course of the antidepressant escitalopram. The proportion of patients who no longer qualified for a major depression diagnosis after treatment was twice as high in the psilocybin group.

This month saw results of one of the largest trials of MDMA-assisted psychotherapy for PTSD published. The phase 3 study used MDMA-assisted psychotherapy to treat 90 patients with severe, chronic PTSD. After three sessions, 67% of participants no longer qualified for a PTSD diagnosis, compared to just 32% of participants undergoing therapy alone.

These latest studies add to a growing number of trials from around the world showing the therapeutic benefit of psilocybin or MDMA in depression, PTSD, anxiety associated with terminal illness, obsessive-compulsive disorder, alcohol and tobacco dependence, and social anxiety in adults with autism.

Scientists are now investigating the use of psilocybin in other conditions for the first time, such as anorexia nervosa, general anxiety disorder, and opioid and cocaine dependence.

A woman appears unhappy.
Studies are showing MDMA and psilocybin can be effective in treating a variety of mental health problems.
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Are MDMA and psilocybin safe?

Unlike many Schedule 8 medicines, psilocybin- or MDMA-assisted psychotherapy treatments are not taken regularly. The substance is usually used just two or three times with trained specialists as part of a psychotherapy program.

Despite the safety concerns cited by the TGA, there haven’t been any serious adverse reported events due to psilocybin or MDMA from dozens of clinical trials. Less serious effects can include temporary anxiety, paranoia, fear, nausea, post-treatment headaches, or mild increases in blood pressure and heart rate.

Of course, these trials use pharmaceutical-grade drugs administered by a doctor.

However, one of the most comprehensive studies of the harms of commonly used illegal drugs found even illicit forms of psilocybin and MDMA are among the least harmful. In fact, “mushrooms” containing psilocybin had the lowest overall harm score, while illicit forms of clinically-used Schedule 8 substances like cocaine, cannabis and ketamine were all more harmful than psilocybin or MDMA.

We don’t know what dose of psilocybin would be lethal to humans, but it’s estimated to be about 1,000 times greater than the therapeutic dose. No overdose deaths due to psilocybin toxicity alone have ever been reported.

Use of illicitly manufactured MDMA — which often contains other drugs or impurities — has occasionally caused deaths. An estimated 600,000 Australians use illegal MDMA each year, and an average of about three deaths per year since 2000 have been associated with MDMA toxicity alone.

But illicit use of MDMA of unknown dose and purity is much more dangerous than administration of pharmaceutical MDMA under medical supervision in a clinical environment.

A growing field

In recent years, respected academic and medical institutions around the world have launched dedicated centres for psychedelic and MDMA research, including Johns Hopkins University and Imperial College London.

And research into the therapeutic effects of psilocybin and MDMA has recently started in Australia. St Vincent’s Hospital in Melbourne is conducting a clinical trial using psilocybin-assisted psychotherapy to treat anxiety and depression in terminally ill patients. A clinical trial at Monash University is looking at psilocybin-assisted psychotherapy for generalised anxiety disorder and MDMA-assisted psychotherapy for PTSD.

The Australian government recently announced A$15 million in funding for research into the medical potential of psychedelics and MDMA.




Read more:
Psychedelics to treat mental illness? Australian researchers are giving it a go


It’s hard to reconcile the TGA’s interim decision to retain Schedule 9 for substances with demonstrated benefit in several mental health conditions and fewer safety concerns than many existing Schedule 8 medicines.

The US medicines regulator recently granted MDMA and psilocybin “breakthrough therapy” designation; a special status for highly promising drugs that speeds up their path to the clinic.

The down-scheduling of psilocybin and MDMA could have enormous medical benefit for Australian patients, especially when Australia spent A$10.6 billion on mental health between 2018-2019.The Conversation

Sarah-Catherine Rodan, PhD candidate, University of Sydney and Samuel Banister, Team Leader in Medicinal Chemistry, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Have Australian researchers developed an effective COVID-19 treatment? Potentially, but we need to wait for human trials


Nial Wheate, University of SydneyThe world is now 18 months into the COVID-19 pandemic and we’ve yet to find a single drug that can stop the virus. At best, we can treat the effects of the virus through oxygen therapy for those who can’t breathe, and with drugs that reduce the inflammation associated with the infection.




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But an Australian-United States research team, led by Griffith University’s Menzies Health Institute, have shown promising results in their mouse trials of a new treatment for COVID-19.

The technology is based on “short interfering RNA”, which prevents the virus from replicating inside human cells. They found a 99.9% drop in the number of virus particles in the mice they studied.

The researchers hypothesise the drug could be injected into patients daily for up to five days, for example for sick patients in hospital, or as a once-off if someone has just been exposed to the coronavirus; however, there’s no data on this specifically, so it’s speculative for now.

While the results are very promising, the technology has only been tested in mice. Human clinical trials will take some time to complete before we know whether a drug will be approved by the government.

 

How viruses work

Viruses are tricky to treat because they are biological molecules made of the same types of materials as the human body. Virus particles are just packets of information on how to make more virus, encoded in a molecule called “ribonucleic acid” or RNA (although some contain DNA instead) within a protein coating.




Read more:
Explainer: what is RNA?


Once a virus particle penetrates into a cell, it either hijacks the machinery of the cell to make copies of itself, or in some cases, has its RNA copied into the host cell’s DNA. Either way, the cell becomes a manufacturing facility making hundreds and thousands of copies of the virus.

So the best way to stop a virus is to stop its RNA information being copied and transcribed by the cell.

We already have drugs capable of doing this for specific viruses. A drug called PrEP (pre-exposure prophylaxis) is available as a prophylactic against infection with HIV and the development of AIDS. A prophylactic can prevent a disease before it takes hold in the body.

The PrEP medicine works because the two active ingredients it contains, tenofovir and emtricitabine, block a molecule called reverse transcriptase which the virus needs to be replicated. Unfortunately, neither drug works to block COVID-19.

Short interfering RNA

Unlike PrEP, the new technology is particularly clever because it uses a molecule called short/small interfering RNA or “siRNA” to prevent the reading and copying of the virus information. This siRNA was specifically designed to recognise a sequence of the coronavirus’ own RNA that is common across COVID-variants.

This means the siRNA can seek out and lock onto the viral RNA because it perfectly complements it, regardless of the COVID-19 strain. When it locks with the virus RNA, the viral information becomes trapped and can’t be copied, or it causes the RNA to be cut and degraded.

At this point there is no virus production, and our immune system can just mop up the small number of virus particles floating around the body.




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To prove their technology, the researchers enclosed their siRNA in lipid nanoparticles, which are essentially tiny fat-like particles. Without this protective coating, the siRNA would be destroyed in the blood stream before it could lock onto the virus. Lipid nanoparticles are also used in the formulation of the Pfizer and Moderna COVID-19 vaccines.

With the protective nanoparticle shell, the siRNA could then be delivered via a water-based injection into veins.

When the researchers administered the siRNA to mice that had been infected with COVID-19, they found the mice didn’t lose as much weight when compared with untreated mice. Weight loss was an indicator of how sick the mice were.

The researchers also found a 99.9% drop in the number of virus particles in the mice.

On occasion, when biological molecules are injected into the blood stream, this can trigger a severe allergic reaction called anaphylaxis. Importantly, the researchers found their siRNA didn’t trigger an immune response in the mice, and therefore will be unlikely to cause anaphylaxis.

So as well as being effective, the technology appears to be relatively safe.

Will this drug be available soon?

As promising as the results are, we shouldn’t get our hopes up that a drug will be available any time soon. Data derived from animal tests doesn’t always translate to success in humans. Often, the way an animal’s body processes a drug can be different from the human body, and it ends up being ineffective.

Also, animal tests are just the first step in a long regulatory process to prove a drug works and is safe. Even with accelerated clinical trials and fast-tracked assessment from governments, an approved drug is still a year or more away.




Read more:
Of mice and men: why animal trial results don’t always translate to humans


Correction: a previous version of this article stated that HIV needed reverse transcriptase to embed the RNA information into human DNA. We’ve amended it to say HIV needs reverse transcriptase to be replicated.The Conversation

Nial Wheate, Associate Professor of the Sydney Pharmacy School, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

How to treat sunburn pain, according to skin experts


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Katie Lee, The University of Queensland and Monika Janda, The University of Queensland

So you’re one of the 21% of Australians who got sunburnt last weekend.

While we should be avoiding sunburn, it’s sometimes easier said than done in the Australian sun.

What can you do once you realise you’re turning into a temporary lobster?

First, the bad news

Once you’re sunburnt, you can’t undo the damage to your DNA and skin structures, and you can’t speed up skin healing. You can only treat the symptoms.

Sunburn is a radiation burn caused by too much exposure to ultraviolet (UV) rays, causing extensive damage to the DNA in your skin. When your skin’s DNA monitoring and repair system judges there’s too much damage to fix, it flags the cells for destruction and calls in the immune system to finish the job.

The immune cells and extra fluid squeezing into the skin cause the swelling, redness, heat and pain we know as sunburn. Blisters develop when whole sheets of cells die and lift away, and fluid fills in the space below. Later, dry peeling results when large sheets of dead cells peel off to make way for fresh ones.

Skin peeling, also called desquamation, after a sunburn.
By the time you get to skin peeling, or ‘desquamation’, your sunburn is almost completely healed.
Rjelves/Wikimedia Commons, CC BY-SA



Read more:
Explainer: what happens to your skin when you get sunburnt?


However, while your skin does its thing, you can manage the symptoms and make yourself more comfortable.

Step 1: Prevent further damage and assess your burn

First, get out of the sun until the redness and pain have subsided, even if this takes several days. The full effects of a sunburn can take up to three days to develop, and further UV exposure will only compound the damage.

Next, assess whether to seek medical help. Severe cases can involve second-degree burns, which disrupt the lower layer of skin, the dermis, and stop the skin from regulating fluid loss effectively. If you have a second-degree burn across a large area of you body, complications can include electrolyte imbalances due to large amounts of fluid loss, or shock, also due to extreme fluid loss. Secondary infections are also possible since the upper layer of skin is no longer acting as a tough barrier to germs. You should definitely see a doctor if you:

  • have large areas of blistered skin, especially on the face

  • have severe swelling

  • can’t manage the pain with over-the-counter painkillers

  • experience fevers, chills, nausea, dizziness or confusion.

Blistered sunburn in children needs immediate attention from your GP.

A severely sunburnt, swollen hand with a pale patch where the skin was protected by a watch.
Swollen sunburn means you need to see a doctor.
Uddey/Wikimedia Commons, CC BY-SA

Step 2: Ease the suffering

As with a thermal burn, water is your friend. Drink plenty to correct any dehydration from being in the sun too long and replenish the fluid being drawn into your skin. Cool baths, showers or damp cloths ease the sensation of heat and can be used as often as you like throughout the day. Avoid putting ice on a sunburn, as this can make matters worse by causing intense vasoconstriction, where blood vessels narrow sharply and cut off local blood supply to already damaged skin.

Moisturising lotions can also help soothe by keeping moisture in, but avoid skin-numbing creams unless prescribed by your doctor. Any water-based moisturiser should do, including aloe vera gel.

Despite its popularity as a home remedy, there’s surprisingly little research on aloe vera for sunburn specifically. There’s promising data for its use in wound healing, but many studies investigated aloe extracts taken orally, rather than gel on the skin. In any case, a commercial aloe vera gel won’t do you any harm if you find it soothing. However, gel straight from the plant in your garden comes with a risk of soil-borne infections in skin that’s already damaged (warning: gruesome pictures in that link).

Over-the-counter painkillers like ibuprofen or paracetamol can take the sting out of your sunburn and help you rest more comfortably. If your skin is very itchy, try an antihistamine. US guidelines also often suggest low-dose (0.5-1%) hydrocortisone cream; there’s not much evidence for its effectiveness, but it also won’t hurt you to try it for a few days.

If you have blisters, try not to pop them as that exposes the damaged skin underneath to infection; cover them up with a wound dressing if you’re tempted.

While none of these remedies will fix the damage in the way antibiotics fix an infection, they will make you more comfortable while your skin gets on with healing itself.




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Monday’s medical myth: we’re not getting enough sun


Step 3: Make a plan

While you’re stuck inside, pinpoint how you got burnt and how you might prevent it next time. Most sunburn happens when you did not expect to be outdoors for long, or when you thought sunburn was unlikely because the weather was cool, windy or cloudy. UV radiation is still present in these conditions, but you don’t have the benefit of feeling hot to remind you to get out of the sun.

A man's sunburnt feet with white lines showing where the skin was protected by his thong straps.
Did you forget to put sunscreen on a section of your body?
Charlie Brewer/Wikimedia Commons, CC BY-SA

Here are a few familiar scenarios:

  • got burnt when you unexpectedly had to park 10 minutes’ walk away? Apply sunscreen as part of your daily routine whenever the UV index will be 3 or over. This will protect you from these sneaky sunburns and also from sub-sunburn levels of UV damage. Don’t worry — there’s no evidence wearing sunscreen every day will make you vitamin D deficient or cause a toxic build-up of chemicals in your body

  • arrived at the cricket and realised you left your hat or sunscreen at home? Many venues offer free sunscreen, so ask at the check-in or the health and safety officer

  • coming in from the beach, garden or bike ride just a bit too late? Sunscreen won’t protect you all day, so make sun-protective clothes part of your regular attire — a rashie, long-sleeved shirt, or UV-protective armguards and leggings

  • got to the park BBQ when all the shady spots were taken? Arrange your next outing to avoid the most UV-intense middle of the day. The SunSmart app or Bureau of Meteorology weather report will tell you the UV forecast and when you need sun protection

  • forgot to reapply sunscreen? Set an alarm on your phone next time to remind you.

The more you practise this kind of thinking, the easier it will become.The Conversation

A screenshot of the SunSmart app showing the UV forecast for Brisbane and recommending sun protection between 7:30am and 3:20pm.
The SunSmart app will tell you when you need to use sun protection based on your location.
SunSmart app

Katie Lee, Research assistant, The University of Queensland and Monika Janda, Professor in Behavioural Science, The University of Queensland

This article is republished from The Conversation under a Creative Commons license. Read the original article.

COVID changed the way we use drugs and alcohol — now it’s time to properly invest in treatment



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Nicole Lee, Curtin University

During crises and disasters, alcohol and other drug use often changes. But the changes are not straightforward and impacts may be different for different groups of people.

There doesn’t seem to have been significant overall increases or decreases in alcohol or other drug use during the COVID-19 pandemic, but some groups are at increased risk. And access to treatment is more limited for those who need it.

It’s a complex picture

There’s a bit of data around, but the picture is still not quite clear.
As researchers from the Centre for Alcohol Policy Research at La Trobe University have argued in an editorial published today, we need more research to understand the influence of the pandemic on use.

There were some early indicators of increases in Australians’ alcohol consumption as the pandemic hit, possibly related to increased stress. But that effect seemed to reduce as we settled into the new normal.

At the beginning of COVID-19 restrictions in March, Commonwealth Bank reported spending had increased on alcohol, but this was then reversed in April.

And in April, a study by the Foundation for Alcohol Research and Education found that most people who had stockpiled alcohol reported drinking more. Also around the same time, Australian Bureau of Statistics data showed more people had increased their drinking (14.4%) than had decreased it (9.5%).

By May, the Australian National University found more people had decreased their drinking (27%) than had increased it (20%). The Global Drug Survey between May and June found similar results among the mostly young people who responded.

However, alcohol use seemed to increase among some groups, possibly those who are more vulnerable to harms.




Read more:
Worried about your drinking during lockdown? These 8 signs might indicate a problem


In both the ABS and ANU studies, more women had increased their drinking than decreased it, which seemed to be related to higher stress linked to increased responsibilities at home.

In a survey of people who use illicit drugs, more people increased (41%) than decreased (33%) drinking. And among people who inject drugs around 11% reported increased drinking.

There have also been indicators that family violence has increased during this time. Alcohol and other drug use is a risk factor for family violence.

We need more data about heavy drug use

Since the onset of the pandemic, two studies found cannabis use had increased but other drug use had decreased or was stable. The respondents were mostly young, used for recreational purposes and were not dependent nor did they have serious problems.

Reductions in use of drugs like MDMA and cocaine, which are associated with festivals and parties, are not surprising since these large events have been restricted for months.

Two studies suggested cannabis use was on the rise, but we still need more and better data on how the pandemic has impacted heavy users.
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Most of the research hasn’t involved people who are heavy or dependent users, so we don’t know much about changes in use in these groups.

One study of people who inject drugs (who tend to use more regularly) reported some changes to availability and purity of some drugs, and small changes in use, but again some people increased and some decreased their use.

With physical distancing and lockdowns, it’s likely more people used alone or with fewer people. This means if anything goes wrong, help is further away.

Telehealth for drug treatment?

A survey of treatment services found that among services that reported changes in demand, most had an increase. Most services also reported that mental health problems, family violence and financial stress had all increased among people who use their services. These factors can make treatment more complex.

There is some evidence fewer people accessed medication treatment for opioids during the restrictions, like methadone.

COVID-19 restrictions have changed the way many services offer treatment. Most residential rehabilitation services have reduced the number of places available so they can ensure physical distancing.

Many treatment services are reporting increased demand.
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Before COVID-19 there were already long waiting lists for residential rehabilitation, so with more than 70% of services reporting reduced capacity, people may have found it harder to access residential treatment.

Non-residential services (like counselling or day programs) haven’t significantly reduced the number of people they see, and most have partially or fully moved to telehealth.

As a result, around 35% of services said fewer people missed appointments. This might be due to the easier access telehealth provides, including the reduced travel time.

However, around 25% of services said more people missed appointments. Anecdotal interviews suggest some of this might be due to difficulty transitioning to online appointments. One person said: “I know they are on Zoom but I don’t know how to use it”.

These adaptations are more complex than they appear. The time and effort required for services to make significant changes takes time away from providing treatment.

The move to telehealth is a significant one, requiring additional hardware and software, training of staff, and help for people who use the service to work out how to use the technology. Things like ensuring confidentiality can be more difficult when someone is receiving counselling at home with family around, for example.

Piecemeal funding for treatment services

The alcohol and other drug sector was already significantly under-resourced and struggling to meet existing demand before COVID-19.

In April, federal health minister Greg Hunt announced A$6 million in funding for alcohol and other drug services. Just over half of this was allocated to three organisations to increase online access to support services. The rest went to information and awareness campaigns. But no funds were set aside for existing treatment services to make COVID-19 related changes to their services.

Various state governments have allocated some funding to support alcohol and other drug services to adjust to COVID-19:

  • Tasmania released a total of A$450,000 to help services transition to telehealth

  • Western Australia allocated a total of A$350,000 for specialist alcohol and other drug services to maintain services amid the pandemic

  • Victoria and South Australia announced additional support to help people access medication treatment.

Further funding is needed to ensure services can continue to provide COVID-safe services.

It’s important for people who use alcohol and other drugs, and for the public, that alcohol and other drug treatment is well-supported to continue to operate during these changes. We know treatment is cost-effective, reduces crime and increases participation in the community. For every dollar invested in drug treatment, $7 is saved to the community.

Getting help

If you’re worried about your own or someone else’s alcohol or other drug use, you can get help by phoning the National Alcohol and Other Drug Hotline on 1800 250 015.

You can also access support online through CounsellingOnline, Hello Sunday Morning and SMART Recovery.

You may also be eligible to access one of the new telehealth services. Talk to your GP to find out more.The Conversation

Nicole Lee, Professor at the National Drug Research Institute (Melbourne), Curtin University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The evidence is in. WHO says corticosteroids really do save lives of people critically ill with COVID-19



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Andrew McLachlan, University of Sydney

Readily available drugs, which dampen the runaway inflammatory response in patients severely ill with COVID-19, save lives, according to evidence released this week.

An analysis by the World Health Organisation (WHO), which drew together results from several studies, confirms the benefit of this group of anti-inflammatory steroid drugs, known as corticosteroids.

While earlier studies showed the apparent benefit of one of these drugs, dexamethasone, this latest evidence goes further.

It shows other cheap and readily available corticosteroid drugs, including hydrocortisone, could benefit patients at the life-threatening stages of coronavirus infection.

Remind me again, what are corticosteroids?

Corticosteroids have been used for decades to treat a variety of inflammatory conditions. These include severe forms of lung inflammation, such as pneumonia, shock due to infection, and severe respiratory syndromes. They are also used to treat more common conditions, including asthma and eczema.

These medicines are on the WHO list of essential medicines, meaning they are widely available (usually at low cost).




Read more:
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What do we already know about corticosteroids for COVID-19?

In June, early release of results from the RECOVERY trial showed dexamethasone reduced the risk of death by up to a third in people hospitalised with COVID-19 who needed a ventilator to help them breathe.

Results of the dexamethasone trial were released early.

Despite the early release of the trial results, and limited details at the time, the findings were compelling and clinical practice changed.

Several other trials were stopped. All patients switched to receive active treatment with a corticosteroid.

The results of the RECOVERY trial have since been formally peer reviewed and published.




Read more:
Dexamethasone: the cheap, old and boring drug that’s a potential coronavirus treatment


What does the latest evidence say?

The WHO drew together results from seven randomised clinical trials, including data from 1,703 critically ill patients with COVID-19.

This is a powerful and compelling way to combine information and truly address the question of whether these medicines benefit people in hospital critically unwell with COVID-19.




Read more:
ICU ventilators: what they are, how they work and why it’s hard to make more


The study, which included patients from Australia and New Zealand, found almost 33% of people treated with corticosteroids died within 28 days of treatment. This was compared with 41% of patients who received supportive care (or placebo). Corticosteroid treatment helped patients whether or not they needed ventilation or oxygen.

Importantly, the analysis also concluded the benefits were not specific to one corticosteroid drug but were the same for dexamethasone and hydrocortisone.

Corticosteroids can also have an impact on the immune system. So the researchers looked at the risk of infection from other causes, for example bacterial pneumonia, and found it was not a major concern.

What does this mean for patients?

The weight of evidence has led WHO guidelines this week to strongly recommend using corticosteroids to treat people with severe or critical COVID-19.

This aligns with current Australian guidelines for treating hospitalised patients with COVID-19 needing oxygen support.

Corticosteroids are not for everyone and are not a cure

It is important to remember these findings only apply to using corticosteroids in critically ill people hospitalised with COVID-19. There is currently limited information to suggest these medicines are appropriate for people with mild COVID-19.

While corticosteroids help treat the body’s response to the coronavirus infection, they are not antiviral drugs. They do not inhibit the virus itself, so they are not a cure.




Read more:
In the fight against coronavirus, antivirals are as important as a vaccine. Here’s where the science is up to


A new way of doing research

Usually, several clinical trials on a common theme are published over a series of years. Then a meta-analysis draws together their results, publishing these combined results much later.

But the amazing thing about this latest evidence is the meta-analysis included data from clinical trials published at the same time. This shows a degree of co-operation and collaboration between researchers to share data to urgently address important research questions that guide clinical care.

Evidence to guide the best treatments and management for people with COVID-19 continues to emerge. You can follow the evidence and how it’s applied in Australia here.




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Ivermectin is still not a miracle cure for COVID-19, despite what you may have read


The Conversation


Andrew McLachlan, Head of School and Dean of Pharmacy, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Multiple sclerosis drug may help treat COVID-19 and lead to faster recovery



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Nial Wheate, University of Sydney and Elise Schubert, University of Sydney

What do multiple sclerosis (MS) and the novel coronavirus have in common? Until this week, not much, but a recent clinical trial has shown a reformulation of a drug used to treat MS can potentially also be used to help patients infected with COVID-19.

SNG001 is an inhaled form of a drug called interferon-beta under development by the UK pharmaceutical company Synairgen. Interferon is normally prescribed for the treatment of symptoms relating to relapsing-remitting MS.

But the clinical trial, Synairgen found that when SNG001 was given to patients with COVID-19, it stopped the development of more severe symptoms, accelerated their recovery, and allowed them to leave hospital earlier.




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Like other clinical trials for COVID-19 treatments, the results still need to be thoroughly checked before SNG001 is included as a standard treatment for coronavirus. The drug’s key risks (potential for severe depression) also need to be weighed against the potential benefits.

How does it work?

MS is a condition of the central nervous system. The nerve impulses between the brain and spinal cord get blocked or mixed up. It happens because the body’s immune system attacks the protective layers around nerve fibres. The result is a loss of muscle control and balance.

In contrast, COVID-19 is a viral infection that affects a patient’s ability to breathe due to inflammation putting pressure on their lungs.

What both diseases have in common is the activation of the body’s immune response, so a drug that modulates the immune system for one can potentially work for the other.

Interferon-beta (interferon), a naturally occurring protein in the body, is used as an immunotherapy drug to combat relapsing-remitting MS by reducing inflammation and easing the symptoms of the disease.

Scientists at Synairgen hypothesised it could also treat COVID-19 through initiating the body’s antiviral response and potentially reducing inflammation on the lungs.

It is believed some at-risk patient groups cannot produce interferon as effectively as other people, reducing their ability to fight the virus and resulting in more severe symptoms.

So giving those patients interferon, in theory, should help them fight the virus, alleviate their symptoms, and improve survival rates.

Take a breath

For the treatment of MS, interferon is given as a weekly injection into muscle tissue.

The SNG001 drug developed by Synairgen contains the same interferon therapy used for MS, but formulated as an inhaled product.

Originally, the company was developing SNG001 as a treatment for a different type of lung condition called chronic obstructive pulomary diease (COPD), but it saw the direct potential for COVID-19 as well.

Instead of an injection, SNG001 is given to patients via a nebuliser, a machine that transforms a water solution of interferon into a fine mist that can be breathed in by patients through a face mask.

Promising results, so far

Between March and May this year, Synairgen sponsored a clinical trial at University Hospital Southampton to test SNG001 for COVID-19 patients. Those eligible for the trial only needed to have mild symptoms of COVID-19.

Other clinical trials conducted in the past for different drugs, such as remdesivir and dexamethasone, required patients to be hospitalised before they were eligible for drug treatment.

In total, 101 patients in a hospital setting were enrolled in the SNG001 trial and were given the drug daily for 14 days. Compared with a placebo, those given SNG001 had a 79% lower risk of developing severe disease.

Patients given the drug were also twice as likely to recover from their infection and were discharged earlier from hospital than those given the placebo.

Before SNG001 becomes standard care for COVID-19 treatment the results of the clinical trial need to be checked by independent scientists.

In the past, trial results for hydroxychloroquine did not stand up to scrutiny after they were announced and the results were subsequently retracted by the research team.

The risks and benefits

If the latest results are shown to be reliable, before doctors decide to make SNG001 a part of the standard treatment for hospitalised COVID-19 patients they will need to weigh its benefits against the potential risks.

One of the most important side effects of the drugs is that it can induce depression.

As a result, interferon is used with caution in patients with pre-existing depression or who have suicidal thoughts. These conditions may already be heightened by the pandemic if a potential patient for the drug has lost their job or they are not dealing well with the isolation of social distancing.

This means doctors would need to undertake a comprehensive mental health screen of all patients they consider for SNG001 treatment.




Read more:
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Other side effects relevant to interferon are that it can worsen seizure disorders or heart failures. So again, it needs to be used with caution in these patient groups.

The results of the SNG001 trial are very promising and potentially give us a treatment to prevent those people mildly infected with COVID-19 from developing more severe symptoms and needing hospitalisation.

But the results need to be checked by independent scientists first, and the drug’s benefits need to be weighed against its risk, as the ability to induce severe depression could cause a wave of mental health problems that make matters worse rather than better.The Conversation

Nial Wheate, Associate Professor | Program Director, Undergraduate Pharmacy, University of Sydney and Elise Schubert, Pharmacist and PhD Candidate, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Alzheimer’s disease: protective gene uncovered in human cell model – bringing promise for new drug discoveries



Our method could someday potentially detect the disease before it starts developing in a person’s brain.
Robert Kneschke/ Shutterstock

Dean Nizetic, Queen Mary University of London

Every three seconds, someone in the world develops dementia. The most common form of dementia is Alzheimer’s disease. While researchers have identified a number of risk factors that are linked to dementia – including genetics, smoking, and high blood pressure – there is currently still no cure.

Part of the reason for this is because of how complicated it is to test potential Alzheimer’s drugs. In order to conduct clinical trials participants need to have symptoms. But by the time symptoms appear, it’s usually too late for treatments to have a large effect as many of their brain cells have already died.

But our latest research developed a new human cell model that is able to rapidly simulate the development of Alzheimer’s disease in the lab. This allowed us to identify a gene, called BACE2, that is naturally able to suppress the signs of Alzheimer’s disease in human brain cells. Our research is the result of around five years’ work, and was the collaborative effort of teams based in London, Singapore, Sweden and Croatia.

Researchers already know a lot about which genes cause Alzheimer’s disease or make someone more likely to develop it. These genes contribute to certain toxic proteins accumulating in the human brain. So our team thought that the opposite must also be true: our brain cells must also have proteins that can naturally slow down the development of Alzheimer’s.

One gene that can definitely cause Alzheimer’s disease is a gene found on the 21st pair of human chromosomes that is responsible for making the amyloid precursor protein (APP). Research shows that 100% of people born with just one extra copy of the APP gene (called “DupAPP”) will develop dementia by age 60.

People with Down’s syndrome are born with three copies of APP because they have a third 21st chromosome. But by age 60, only 60% of them will develop clinical dementia. We wanted to know why some people with Down’s syndrome have delayed development of – or never develop – Alzheimer’s dementia compared to those who have one extra DupAPP gene.

The simple answer for this is because they have an extra dose of all other genes located in chromosome 21. We believed that there could be some dose-sensitive genes on chromosome 21 that, when triplicated, protect against Alzheimer’s disease by counteracting the effects of the third APP gene.

These genes must then appear to delay the onset of clinical dementia in some people with Down’s syndrome by approximately 20 years. Studies have even shown that any future drug able to delay dementia onset by just five years would reduce the prevalence of Alzheimer’s in the general population by half.

We re-programmed cells, turning them into brain cells.
arrideo/ Shutterstock

To study the potential of the extra genes, we took hair follicle cells from people with Down’s syndrome and re-programmed the cells to become like stem cells. This allowed us to turn them into brain cells in a Petri dish.

We then grew them into 3D balls of cells that imitated the tissue of the grey matter (cortex) of the human brain. The 3D nature of the culturing allowed misfolded and toxic proteins to accumulate, which are crucial changes that lead to Alzheimer’s disease in the brain.

We found all three major signs of Alzheimer’s disease (plaque build-up in the brain, misfolded “tau” proteins and dying brain neurons) in cell cultures from 71% of people with Down’s syndrome who donated samples. This proportion was similar to the percentage of clinical dementia among adults with Down’s syndrome.

We were also able to use CRISPR – a technology that allows researchers to alter DNA sequences and modify a gene’s function – to reduce the number of BACE2 genes from three copies to two copies on chromosome 21. This was only done in cases where there were no indications of Alzheimer’s disease in our cellular model. Surprisingly, reducing the number of BACE2 genes on chromosome 21 provoked signs of the disease. This strongly suggest that having extra copies of a normal BACE2 gene could prevent Alzheimer’s.

The protective action of BACE2 reduces the levels of toxic amyloid proteins. This was verified in our cellular models, as well as in cerebrospinal fluid and post-mortem brain tissue from people with Down’s syndrome.

Our study provides proof that natural Alzheimer’s-preventing genes exist, and now we have a system to detect new potential protective genes. Importantly, recent research showed the protective action of BACE2 might also be relevant to people who don’t have Down’s syndrome.

Our results also show that all three signs of Alzheimer’s disease can be potentially detected in cells from live donors. Though this requires a lot more research, it means we may be able to develop tests that identify which people are at higher risk of Alzheimer’s disease by looking at their cells.

This would allow us to detect the disease before it starts developing in a person’s brain, and could make it possible to design personalised preventative treatments. However, we are still a long way from reaching this goal.

Most importantly, our work shows that all three signs of Alzheimer’s disease detected using our model could be prevented by drugs known to inhibit the production of the toxic amyloid protein – and this can be detected in as little as six weeks in the lab. We hope our discovery could lead to the development of new drugs aimed at delaying or preventing Alzheimer’s disease, before it causes brain cell death.The Conversation

Dean Nizetic, Professor of Cellular and Molecular Biology, Queen Mary University of London

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Dexamethasone: the cheap, old and boring drug that’s a potential coronavirus treatment




Nial Wheate, University of Sydney

First, we tried the antimalarial drug hydroxychloroquine. Then we tested the antiviral drug remdesivir. But new UK research gives the strongest indication yet we may have found a useful treatment for COVID-19.

This time it’s an old anti-inflammatory drug, dexamethasone, which has been described as cheap, old and boring.

Preliminary results from a clinical trial just released indicate the drug seems to reduce your chance of dying from COVID-19 if you’re in hospital and need oxygen or a machine to help you breathe.

The results were significant enough for the UK to recommend its use for severe COVID-19.

Before we roll it out in Australia, we need to balance the drug’s risks with its benefits after peer-review of the full trial data.

What is dexamethasone?

Dexamethasone has been used since the late 1950s, so doctors are familiar with it. It’s also inexpensive, with a packet of 30 tablets costing around A$22 (for general patients) under Australia’s Pharmaceutical Benefits Scheme.

So if it does work for COVID-19, this cheap and boring drug, already available in Australia with a prescription, would be easy to add to current treatments.

Dexamethasone belongs to a class of drugs known as corticosteroids and is used to treat a range of conditions related to inflammation. These include severe allergies, some types of nausea and vomiting, arthritis, swelling of the brain and spinal cord, severe asthma, and for breathing difficulties in newborn babies.

And it’s dexamethasone’s application to those latter two respiratory conditions that prompted doctors to think it may also help patients severely affected by COVID-19.




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ICU ventilators: what they are, how they work and why it’s hard to make more


What did the trial find?

The recently reported results come from the Randomised Evaluation of COVID-19 Therapy, or RECOVERY, trial.

The researchers put patients into one of three groups: those needing ventilation (a machine that helps them breath); those who just needed oxygen therapy; and those who needed no treatment to help them breathe.

Patients in each of those groups were given dexamethasone (6mg once a day, either as a tablet or via intravenous injection), for ten days. A fourth group (a control group) was not given the drug.

Dexamethasone was most useful for the ventilated patients; deaths for this group dropped by about one-third with drug treatment. In contrast, deaths only dropped by one-fifth for those patients who were only receiving oxygen therapy. There was no benefit to patients who could breathe normally.

Results of the dexamethasone trial have just been released.

The researchers calculated that giving dexamethasone to eight ventilated patients would prevent one from dying, on average. And giving it to around 25 patients needing oxygen alone would prevent one death.




Read more:
The fascinating history of clinical trials


How might dexamethasone work for COVID-19?

When a patient has severe COVID-19, their immune system ramps up to catch and control the virus in the lungs.

In doing this, their body produces more infection-fighting white blood cells. This results in inflammation and pressure on their lungs, making it very difficult for them to breath.

It’s therefore likely dexamethasone reduces this inflammation, and so reduces pressure on the lungs.




Read more:
How does coronavirus kill?


What are the downsides?

There are potential complications with using dexamethasone.

First, dexamethasone also suppresses the immune system when it reduces inflammation. So, it’s not usually recommended for people who are sick, or could be sick, from other infections. So doctors will need to make sure patients have no other infections before they are prescribed the drug.

If the results of this trial are correct though, the drug doesn’t appear to compromise the patient’s ability to fight COVID-19; it might just affect their ability to fight off other diseases.

Second, the drug is only useful for patients with difficulty breathing and needing some assistance either through ventilation in a hospital or from oxygen therapy.

There appears to be no benefit for patients who don’t need help breathing. So we shouldn’t be giving it to everyone who tests positive to the virus.




Read more:
In the fight against coronavirus, antivirals are as important as a vaccine. Here’s where the science is up to


Third, like all drugs, dexamethasone has side effects that need to be monitored. Serious, but rare ones include: severe stomach or intestinal pain, sudden changes with vision, fits, significant psychiatric or personality changes, severe dizziness, fainting, weakness and chest pain or irregular heartbeat, and swelling of the face, lips, mouth, tongue or throat, which may cause difficulty in swallowing or breathing.

What happens next?

The results of the clinical trial are preliminary. So we need to wait for the full study data and scientific peer-review before we can make a definitive decision as to whether dexamethasone treatment is a worthwhile, and safe, addition to COVID-19 therapy in Australia.




Read more:
What if the vaccine or drugs don’t save us? Plan B for coronavirus means research on alternatives is urgently needed


The Conversation


Nial Wheate, Associate Professor | Program Director, Undergraduate Pharmacy, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.