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The disease-resistant patients exposing Covid-19’s weak spots – BBC News

Posted: February 25, 2021 at 1:32 am

There are some clues already. Researchers have identified an association between type O and rhesus negative blood groups, and a lower risk of severe disease. But while scientists have hypothesised that people with certain blood types may naturally have antibodies capable of recognising some aspect of the virus, the precise nature of the link remains unclear.

But Bobe is far from the only scientist attempting to tease apart what makes Covid-19 outliers unique. Mayana Zatz, director of the Human Genome Research Centre at the University of So Paulo has identified 100 couples, where one person got Covid-19 but their partner was not infected. Her team is now studying them in the hope of identifying genetic markers of resilience. "The idea is to try and find why some people who are heavily exposed to the virus do not develop Covid-19 and remain serum negative with no antibodies," she says. "We found out that this is apparently relatively common. We received about 1,000 emails of people saying that they were in this situation."

Zatz is also analysing the genomes of 12 centenarians who have only been mildly affected by the coronavirus, including one 114-year-old woman in Recife who she believes to be the oldest person in the world to have recovered from Covid-19. While Covid-19 has been particularly deadly to the older generations, elderly people who are remarkably resistant could offer clues for new ways to help the vulnerable survive future pandemics.

But while cases of remarkable resilience are particularly eye-catching for some geneticists, others are much more interested in outliers at the other end of the spectrum. Over the past couple of months, studies of these patients have already yielded key insights into exactly why the Sars-CoV-2 virus can be so deadly.

Disrupting the body's alarm system

Last summer, Qian Zhang had arrived for a dental appointment when her dentist turned to her and asked, "How come some people end up in intensive care with Covid-19, while my sister got it and didn't even know she was positive?"

As a geneticist working at The Rockefeller University, New York, it was a question that Zhang was particularly well equipped to answer. Over the past 20 years, Rockefeller scientists have probed the human genome for clues as to why some people become unexpectedly and severely ill when infected by common viruses ranging from herpes to influenza. "In every infectious disease we've looked at, you can always find outliers who become severely ill, because they have genetic mutations which make them susceptible," says Zhang.

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Study finds 20% of people are genetically resilient to the cold – Canadian Running Magazine

Posted: at 1:32 am

Have you ever wondered why some people can walk out in a t-shirt when its -15 C while others start shivering as soon as the temperature drops into the single digits? A new study published in the American Journal of Human Geneticsmay finally have your answer. Researchers have found that people lacking a certain protein in their muscles are more resilient to the cold, and interestingly enough, this genetic mutation may also give you a higher capacity for endurance athletics.

RELATED: The science behind cold weather and running performance

In the study, 42 men between the age of 18 and 40 sat in cold water (14 C) until their body temperature had dropped to 35.5 C. While the participants were submerged in the water, researchers used electromyography to measure their muscle electrical activity, and took biopsies of their muscles to observe their protein content and fibre-type composition.

The results found that people who lacked the protein -aktinin-3 were better at keeping warm and, from an energy perspective, were better at enduring a toucher climate. This protein is found only in fast-twitch muscle fibres, and is lacking in about 20 per cent of the population. Its absence is due to a genetic mutation, and scientists believe that the presence of this mutated gene increased when humans migrated from Africa to colder climates in central and Northern Europe. According to the authors of the study, this is the first direct experimental evidence that this gene provides resilience to the cold.

We here show an improved body temperature defence during cold-water immersion in humans deficient of the sarcomeric protein -actinin-3 expressed in fast-twitch skeletal muscle, they said in their report.

The participants who lacked -aktinin-3 had a greater proportion of slow-twitch muscle fibres, and their genetic mutation allowed them to maintain their body temperature in a more energy-efficient way while their body was cooling. They also shivered less, which is a reaction activated by fast-twitch fibres, and instead increased the activation of slow-twitch fibres that produce heat by increasing baseline contraction.

The authors also noted that people who lack -aktinin-3 rarely excel at sports that require explosive power or strength, likely because they have fewer fast-twitch muscle fibres. These people tend to have a greater capacity for endurance sports, which is not surprising since endurance athletes tend to have more slow-twitch muscle fibres. Of course, there are other factors that can affect your bodys ability to handle cold, so not every runner is going to thrive in cold conditions, and being a runner doesnt automatically mean you have this genetic mutation (nor does having it mean youll be a better distance runner). Even if you are a dedicated runner, you still only have a one in five chance of lacking -aktinin-3.

So if youre one of the lucky ones who doesnt mind the cold, maybe you have this genetic mutation. The rest of us will just continue to bundle up and wait for summer.

RELATED: The key to winter running? Modify your expectations

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The human genome at 20: how biology’s most-hyped breakthrough led to anticlimax and arrests – Yahoo Eurosport UK

Posted: at 1:32 am

When President Bill Clinton took to a White House lectern 20 years ago to announce that the human genome sequence had been completed, he hailed the breakthrough as the most important, most wondrous map ever produced by humankind. The scientific achievement was placed on par with the moon landings.

It was hoped that having access to the sequence would transform our understanding of human disease within 20 years, leading to better treatment, detection and prevention. The famous journal article that shared our genetic ingredients with the world, published in February 2001, was welcomed as a Book of Life that could revolutionise medicine by showing which of our genes led to which illnesses.

But in the two decades since, the sequence has underwhelmed. The potential of our newfound genetic self-knowledge has not been fulfilled. Instead, what has emerged is a new frontier in genetic research: new questions for a new batch of researchers to answer.

Today, the gaps between our genes, and the switches that direct genetic activity, are emerging as powerful determinants behind how we look and how we get ill perhaps deciding up to 90% of what makes us different from one another. Understanding this genetic dark matter, using the knowledge provided by the human genome sequence, will help us to push further into our species genetic secrets.

Cracking the human genetic code took 13 years, US$2.7 billion (1.9 billion) and hundreds of scientists peering through over 3 billion base pairs in our DNA. Once mapped, our genetic data helped projects like the Cancer Dependency Map and the Genome Wide Association Studies better understand the diseases that afflict humans.

But some results were disappointing. Back in 2000, as it was becoming clear the genome sequence was imminent, the genomics community began excitedly placing bets predicting how many genes the human genome would contain. Some bets were as high as 300,000, others as low as 40,000. For context, the onion genome contains 60,000 genes.

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Read more: Explainer: what is a gene?

Dispiritingly, it turned out that our genome contains roughly the same number of genes as a mouse or a fruit fly (around 21,000), and three times less than an onion. Few would argue that humans are three times less complex than an onion. Instead, this discovery suggested that the number of genes in our genome had little to do with our complexity or our difference from other species, as had been previously assumed.

Access to the human genome sequence also presented the scientific community with a huge number of important ethical questions, underscored in 2000 by Prime Minister Tony Blair when he cautioned: With the power of this discovery comes the responsibility to use it wisely.

Ethicists were particularly concerned about questions of genetic discrimination, like whether our genes could be used against us as evidence in a court of law, or as a basis for exclusion: a new kind of twisted hierarchy determined by our biology.

Some of these concerns were addressed by legislation against genetic discrimination, like the US Genetic Information Nondiscrimination Act of 2008. Other concerns, like those around so-called designer babies, are still being put to the test today.

Read more: Should we edit the genomes of human embryos? A geneticist and social scientist discuss

In 2018, human embryos were gene edited by a Chinese scientist, using a method called CRISPR which allows targeted sections of DNA to be snipped off and replaced with others. The scientist involved was subsequently jailed, suggesting that there remains little appetite for human genetic experimentation.

On the other hand, to deny available genetic treatments to willing patients may one day be considered unethical just as some countries have chosen to legalise euthanasia on ethical grounds. Questions remain about how humanity should handle its genetic data.

With human gene editing still highly contentious, researchers have instead looked to find out which genes may be responsible for humanitys illnesses. Yet when scientists investigated which genes are linked to human diseases, they were met with a surprise. After comparing huge samples of human DNA to find whether certain genes led to certain illnesses, they found that many unexpected sections of the genome were involved in the development of human disease.

The genome contains two sections: the coding genome, and the non-coding genome. The coding genome represents just 1.7% of our DNA, but is responsible for coding the proteins that are the essential building blocks of life. Genes are defined by their ability to code proteins: so 1.7% of our genome consists of genes.

The non-coding genome, which makes up the remaining 98.3% of our DNA, doesnt code proteins. This largely unknown section of the genome was once dismissed as junk DNA, previously thought to be useless. It contained no protein-creating genes, so it was assumed the non-coding genome had little to do with the stuff of life.

Bewilderingly, scientists found that the non-coding genome was actually responsible for the majority of information that impacted disease development in humans. Such findings have made it clear that the non-coding genome is actually far more important than previously thought.

Within this non-coding part of the genome, researchers have subsequently found short regions of DNA called enhancers: gene switches that turn genes on and off in different tissues at different times. They found that enhancers needed to shape the embryo have changed very little during evolution, suggesting that they represent a major and important source of genetic information.

These studies inspired one of us, Alasdair, to explore the possible role of enhancers in behaviours such as alcohol intake, anxiety and fat intake. By comparing the genomes of mice, birds and humans we identified an enhancer that has changed relatively little over 350 million years suggesting its importance in species survival.

When we used CRISPR genome editing to delete this enhancer from the mouse genome, those mice ate less fat, drank less alcohol, and displayed reduced anxiety. While these may all sound like positive changes, its likely that these enhancers evolved in calorifically poor environments full of predators and threats. At the time, eating high-calorie food sources such as fat and fermented fruit, and being hyper-vigilant of predators, would have been key for survival. However, in modern society these same behaviours may now contribute to obesity, alcohol abuse and chronic anxiety.

Intriguingly, subsequent genetic analysis of a major human population cohort has shown that changes in the same human enhancer were also associated with differences in alcohol intake and mood. These studies demonstrate that enhancers are not only important for normal physiology and health, but that changing them could result in changes in behaviour that have major implications for human health.

Given these new avenues of research, we appear to be at a crossroads in genetic biology. The importance of gene enhancers in health and disease sits uncomfortably with our relative inability to identify and understand them.

And so in order to make the most of the sequencing of the human genome two decades ago, its clear that research must now look beyond the 1.7% of the genome that encodes proteins. In exploring uncharted genetic territory, like that represented by enhancers, biology may well locate the next swathe of healthcare breakthroughs.

This article was updated on February 21, 2021 to clarify that DNA base pairs are not made from proteins.

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

The Conversation

Alasdair Mackenzie receives funding from the BBSRC, Tenovus (Scotland) and Medical Research Scotland

Andreas Kolb does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

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The human genome at 20: how biology's most-hyped breakthrough led to anticlimax and arrests - Yahoo Eurosport UK

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How Research Not Intended To Be About Disease Can End up Being Medically Relevant – The Wire Science

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Dictyostelium fruiting body. Image: Bruno in Columbus/Wikimedia Commons.

In 1989, in my newly set up laboratory at the Centre for Cellular and Molecular Biology (CCMB), Hyderabad, I began to explore how free-living soil amoebae called cellular slime moulds respond to anti-fungal compounds called phytoalexins.

Plants make phytoalexins in response to fungal attack and injury. It is likely that amoebae encounter these compounds in the soil around plant roots. This research led us, in ten years, to discover the human gene encoding an enzyme, C-14 reductase, for making cholesterol, which is an important constituent of our cell membranes although having too much of it is bad for the heart.

Other scientists subsequently showed that mutations in this gene cause a severe genetic condition called Greenberg dysplasia, which kills foetuses before birth because their bones fail to develop properly. This story illustrates how research not intended to investigate human health and disease can sometimes end up being medically relevant.

Cellular slime mould amoebae feed and multiply on bacteria growing on decaying organic matter. When the bacteria run out, the amoebae starve, and this prompts them to gather in their hundreds of thousands and form multi-cellular aggregates. Each aggregate then transforms itself into a small fruiting body composed of a slender stalk that holds aloft a droplet of cells. These cells develop into long-lived vegetative spores.

Ants, snails, and other small animals brushing past the droplet disperse the spores to new food sources, where each spore germinates to release a single amoeba that forages for bacteria, multiplies and repeats this life cycle.

We examined the response of the cellular slime mould Dictyostelium discoideum to pisatin, the major phytoalexin of the garden pea (Pisum sativum). Pisatin, extracted from pea seedlings, at a dose of 150 g /ml in salt solution quickly killed the amoebae suspended therein but a lower dose (50 g/ml) did not.

Interestingly, amoebae exposed for 30 minutes to the low dose acquired resistance to a subsequent challenge at the high dose. Since in their natural setting amoebae likely encounter a low concentration first, pisatin might not trouble the amoebae too much.

Intriguingly, still lower concentrations (5 g/ml) prevented starving amoebae from aggregating. Amoebae are great foragers of bacteria, and pisatin might be the plants way to recruit them to continue foraging around root lesions and help disinfect the lesion of potentially pathogenic bacteria.

Alternatively, the presence of pisatin might signal to the amoebae that a nearby plant is in trouble, with promise of an imminent windfall of decaying organic matter and bacteria, and hence to defer fruiting body formation.

Exposure to the low dose, however, did not induce pisatin-resistance in a D. discoideum mutant whose mutation had to do with the synthesis of a compound called sterol. Why did we examine this mutant? Because we had previously used the sterol mutants for genetic analysis, so they were readily available at hand, and it is always a good practice to test any new phenomenon in a variety of different strains.

In 1990, the famous geneticist Robin Holliday visited the CCMB and advised us to explore these phenomena in fungi. I wrote to the Fungal Genetics Stock Center, USA, requesting them to send us standard and sterol mutant strains of the bread mould Neurospora crassa.

The very first experiment with Neurospora revealed the mutants were much more sensitive to pisatin concentrations that had no effect on the wild type (i.e. non-mutant).

Also read: With an Eye on the Future, India Needs More Cryo-Electron Microscopes

Around then, I received a Rockefeller Foundation Fellowship to visit the University of Arizona, to use reagents available there to examine whether the inducible pisatin resistance of the Dictyostelium amoebae depended on their turning on an enzyme to degrade pisatin. It did not.

Contemporaneously, Marc Orbach had joined the university as a new faculty member. In his earlier research, Orbach had constructed a library of the Neurospora genome. Under his tutelage, I used the library to select for a DNA sequence that when introduced into the Neurospora mutant reversed its pisatin-sensitive character because it carried a functional copy of the missing gene.

Back at CCMB, K.G. Papavinasasundaram, a postdoctoral scientist, sequenced the selected DNA and found that it shared extensive similarity with the gene for C-14 reductase in yeast. This was not very surprising because yeast and Neurospora are evolutionarily closer to each other than, say, to chickens. But very unexpectedly, the Neurospora gene also shared an equal similarity with a chicken protein called LBR.

LBR has an important role in the vertebrate cell nucleus but no one suspected it also had a role in cholesterol biosynthesis. We were lucky that the Neurospora genes sequence followed the yeast and chicken gene sequences into the DNA sequence database, because it fell to us to spot the similarity between the three sequences.

We dont know why the scientists who uploaded the second sequence failed to find its similarity with the first. Subsequently, we showed that expression of a segment of human LBR in the Neurospora mutant could reverse its pisatin-sensitive phenotype. This established that LBR is a sterol biosynthetic enzyme.

LBR is one of two human genes coding for C-14 reductase. Mutations in it disrupt normal cholesterol synthesis and possibly allow build up of toxic byproducts, but we still do not know how this results in foetal bone growth and development defects.

The other human gene coding for C-14 reductase is TM7SF2. Mice whose TM7SF2 gene was knocked-out were healthy, suggesting that in them the LBR version fully compensates the loss.

It is possible that LBR is the housekeeping enzyme whereas TM7SF2 is a tunable version that can adjust to the local cholesterol demand. Human TM7SF2 did not rescue either the Neurospora or yeast sterol mutants. The TM7SF2 protein might need to be modified before its enzyme activity can be turned on, and yeast and Neurospora cells might not be capable of making the modification.

If this hypothesis is correct, then by testing different LBR/TM7SF2 chimeric proteins for function in Neurospora or yeast, one might be able to identify the modification target.

The twists and turns of our research as it meandered from the high-altitude isolation of phytoalexin-responses of soil amoebae to the busy delta of studies on human genes and disease exemplifies the contingent nature of research.

D.P. Kasbekar is a retired scientist.

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Gaucher Disease Treatment Market is projected to grow at a healthy CAGR over the next years by regions | Keyplayers :Acetelion Pharmaceutical (J&J…

Posted: at 1:32 am

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Gaucher Disease Treatment Market is projected to grow at a healthy CAGR over the next years by regions | Keyplayers :Acetelion Pharmaceutical (J&J...

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Atopic dermatitis (eczema) – Diagnosis and treatment …

Posted: at 1:22 am

Diagnosis

No lab test is needed to identify atopic dermatitis (eczema). Your doctor will likely make a diagnosis by examining your skin and reviewing your medical history. He or she may also use patch testing or other tests to rule out other skin diseases or identify conditions that accompany your eczema.

If you suspect a certain food caused your child's rash, tell the doctor and ask about identifying potential food allergies.

Atopic dermatitis can be persistent. You may need to try various treatments over months or years to control it. And even if treatment is successful, signs and symptoms may return (flare).

It's important to recognize the condition early so that you can start treatment. If regular moisturizing and other self-care steps don't help, your doctor may suggest one or more of the following treatments:

Creams that control itching and help repair the skin. Your doctor may prescribe a corticosteroid cream or ointment. Apply it as directed, after you moisturize. Overuse of this drug may cause side effects, including thinning skin.

Other creams containing drugs called calcineurin inhibitors such as tacrolimus (Protopic) and pimecrolimus (Elidel) affect your immune system. They are used by people older than age 2 to help control the skin reaction. Apply it as directed, after you moisturize. Avoid strong sunlight when using these products.

These drugs have a black box warning about a potential risk of cancer. But the American Academy of Allergy, Asthma & Immunology has concluded that the risk-to-benefit ratios of topical pimecrolimus and tacrolimus are similar to those of most other conventional treatments of persistent eczema and that the data don't support the use of the black box warning.

Light therapy. This treatment is used for people who either don't get better with topical treatments or who rapidly flare again after treatment. The simplest form of light therapy (phototherapy) involves exposing the skin to controlled amounts of natural sunlight. Other forms use artificial ultraviolet A (UVA) and narrow band ultraviolet B (UVB) either alone or with medications.

Though effective, long-term light therapy has harmful effects, including premature skin aging and an increased risk of skin cancer. For these reasons, phototherapy is less commonly used in young children and not given to infants. Talk with your doctor about the pros and cons of light therapy.

Treatment for eczema in babies (infantile eczema) includes:

See your baby's doctor if these measures don't improve the rash or if the rash looks infected. Your baby may need a prescription medication to control the rash or to treat an infection. Your doctor may also recommend an oral antihistamine to help lessen the itch and to cause drowsiness, which may be helpful for nighttime itching and discomfort.

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition.

To help reduce itching and soothe inflamed skin, try these self-care measures:

Atopic dermatitis can be especially stressful, frustrating or embarrassing for adolescents and young adults. It can disrupt their sleep and even lead to depression. And close family members of people with this condition may face financial, social and emotional problems.

Seek psychological support from counselors, support groups, friends or family.

You're likely to start by seeing your family or primary care doctor. But in some cases when you call to set up an appointment, you may be referred to a specialist in skin diseases (dermatologist).

Here's some information to help you prepare for your appointment.

For atopic dermatitis, some basic questions you might ask your doctor include:

Your doctor is likely to ask you several questions, including:

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Last-Itch Effort: Fighting the Bacteria That Exacerbate Eczema with Bacteria – UC San Diego Health

Posted: at 1:22 am

In a new study out of University of California San Diego School of Medicine, researchers have identified a universal strain of bacteria derived from healthy human skin that can treat the most common type of eczema, also known as atopic dermatitis.

In the paper published Feb. 22, 2021, in Nature Medicine, the research team investigated the safety and mechanisms of this certain bacteria in a first-in-human, Phase I, double-blinded clinical trial looking to treat people living with eczema. Of the 54 participants, two-thirds reported improvements in their symptoms, including fewer complaints of itchiness and inflammation.

The main question we wanted to answer was if this was safe. This was a safety study, said Richard Gallo, MD, PhD, Ima Gigli Distinguished Professor of Dermatology and chair of the Department of Dermatology at UC San Diego School of Medicine. We found exactly what we hoped to find. The eczema of participants who received the bacterial treatment improved and there were no adverse events.

Researchers screened more than 8,000 isolates of Staphylococcal bacteria derived from the skin of individuals without eczema, and identified a few strains that inhibited growth of Staphylococcal aureus, a pathogenic bacterium that aggravates skin conditions, such as eczema. These strains were evaluated for additional characteristics, such as decreased capacity to damage skin, and sensitivity to common antibiotics.

The screening resulted in the identification of a single strain of bacteria called Staphylococcus hominis A9 that could be used for the treatment of atopic dermatitis.

Thats how we found the universal strain. This was one out of 8,000 strains that were tested in a dish for their ability to kill Staphylococcal aureus and treat atopic dermatitis, said Gallo. And it worked.

The first tests were performed in animal models where mice were given an experimental version of eczema. Researchers then mixed Staphylococcus hominis with unscented lotion and applied the mixture to the mice twice daily for three days. After treatment, also known as bacteriotherapy, the mice were essentially cured of the eczema.

Success with these animal models led to the Phase I clinical trial using bacteriotherapy to treat 54 trial participants with eczema. Two-thirds of the participants showed a large reduction in S. aureus populations on their skin and improvement in their eczema.

This research is a unique approach to targeting the harmful Staphylococcal aureus on atopic dermatitis skin with beneficial bacteria, said study co-author Donald Leung, MD, allergist and immunologist at National Jewish Health and a co-author of the study. Its our hope this will help patients with eczema rid their skin of the harmful bacteria causing the inflammation. Future studies will determine if this new cream can be used for long periods of time to reduce the severity of eczema and improve the patients quality of life.

Healthy human skin is alive with bacteria there are more microorganisms living in and on the human body than there are human cells. Most microbes reside on human skin without causing harm, but in some people, bacterial pathogens can negatively alter a persons health.

According to the National Eczema Association, nearly 18 million people in the United States have atopic dermatitis, the most common form of eczema, which is a chronic, itchy rash that commonly appears on the arms, legs and cheeks.

From our research, weve determined this rational therapeutic approach for atopic dermatitis appears to be safe for people to use to treat their eczema, said Gallo. And its easy, too, because its just a cream and avoids the side effects of steroids and other drugs that target the immune system.

Co-authors of the study include: Teruaki Nakatsuji, Tissa R. Hata, Yun Tong, Joyce Y. Cheng, Faiza Shafiq, Anna M. Butcher, Secilia S. Salem, Samantha L. Brinton, UC San Diego; Amanda K. Rudman Spergel, National Institutes of Health; Keli Johnson, Brett Jepson, Agustin Calatroni, Gloria David, Rho Federal Systems Division, Inc.; Marco Ramirez-Gama, and Patricia Taylor, National Jewish Health.

This research was funded, in part, by the Atopic Dermatitis Research Network (U19AI117673) and National Institute of Health (R01AR076082, R01AR064781 and R01AI116576).

Disclosure: Richard L. Gallo is a cofounder, consultant, member of the scientific advisory board and holds equity in MatriSys Bioscience, a company that is developing skin bacteriotherapy.

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Health Canada approves DUPIXENT (dupilumab injection) as the first biologic for the treatment of moderate-to-severe atopic dermatitis in children aged…

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MISSISSAUGA, ON, Feb. 23, 2021 /CNW/ - Sanofi Canada announced today that Health Canada has approved DUPIXENT (dupilumab injection) for the treatment of moderate-to-severe atopic dermatitis (AD) in children aged six to 11 years whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.3

"As the first biologic treatment for atopic dermatitis approved for this age group, DUPIXENT is a promising new option for treating children living with this chronic disease," says Dr. Melinda Gooderham, Dermatologist and Medical Director at the SKiN Centre for Dermatology. "Because it targets type 2 inflammation, the underlying cause of the disease, it may help young patients gain more control over their symptoms during childhood, a pivotal time in their development."

DUPIXENT is a fully human monoclonal antibody that inhibits the signaling of the interleukin-4 (IL-4) and interleukin-13 (IL-13) proteins and is not an immunosuppressant. Data from DUPIXENT clinical trials have shown that IL-4 and IL-13 are key drivers of the type 2 inflammation that plays a major role in AD, asthma, and severe chronic rhinosinusitis with nasal polyposis (CRSwNP).4

AD, the most common form of eczema, is an inflammatory disease classified by dry, itchy skin. In its moderate-to-severe form, it is characterized by rashes that can cover much of the body, and can include intense, persistent itching, skin lesions and skin dryness, cracking, redness or darkness, crusting and oozing.5 Inadequately controlled AD can have a physical, emotional and psychosocial impact, causing sleep disturbance, symptoms of anxiety and depression, and feelings of isolation.6

For children living with AD, studies showed that the impact extends beyond its physical symptoms. A survey conducted by the Eczema Society of Canada among Canadian children from infancy up to the age of 18 (and their caregivers) living with AD found that 70 per cent experienced loss of sleep due to their condition, 20 per cent missed school days and 30 per cent experienced anxiety.7 These factors can have a negative psychological impact on children, particularly in regard to their concentration and performance at school along with their willingness to socialize.8

"Atopic dermatitis is a chronic disease that has an indelible impact on all patients, both physically and psychologically, and can be devasting to children during a vulnerable time in their life," says Marissa Poole, Country Lead, Sanofi Canada and General Manager, Sanofi Genzyme Canada. "With this new indication, DUPIXENT now has the potential to help the many Canadians who experience this disease including children, adolescents and adults."

About DUPIXENT

Since its initial approval in 2017, DUPIXENT remains the only biologic medicine approved by Health Canada for the treatment of patients six years and older with moderate-to-severe AD whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.9 DUPIXENT is also approved in Canada for the treatment of adult patients with severe CRSwNP and for the treatment of severe asthma in patients 12 years and older.10

DUPIXENT is jointly developed by Sanofi and Regeneron under a global collaboration agreement.

About Sanofi

Sanofi is dedicated to supporting people through their health challenges. We are a global biopharmaceutical company focused on human health. We prevent illness with vaccines, provide innovative treatments to fight pain and ease suffering. We stand by the few who suffer from rare diseases and the millions with long-term chronic conditions.

With more than 100,000 people in 100 countries, Sanofi is transforming scientific innovation into healthcare solutions around the globe.

Sanofi entities in Canada employ approximately 2,000 people. In 2018, we invested more than $127 million in R&D in Canada, creating jobs, business and opportunity throughout the country.

Follow us on Twitter @SanofiCanada and on YouTube.

Sanofi, Empowering Life

References

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1 Ben-Gashir MA, Seed PT, Hay RJ. Quality of life and disease severity are correlated in children with AD. Br J Dermatol. 2004;150(2):284-90. Available from https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2133.2004.05776.x?sid=nlm%3Apubmed. Accessed February 19, 2021.

2Eczema Society of Canada. Atopic Dermatitis Quality of Life Report. Available from https://eczemahelp.ca/wp-content/uploads/2019/02/ESC_Quality-of-Life-Report_Nov-2017-1.pdf. Accessed February 19, 2021.

3 DUPIXENT Canada Product Monograph. February 22, 2021.

4DUPIXENT Canada Product Monograph. February 22, 2021.

5 Mount Sinai. Patient Care Atopic Dermatitis. Available from http://www.mountsinai.org/patient-care/health-library/diseases-and-conditions/atopic-dermatitis#risk. Accessed February 19, 2021.

6 Eczema Society of Canada. Atopic Dermatitis Quality of Life Report. Available from https://eczemahelp.ca/wp-content/uploads/2019/02/ESC_Quality-of-Life-Report_Nov-2017-1.pdf. Accessed February 19, 2021.

7 Eczema Society of Canada. Atopic Dermatitis Quality of Life Report. Available from https://eczemahelp.ca/wp-content/uploads/2019/02/ESC_Quality-of-Life-Report_Nov-2017-1.pdf. Accessed February 19, 2021.

8 Sick Kids. Eczema: School and activities. Available from https://www.aboutkidshealth.ca/Article?contentid=1113&language=English. Accessed February 19, 2021.

9 DUPIXENT Canada Product Monograph. February 22, 2021.

10 DUPIXENT Canada Product Monograph. February 22, 2021.

SOURCE Sanofi Canada

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Mums agony at sons screams from blistered skin and bowel movements like acid water – The Sun

Posted: at 1:22 am

A MUM has described how her sons milk allergy left him skin blistered from head to toe and his poo like acid water.

Charlotte Smallwood, 25, says her baby Arthur screamed in pain and was "inconsolable" for seven months before he finally got the treatment he needed.

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Doctors reportedly misdiagnosed Arthur, now 10 months old, with colic - when babies cry an abnormal amount - and acid reflux.

But Charlottes first child, three-year-old Thea, had suffered from both of these conditions, and she thought there was something more to Arthurs suffering.

The mum believed that milk was the problem but claims doctors continuously insisted Arthur did not have a cow's milk protein allergy (CMPA).

She and husband Lewis, 28, tried steroid creams, bath creams and milk formulas prescribed by doctors to help their constantly upset and sleep deprived baby - but to no avail.

Eventually, dermatologists at a children hospital urgently requested to see Arthur and were reportedly shocked and disgusted at his treatment to that point.

They prescribed a regime that worked miracles within 24 hours, according to Charlotte, who said Arthur was laughing and rolling around within a week.

Now, Arthur only has flare ups of his allergic symptoms.

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Charlotte, from Romford, Essex, said: The eczema and reactions grew worse and worse, and in the end his skin was reacting to everything that went into or onto his body.

His skin and bowels would bear the brunt of his reactions he would have uncontrollable bowel movements that were like acid water, which left him blistered and raw.

It seemed as though whatever had just gone into him was trying to get out via his skin.

He couldnt do anything he never laughed, couldnt roll, sit up, play or grab things.

Charlotte felt overwhelmed trying to help her son when everything seemed to either have no affect or make him worse.

She said: The toughest part was watching Arthur scream, cry, scratch, throw himself around and bleed.

He would be absolutely uncontrollable and inconsolable.

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Knowing that there wasnt anything that I could do to help my child was absolutely heartbreaking.

Charlotte noticed problems with baby Arthurs skin the day after he was born in April 2020.

His face was patchy and swollen, which doctors reportedly dismissed as baby acne and swelling due to being born by caesarean.

But when Arthur was taken home and started having infant formula, he began suffering episodes of screaming after eating, vomiting up the formula and arching his back in pain.

After swapping Arthur's milk back to pre-made bottles she saw an improvement in his behaviour but the symptoms soon started up again.

She tried over the counter colic and reflux medicines - after Arthurs GP suggested this was the cause - but nothing helped the poor baby.

Arthur was also suffering with severe cradle cap and constipation, and at four weeks old patches of eczema appeared on his cheeks and arms.

From one to four months old, I was back and forth on the phone to the doctor, Charlotte said.

He was given antibiotics, mild steroid creams, bath creams and over the counter creams nothing helped, it just made him worse and worse.

Some creams would even make him look as though he had been burned.

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Cow's milk allergy - the facts

Cows milk protein allergy (CMPA) is one of the most common food allergies to affect babies and young children in the United Kingdom it is still rare.

Symptoms of CMPA often start in the early weeks and months of life.

It affects formula fed babies, but also breastfed babies in very rare cases.

CMPA is an abnormal response by the bodys immune system in which proteins in cows milk are recognised as a potential threat.

This can causethe immune system to be "sensitised". When this happens, there is the potential that when cow's milk is consumed the immune system remembers this protein and may react to it by producing allergic symptoms.

Allergic symptoms can affect one or more of thebodys systems, including the skin, digestive and, less commonly, breathing or blood circulation.

The symptoms can be "immediate", within a few minutes of consuming cows milk or up to two hours afterwards.

The other type of milk allergy happens when symptoms are "delayed", appearing up to 72 hours after cow's milk consumption.

This is caused by a different part of the immune system reacting ina different way.

If cows milk continues to be consumed in the diet, the immune system will continue to produce such symptoms over days or even weeks.

Source: Allergy UK

Unable to get a face-to-face appointment due to Covid-19 restrictions, Charlotte took Arthur to A&E.

Within 10 minutes, he was diagnosed with CMPA and severe infected eczema.

CMPA is when the immune system sees proteins in cows milk as a threat.

It can cause the immune system to be sensitised - it recognises the protein and produces allergic symptoms every time it sees the protein, according to Allergy UK.

This can affect the skin, digestive system, breathing and blood circulation.

Doctors prescribed Arthur a new formula, stronger steroid creams and bath creams, and within a week his skin started to clear up.

But when Charlotte tried to wean him off it, the skin issues came back with a vengeance.

She said: The sleep deprivation was something else I went seven months without sleeping more than three hours of broken sleep a night.

Arthur would just scratch, cry and scream all night long. I had to wrap his arm up close to his body just so he would stop scratching for five minutes.

His sister would get very upset watching him and it was tough trying to explain things to her.

She would give me a cuddle when I would break down in tears, which was a lot.

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In October, Arthur was taken again to A&E after a bad reaction to a teething gel.

His dietician pushed for an appointment at Homerton University Hospital in London for allergy tests when he was seven months old.

Sadly, the condition of his skin was then too severe to carry out allergy testing and his body was 98 per cent covered in severe eczema.

We went home feeling very deflated and wondering how long we would have to wait for someone to see him again, Charlotte said.

But I received a phone call the next day from the Homerton childrens dermatology department asking me to take him there that second we couldnt believe it.

When Arthur was seen by the specialists, Charlotte said they were "shocked" and disgusted by how previous doctors had cared for his skin and couldn't understand how he had been left so long without proper treatment.

His new dermatologist gave him a strict skin routine which they said should help within one week.

It involved three different ointments, a gel for his scalp, and a special bath product.

Charlotte would apply steroid ointments over his whole face and body in the morning, followed by a cream 15 minutes later.

She had to reapply the cream every two hours, which dropped to every four hours in the second week.

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The mum said: At the time, I was very sceptical and didnt believe them, but he was clear in just 24 hours.

By the end of the first week, he was laughing, rolling, sitting up, grabbing things and playing.

I could change his nappy on my own without him scratching and he slept through the night for the first time ever.

His big sister found it so amazing that she could finally play with her baby brother as she couldnt touch him before.

Now, sweet Arthur is flourishing and only suffers mild eczema flare-ups occasionally, caused by environmental factors such as dust and washing detergents.

He is still on the special formula but is weaning and loving all of his food, having had his allergies retested.

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Charlotte is careful to read food labels to ensure no dairy gets into Arthurs diet, which would cause another devastating flare-up.

She added: A lot of doctors seem very standoffish when it comes to CMPA, sort of like they dont believe its a real allergy.

I have come across many people and children like our family that have gone through the same situation.

But do not give up and dont be scared to go over somebodies head to get to where your child needs to be.

Arthur is now a happy, healthy 10-month-old who is thriving he has come so far.

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Eczema Therapeutics Market 2020, Global Statistics, Facts and Figures, Investment Trends, Analysis Of Major Manufacturer Trends and Forecast By 2026 -…

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Eczema Therapeutics Market Report 2021: To Know the impact of COVID-19 on the global market, Request For Free Sample

The Eczema Therapeutics Market Report is a systematic survey of the global Eczema Therapeutics market that depicts shows the current state of the business at the observatory. The Supply and demand, revenue estimates, and volume share are widely covered in the report. This predicts market progress over the forecast year 2020 to 2027. The report includes key strategies of companies operating in the market and their impact analysis. The report features an outline of the determined vendors of the market along with an overview of the major market players. Thekey players in the Eczema Therapeutics market areEncore Dermatology Inc, Eli Lilly and Co, Sanofi, LEO Pharma AS, Alliance Pharma Plc, Pfizer Inc, AbbVie Inc, Mylan NV, Bausch Health Companies Inc, Bayer AG.The report contains inventions that provide revenue segmentation and business overview, layouts for key market players. It takes into account the latest enhancements in the global Eczema Therapeutics market while assessing the market share of key players over the forecast period 2021-2027. The report estimates growth in the global Eczema Therapeutics market by estimating the limits and strengths of key players through SWOT analysis. In addition, the report highlights key product overviews and Market segments [By Product Type: Atopic Dermatitis, Contact Dermatitis, Others], and global market subsegment By Application: Hospital, Clinic, Others of the global market

Download FREE Sample Report:@ https://www.globalmarketers.biz/report/life-sciences/global-eczema-therapeutics-market-report-2020-by-key-players,-types,-applications,-countries,-market-size,-forecast-to-2026-(based-on-2020-covid-19-worldwide-spread)/154779#request_sample

This study analyzes the economic adverse effects of COVID-19 with Eczema Therapeutics supply chain scenarios, global demand, and consumers are analyzed in this report. It also provides a robust Eczema Therapeutics business strategy adopted by industry players to gain traction in the industry. It provides detailed info on marketing channels, upstream raw material suppliers, and downstream buyer analysis.The extensive assessment of Eczema Therapeutics manufacturing processes, consumption patterns, company profiles, and gross margins has been analyzed in this study. It also provides additional evaluation/analysis on pricing and demand for each product type, application, the end-users study is also offered in this research. The opportunities, restraints, growth drivers, future trends are presented effectively by Global Marketers

Main highlights from the table of contents:1. Market overview

MarketScope

Definition, classification, purpose

Eczema Therapeutics market momentum, opportunity map analysis

Analysis of market concentration and maturity

2. Market segmentation

Industry classification by top companies

By product type

Depends on the application and end-user

3. Regional diversification of the Eczema Therapeutics industry

North America

Europe

Asia Pacific

Latin America

Middle East and Africa

Other parts of the world

4. Competitive analysis

Market share, sales, revenue analysis

Import-Export details, supply and demand statistics

M & A, growth strategies, opportunities, and risk assessment

5. Important data coverage by region

Volume and value analysis

Consumption and market share survey

Revenue, price trends, and market size assessment

6. Manufacturer/Top Company Profile

Business overview

Eczema Therapeutics product analysis

Sales by region

Price, revenue, gross profit

7. Global Eczema Therapeutics Market Forecast by Type, Application, and End User

Forecast by size, share, and revenue

Predict growth opportunities, investment scope, and development

Pricing, consumption, and volume forecasts for Eczema Therapeuticss

8. Important survey results and survey methods

9. Reliable data source

10. Conclusions, analysts opinions, and appendices

Browse Detailed TOC https://www.globalmarketers.biz/report/life-sciences/global-eczema-therapeutics-market-report-2020-by-key-players,-types,-applications,-countries,-market-size,-forecast-to-2026-(based-on-2020-covid-19-worldwide-spread)/154779#table_of_contents

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