Marketing Scoops: Why Sleep Disturbance and Atopic Dermatitis (AD) Go Hand in Hand

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If you have atopic dermatitis (AD), also known as eczema, then you know the struggle: You climb into bed ready to catch some zzz’s, but can’t sleep because of the intense, relentless itching. Thanks to my current flareup (courtesy of the dry, cold weather), symptoms that are usually just minor irritations during the day have suddenly become hard to ignore at night. It’s an exhausting, frustrating cycle……..Continue reading….

By : Kendra Cherry, MSEd

Source: Very Well Mind

Critics:

Symptoms refer to the sensations that people with AD feel, whereas signs refer to a description of the visible changes that result from AD.The main symptom of AD is itching which can be intense. Some people experience burning, soreness, or pain. People with AD often have generally dry skin that can look greyish in people with darker skin tones of colour. Areas of AD are not well-defined, and they are typically inflamed (red in a light coloured skin or purple or dark brown in people with dark skin of colour). Surface changes include:

scaling cracking (skin fissures)
swelling (oedema)
scratch marks (excoriation)
bumpiness (papulation)
oozing of clear fluid
thickening of the skin (lichenification) where the AD has been present for a long time.

Eczema often starts on the cheeks and outer limbs and body in infants and frequently settles in the folds of the skin, such as behind the knees, folds of the elbows, around the neck, wrists, and under the buttock folds as the child grows.^[13] Any part of the body can be affected by AD. Atopic dermatitis commonly affects the eyelids, where an extra prominent crease can form under the eyelid due to skin swelling known as Dennie-Morgan infraorbital folds.

Cracks can form under the ears, which can be painful (infra-auricular fissure). The inflammation from AD often leaves “footprints” known as postinflammatory pigmentation that can be lighter than the normal skin or darker. These marks are not scars and eventually go back to normal over months, provided the underlying AD is treated effectively.

People with AD often have dry and scaly skin that spans the entire body, except perhaps the diaper area, and intensely itchy red, splotchy, raised lesions to form in the bends of the arms or legs, face, and neck. Genes that may contribute to AD are mainly those responsible for immune response (e.g., TH2 cytokine and JAK-STAT pathway genes) and skin barrier (e.g., filaggrin, claudin-1, loricrin).

Immune response: Many people with AD have a family history or a personal history of atopy. Atopy is a term used to describe individuals who produce substantial amounts of IgE. Such individuals have an increased tendency to develop asthma, hay fever, eczema, urticaria and allergic rhinitis. Up to 80% of people with atopic dermatitis have elevated total or allergen-specific IgE levels.

Skin barrier: About 30% of people with AD have mutations in the gene for the production of filaggrin (FLG), which increases the risk for early onset of atopic dermatitis and developing asthma. However, expression of filaggrin protein or breakdown products offer no predictive utility in atopic dermatitis risk. People with atopic dermatitis also have decreased expression of tight junction protein Claudin-1, which deteriorates the bioelectric barrier function in the epidermis.

According to the hygiene hypothesis, early childhood exposure to certain microorganisms (such as gut flora and helminth parasites) protects against allergic diseases by contributing to the development of the immune system. This exposure is limited in a modern “sanitary” environment, and the incorrectly developed immune system is prone to develop allergies to harmless substances. Some support exists for this hypothesis with respect to AD. Those exposed to dogs while growing up have a lower risk of atopic dermatitis.

Also, epidemiological studies support a protective role for helminths against AD. Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurized milk. In a small percentage of cases, atopic dermatitis is caused by sensitization to foods such as milk, but there is growing consensus that food allergy most likely arises as a result of skin barrier dysfunction resulting from AD, rather than food allergy causing the skin problems.

Atopic dermatitis sometimes appears associated with coeliac disease and non-coeliac gluten sensitivity. Because a gluten-free diet (GFD) improves symptoms in these cases, gluten seems to be the cause of AD in these cases. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for heavily processed foods. Exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis. Exposure to dust mites, for example, is believed to contribute to the risk of developing AD.

The prevalence of atopic dermatitis in children may be linked to the level of calcium carbonate or “hardness” of household drinking water. Living in areas with hard water may also play a part in the development of AD in early life. However, when AD is already established, using water softeners at home does not reduce the severity of the symptoms. Colonization of the skin by the bacterium S. aureus is prevalent in those with atopic dermatitis.

Abnormalities in the skin barrier of persons with AD are exploited by S. aureus to trigger cytokine expression, thus aggravating the condition. However, atopic dermatitis is non-communicable and therefore could not be directly caused by a highly infectious organism. Furthermore, there is insufficient evidence for the effectiveness of anti-staphylococcal treatments for treating S. aureus in infected or uninfected eczema.

The role of S. aureus in skin irritation occurs via inflammation factors that induce itching, which may damage the skin, further driving inflammation, and facilitating the growth of S. aureus, thus promoting a chronic cycle. There are no established clinical methods using dietary or topical strategies to inhibit or prevent atopic dermatitis. Specific dietary plans during pregnancy and in early childhood, such as eating fatty fish (or taking omega-3 supplements), are not effective.

Taking probiotics (for example Lactobacillus rhamnosus) during pregnancy and feeding probiotics to infants are strategies under research, with only preliminary evidence that they may be preventative. Using moisturizers daily in infants during the first year of life does not help to prevent atopic dermatitis, and might even increase the risk of skin infections. No cure for AD is known, although treatments may reduce the severity and frequency of flares.

The most commonly used topical treatments for AD are topical corticosteroids (to get control of flare-ups) and moisturisers (emollients) to help keep control. Clinical trials often measure the efficacy of treatments with a severity scale such as the SCORAD index or the Eczema Area and Severity Index. Daily basic care stabilizes the barrier function of the skin to mitigate its sensitivity to irritation and penetration of allergens.

Affected persons often report that improvement in skin hydration parallels improvement in AD symptoms. Moisturisers (or emollients) can improve skin comfort and may reduce disease flares. They can be used as leave-on treatments, bath additives, or soap substitutes. There are many different products, but the majority of leave-on treatments (least to most greasy) are lotions, creams, gels or ointments.

All of the different types of moisturisers are equally effective, so people need to choose one or more products based on what suits them, according to their age, body site affected, climate/season, and personal preference. Non-medicated prescription moisturisers may also be no more effective than over-the-counter moisturisers. The use of emollient bath additives does not provide any additional benefits. Creams and ointments containing corticosteroids applied directly on skin (topical) are effective in managing atopic dermatitis.

Newer (second generation) corticosteroids, such as fluticasone propionate and mometasone furoate, are more effective and safer than older ones. Strong and moderate corticosteroids are more effective than weaker ones. They are also generally safe and do not cause skin thinning when used intermittently to treat AD flare-ups. They are also safe when used twice a week for preventing flares (also known as weekend treatment).

Applying once daily is as effective as twice or more daily application. In addition to topical corticosteroids, topical calcineurin inhibitors, such as tacrolimus or pimecrolimus, are also recommended as first-line therapies for managing atopic dermatitis. Both tacrolimus and pimecrolimus are effective and safe to use in AD. Crisaborole, an inhibitor of PDE-4, is also effective and safe as a topical treatment for mild-to-moderate AD. Ruxolitinib, a Janus kinase inhibitor, has uncertain efficacy and safety.

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