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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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According to the hygiene hypothesis, when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD. Those exposed to dogs while growing up have a lower risk of atopic dermatitis. There is also support from epidemiological studies for 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 unpasteurised milk.
In a small percentage of cases, atopic dermatitis is caused by sensitization to foods. Also, 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 one's risk of developing AD. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods. Atopic dermatitis sometimes appears to be associated with celiac disease and non-celiac gluten sensitivity, and the improvement with a gluten-free diet indicates that gluten is a causative agent in these cases.
Although wetness alone has the effect of macerating the skin, softening the stratum corneum, and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases pH because ammonia is released, which in turn promotes the activity of fecal enzymes such as protease and lipase. These fecal enzymes increase the skin's hydration and permeability to bile salts which also act as skin irritants.
There is no detectable difference in rates of diaper rash in conventional disposable diaper wearers and reusable cloth diaper wearers. "Babies wearing superabsorbent disposable diapers with a central gelling material have fewer episodes of diaper dermatitis compared with their counterparts wearing cloth diapers. However, keep in mind that superabsorbent diapers contain dyes that were suspected to cause allergic contact dermatitis (ACD)." Whether wearing cloth or disposable diapers they should be changed frequently to prevent diaper rash, even if they don't feel wet. To reduce the incidence of diaper rash, disposable diapers have been engineered to pull moisture away from the baby's skin using synthetic non-biodegradable gel. Today, cloth diapers use newly available superabsorbent microfiber cloth placed in a pocket with a layer of light permeable material that contacts the skin. This design serves to pull moisture away from the skin in to the microfiber cloth. This technology is used in most major pocket cloth diapers brands today.
The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked because fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have higher pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.
The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treating with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be because fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract.
Urushiol-induced contact dermatitis is caused by contact with a plant or any other object containing urushiol oil. The oil adheres to almost anything with which it comes in contact, such as towels, blankets, clothing, and landscaping tools. Clothing or other materials that touch the plant and then, before being washed, touch the skin are common causes of exposure.
For people who have never been exposed or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to occur the first time. Once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the oil. Typically, individuals have been exposed at least once, if not several times, before they develop a rash. The rash typically persists one to two weeks, but in some cases may last up to five weeks.
Urushiol is primarily found in the spaces between cells beneath the outer skin of the plant, so the effects are less severe if the plant tissue remains undamaged on contact. Once the oil and resin are thoroughly washed from the skin, the rash is not contagious. Urushiol does not always spread once it has bonded with the skin, and cannot be transferred once the urushiol has been washed away.
Although simple skin exposure is most common, ingestion of urushiol can lead to serious, systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes a systemic reaction, as well as a rash in the throat and eyes. Firefighters often get rashes and eye inflammation from smoke-related contact. A high-temperature bonfire may incinerate urushiol before it can cause harm, while a smoldering fire may vaporize the volatile oil and spread it as white smoke. However, some sources dispute the danger of burning urushiol-containing plant material.
There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.
People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.
Paederus dermatitis (also called linear dermatitis or dermatitis linearis) is skin irritation resulting from contact with the hemolymph of certain rove beetles, a group that includes the genus Paederus. Other local names given to Paederus dermatitis include spider-lick, whiplash dermatitis, and Nairobi fly dermatitis.
The active agent is commonly referred to as pederin, although depending on the beetle species it may be one of several similar molecules including pederone and pseudopederin.
"Blister beetle dermatitis," a term more properly used for the different dermatitis caused by cantharidin from blister beetles, is also sometimes used to describe paederus dermatitis caused by rove beetles.
Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include: solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues).
Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning. Also, many plants directly irritate the skin.
The diagnosis of flea allergy dermatitis is complicated by the grooming habits of pets. Cats in particular are very efficient at grooming out fleas, often removing any evidence of infestation. Fleas begin biting within 5 minutes of finding a host, and there are no flea treatments that kill fleas before biting occurs.
With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.
Most cases are well managed with topical treatments and ultraviolet light. About 2% of cases are not. In more than 60% of young children, the condition subsides by adolescence.
Once pederin is on the skin from the initial beetle contact, it may also be spread elsewhere on the skin. "Kissing" or "mirror-image" lesions where two skin areas come in contact (for example, the elbow flexure) are often seen. Washing the hands and skin with soap and water is strongly recommended, if contact with a rove beetle has occurred.
Initial skin contact with pederin shows no immediate result. Within 12–36 hours, however, a reddish rash (erythema) appears, which develops into blisters. Irritation, including crusting and scaling, may last from two to three weeks.
One study reported best results with a treatment regimen that combined topical steroids with oral antihistamines and antibiotics. The authors hypothesized that antibiotics were helpful because of the possible contamination of skin by pederin-producing bacteria.
Cosmetics play an important role as causal factors for perioral dermatitis. Regular generous applications of moisturising creams cause persistent hydration of the horny layer causing impairment and occlusion of the barrier function, irritation of the hair follicle and proliferation of skin flora. Combining this with night cream and foundation significantly increases risk of perioral dermatitis by 13-fold.
The cause of perioral dermatitis is unclear. The use of topical steroids and cosmetics have the most important role. Although light exposure has been discounted as a causal factor, some reports of perioral dermatitis have been made by some patients receiving Psoralen and ultraviolet A therapy.
The aim of treatment is to relieve the allergy-induced itch and to remove the fleas from the pet and its home environment. In some cases, secondary bacterial or yeast infections will also need treatment before the itching subsides. Environmental flea control includes using flea foggers or bombs, vacuuming, and treating pet bedding by washing on a hot cycle (over 60 degrees Celsius) in the washing machine. The current on-pet treatment recommended by veterinary dermatologists is spinosad (Comfortis) monthly and nitenpyram (Capstar or generics) every 48 hours until improvement.
Many pets with FAD may also have other allergies, such as allergies to food, contact allergies, and atopic dermatitis.
A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects.
Common causes of allergic contact dermatitis include: nickel allergy, 14K or 18K gold, Balsam of Peru ("Myroxylon pereirae"), and chromium. In the Americas they include the oily coating from plants of the "Toxicodendron" genus: poison ivy, poison oak, and poison sumac. Millions of cases occur each year in North America alone. The alkyl resorcinols in "Grevillea banksii" and "Grevillea" 'Robyn Gordon' are responsible for contact dermatitis. Bilobol, another alkyl resorcinol found in "Ginkgo biloba" fruits, is also a strong skin irritant.
Common causes of irritant contact dermatitis include solvents, metalworking fluids, latex, kerosene, ethylene oxide, paper, especially papers coated with chemicals and printing inks, certain foods and drink, food flavorings and spices, perfume, surfactants in topical medications and cosmetics, alkalis, low humidity from air conditioning, and many plants. Other common causes of irritant contact dermatitis are harsh, alkaline soaps, detergents, and cleaning products.
There are three types of contact dermatitis: irritant contact dermatitis; allergic contact dermatitis; and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.
Common allergens implicated include the following:
- Nickel (nickel sulfate hexahydrate) – has been recognized as a significant cause of allergy. This metal is frequently encountered in stainless steel cookware, jewelry and clasps or buttons on clothing. Current estimates gauge are that roughly 2.5 million US adults and 250,000 children suffer from nickel allergy, which costs an estimated $5.7 billion per year for treatment of symptoms. A significant portion of nickel allergy is preventable.
- Gold (gold sodium thiosulfate) – precious metal often found in jewelry and dental materials
- Balsam of Peru (Myroxylon pereirae) – used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties; derived from tree resin. It may also be a component of artificial vanilla and/or cinnamon flavorings.
- Chromium – used in the tanning of leather. Also a component of uncured cement/mortar, facial cosmetics and some bar soaps.
- Urushiol – oily coating from plants of Toxicodendron genus – poison ivy, poison oak, and poison sumac. Also found in mango plants and cashews.
- Sap from certain species of mangrove and agave
- Thiomersal – mercury compound used in local antiseptics and in vaccines
- Neomycin – topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap, and pet food. Found by itself, or in Neosporin or Triple Antibiotic
- Fragrance mix – group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes, and dental products
- Formaldehyde – preservative with multiple uses, "e.g.", in paper products, paints, medications, household cleaners, cosmetic products, and fabric finishes. Often released into products by the use of formaldehyde releasers such as imidazolidinyl urea, diazolidinyl urea, Quaternium-15, DMDM Hydantoin, and 2-bromo-2-nitropropane-1,3-diol.
- Cobalt chloride – metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment
- Bacitracin – topical antibiotic found by itself, or as Polysporin or Triple Antibiotic
- Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).
- Colophony (Rosin) – rosin, sap or sawdust typically from spruce or fir trees
- Topical steroid – "see" steroid allergy
- Photographic developers, especially those containing metol
- Topical anesthetics – such as pramoxine or diphenhydramine, after prolonged use
- Isothiazolinones – preservatives used in many personal care, household, and commercial products.
- Mercaptobenzothiazole – in rubber products, notably shoes, gloves, and car tires.
- Soluble salts of platinum – "see" platinosis
Garlic allergy or allergic contact dermatitis to garlic is a common inflammatory skin condition caused by contact with garlic oil or dust. It mostly affects people who cut and handle fresh garlic, such as chefs, and presents on the tips of the thumb, index and middle fingers of the non-dominant hand (which typically hold garlic bulbs during the cutting). The affected fingertips show an asymmetrical pattern of fissure as well as thickening and shedding of the outer skin layers, which may progress to second- or third-degree burn of injured skin.
Garlic dermatitis is similar to the tulip dermatitis and is induced by a combined mechanical and chemical action. Whereas the former mechanism acts via skin rubbing which progresses into damage, the major cause of the latter is the chemical diallyl disulfide (DADS), together with related compounds allyl propyl disulfide and allicin. These chemicals occur in oils of plants of the genus "Allium", including garlic, onion and leek.
Garlic allergy has been known since at least 1950. It is not limited to hand contact, but can also be induced, with different symptoms, by inhaling garlic dust or ingesting raw garlic, though the latter cases are relatively rare. DADS penetrates through most types of commercial gloves, and thus wearing gloves while handling garlic has proven inefficient against the allergy. Treatment includes avoiding any contact with garlic oil or vapours, as well as medication, such as administering acitretin (25 mg/day, orally) or applying psoralen and ultraviolet light to the affected skin area over a period of 12 weeks (PUVA therapy).
Many contact sensitizers or irritants are known to cause contact dermatitis superimposed on nummular dermatitis. Studies have implicated nickel, cobalt, chromate, and fragrance as likely culprits. Xerosis, or dehydration of skin is also a likely cause. Infection with "Staphylococcus aureus" bacteria or "Candida" may also play a role.
Other rashes that occur in a widespread distribution can look like an id reaction. These include atopic dermatitis, contact dermatitis, dyshidrosis, photodermatitis, scabies and drug eruptions.
If the condition thickens, turns red and irritated, starts spreading, appears on other body parts, or if the baby develops thrush (fungal mouth infection), fungal ear infection (an ear infection that does not respond to antibiotics) or a persistent diaper rash, medical intervention is recommended.
Severe cases of cradle cap, especially with cracked or bleeding skin, can provide a place for bacteria to grow. If the cradle cap is caused by a fungal infection which has worsened significantly over days or weeks to allow bacterial growth (impetigo, most commonly), a combination treatment of antibiotics and antifungals may be necessary. Since it is difficult for a layperson to distinguish the difference between sebaceous gland cradle cap, fungal cradle cap, or either of these combined with a bacterial infection, medical advice should be sought if the condition appears to worsen.
Cradle cap is occasionally linked to immune disorders. If the baby is not thriving and has other problems (e.g. diarrhea), a doctor should be consulted.
Atopy is a hereditary and chronic (lifelong) allergic skin disease. Signs usually begin between 6 months and 3 years of age, with some breeds of dog, such as the Golden Retriever showing signs at an earlier age. Dogs with atopic dermatitis are itchy, especially around the eyes, muzzle, ears and feet. In severe cases the irritation is generalised. If the allergens are seasonal, the signs of irritation are similarly seasonal. Many dogs with house dust mite allergy have perennial disease. Some of the allergens associated with atopy in dogs include pollens of trees, grasses and weeds, as well as molds and House dust mite. Ear and skin infections with the bacteria "Staphylococcus pseudintermedius" and the yeast "Malassezia pachydermatis" are common secondary to atopic dermatitis.
Food allergy can be associated with identical signs and some authorities consider food allergy to be a type of atopic dermatitis.
Diagnosis of atopic dermatitis is by elimination of other causes of irritation including fleas, scabies and other parasites such as Cheyletiella and lice. Food allergy can be identified through the use of elimination diet trials in which a novel or hydrolysed protein diet is used for a minimum of 6 weeks and allergies to aeroallergens can be identified using intradermal allergy testing and/or blood testing (allergen-specific IgE ELISA).
Treatment includes avoidance of the offending allergens if possible, but for most dogs this is not practical or effective. Other treatments modulate the adverse immune response to allergens and include antihistamines, steroids, ciclosporin and immunotherapy (a process in which allergens are injected to try to induce tolerance). In many cases shampoos, medicated wipes and ear cleaners are needed to try to prevent the return of infections.
New research into T-cell receptor peptides and their effects on dogs with severe, advanced atopic dermatitis are being investigated.
Irritant contact dermatitis is a form of contact dermatitis that can be divided into forms caused by chemical irritants and those caused by physical irritants.
The prevalence of nummular dermatitis in the United States is approximately 2 per 1,000. It is considered a disease of adulthood, for it is rare in children.