Atopic eczema is an allergic disease believed to have a hereditary component and often runs in families whose members also have asthma. Itchy rash is particularly noticeable on head and scalp, neck, inside of elbows, behind knees, and buttocks. Experts are urging doctors to be more vigilant in weeding out cases that are, in actuality, irritant contact dermatitis. It is very common in developed countries, and rising.
Contact dermatitis is of two types: allergic (resulting from a delayed reaction to some allergen, such as poison ivy ), and irritant (resulting from direct reaction to a detergent, such as sodium lauryl sulfate). Some substances act both as allergen and irritant (wet cement). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis. About three quarters of cases of contact eczema are of the irritant type, which is the most common occupational skin disease. Contact eczema is curable, provided the offending substance can be avoided and its traces removed from one’s environment.
Xerotic eczema (winter itch, pruritus hiemalis) is dry skin that becomes so serious it turns into eczema. It worsens in dry winter weather, and limbs and trunk are most often affected. The itchy, tender skin resembles a dry, cracked, river bed. This disorder is very common among the older population.
Seborrhoeic dermatitis or Seborrheic dermatitis (“cradle cap” in infants) is a condition sometimes classified as a form of eczema that is closely related to dandruff. It causes dry or greasy peeling of the scalp, eyebrows, and face, and sometimes trunk. The condition is harmless except in severe cases of cradle cap. In newborns it causes a thick, yellow crusty scalp rash called cradle cap, which seems related to lack of biotin and is often curable.
Dyshidrosis (dyshidrotic e., pompholyx, vesicular palmoplantar dermatitis, housewife’s eczema) only occurs on palms, soles, and sides of fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching, which gets worse at night. A common type of hand eczema, it worsens in warm weather.
Discoid eczema (aka nummular e., exudative e., microbial e.) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to come and go.
Venous eczema (aka gravitational e., stasis dermatitis, varicose e.) occurs in people with impaired circulation, varicose veins and edema, and is particularly common in the ankle area of people over fifty . There is redness, scaling, darkening of the skin and itching. The disorder predisposes to leg ulcers.
Dermatitis herpetiformis (aka Duhring’s Disease) causes intensely itchy and typically symmetrical rash on arms, thighs, knees, and back. It is directly related to celiac disease, can often be put into remission with appropriate diet, and tends to get worse at night.
Neurodermatitis (aka lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch that results from habitual rubbing and scratching. Usually there is only one spot. Often curable through behavior modification and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps.
Auto eczematization (reaction, autosensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending on the cause. It always occurs some distance away from the original infection.
There are also eczemas overlaid by viral infections (. herpeticum, . vaccinatum), and eczemas resulting from underlying disease (. lymphoma). Eczemas originating from ingestion of medications, foods, and chemicals.
The exact cause of eczema is unknown, but it is thought to be linked to an overactive response by the body’s immune system to unknown triggers.
In addition, eczema is commonly found in families with a history of other allergies or asthma.
Some people may suffer “flare-ups” of the itchy rash in response to certain substances or conditions. For some, coming into contact with rough or coarse materials may cause the skin to become itchy. For others, feeling too hot or too cold, exposure to certain household products like soap or detergent, or coming into contact with animal dander may cause an outbreak. Upper respiratory infections or colds may also be triggers. Stress may cause the condition to worsen.
The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment. It is supported by epidemiologic studies for asthma. The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases risk for asthma and allergy.
While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites, with up to five percent of people showing antibodies to the mites, the overall role this plays awaits further corroboration.
It cannot be spread from person to person.
Typical skin changes may include:
- Blisters with oozing and crusting
- Ear discharge or bleeding
- Raw areas of the skin from scratching
- Skin coloring changes more or less coloring than the normal skin tone (See: Skin abnormally dark or light)
- Skin redness or inflammation around the blisters
- Thickened or leather-like areas, called lichenification, which can occur after long-term irritation and scratching
Both the type of rash and where the rash appears can depend on the age of the patient:
In children younger than age two, skin lesions begin on the face, scalp, hands, and feet. It is often a crusting, bubbling, or oozing rash.
In older children and adults, the rash is more commonly seen on the inside of the knees and elbows, as well as the neck, hands, and feet.
During a severe outbreak, rashes may occur anywhere on the body.
Itching, which is sometimes intense, almost always occurs. Itching may start even before the rash appears.
There is no known cure for eczema; therefore, treatments aim to control the symptoms by reducing inflammation and relieving itching.
SKIN CARE AT HOME
Taking care of your skin at home may reduce the need for medications.
Avoid scratching the rash or skin if you can:
- Relieve the itch by using a cold compress and taking antihistamines to reduce severe itching.
- Keep your child’s fingernails cut short. Consider light gloves if nighttime scratching is a problem.
Keep the skin moist (called lubricating or moisturizing the skin). Use ointments (such as petroleum jelly), creams, or lotions ( 2 – 3 ) times a day. Moisturizers should be free of alcohol, scents, dyes, fragrances, or other chemicals. A humidifier in the home will also help.
Avoid anything that makes your symptoms worse. This may include:
- Foods such as eggs in a very young child (always discuss with your doctor first)
- Irritants such as wool and lanolin
- Strong soaps or detergents, as well as chemicals and solvents
- Sudden changes in body temperature and stress, which may cause sweating and worsen the condition
- Triggers that cause allergy symptoms
When washing or bathing:
- Keep water contact as brief as possible and use less soap than usual. Short, cooler baths are better then long, hot baths.
- Do not scrub or dry the skin too hard or for too long.
- After bathing, it is important to apply lubricating creams, lotions, or ointment on the skin while it is damp. This will help trap moisture in the skin.
Antihistamines taken by mouth may help with itching or if you have allergies. Often you can buy them without a prescription.
Some antihistamines can cause sleepiness, but they may help with scratching while sleeping.
Newer antihistamines cause little or no sleepiness. Some are available over the counter. These medications include fexofenadine (Allegra), loratadine (Claritin, Alavert), and cetirizine (Zyrtec).
Most causes of atopic eczema are treated with medications that are placed directly on the skin or scalp (called topical medicines):
- At first, you will probably be prescribed a mild cortisone (or steroid) cream or ointment. If this does not work, you may need a stronger steroid medicine. You may need different strengths of steroids for different areas of skin.
- Medicines called topical immunomodulators (TIMs) may be prescribed for anyone over 2 years old. TIMs include tacrolimus(protopic) and pimecrolimus (Elidel). Ask your doctor about concerns over a possible cancer risk with the use of these medicines.
- Creams or ointments that contain coal tar or anthralin may be used for thickened areas.
- Barrier repair creams containing ceramides
Other medicines that may be used include:
- Oral or injected corticosteroids when the eczema is severe
- Antibiotic creams or pills if the skin is infected
- Allergy shots (immunotherapy)
- Oral immunosuppressants, such as cyclosporine, methotrexate, or mycophenolate mofetil
Eczema is a chronic condition, but you can control it with treatment, by avoiding irritants, and by keeping the skin well-moisturized.
In children, it often clears beginning around age 5 – 6, but flare ups will often occur. In adults, it is generally a long-term or recurring condition.
People with eczema tend to have dry skin that flares up more in the winter, when the air is cold and dry.
- Infections of the skin caused by bacteria, fungi, or viruses
- Permanent scars
Various measures may reduce the amount of mite antigens, in particular swapping carpets for hard surfaces. However it is not clear whether such measures actually help with eczema. A controlled study suggested that a number of environmental factors such as air exchange rates, relative humidity and room temperature (but not the level of house dust mites) might have an effect on the condition.
Light therapy (or deep penetrating light therapy) using ultraviolet light can help control eczema. UVA is mostly used, but UVB and Narrow Band UVB are also used. Overexposure to ultraviolet light carries its own risks, particularly potential skin cancer from exposure.
When light therapy alone is found to be ineffective, the treatment is performed with the application (or ingestion) of a substance called psoralen. This PUVA (Psoralen + UVA) combination therapy is termed photo-chemotherapy. Psoralens make the skin more sensitive to UV light, thus allowing lower doses of UVA to be used. However, the increased sensitivity to UV light also puts the patient at greater risk for skin cancer.
Recent studies provide hints that food allergy may trigger atopic dermatitis. For these people, identifying the allergens could lead to an avoidance diet to help minimize symptoms, although this approach is still in an experimental stage. Dietary elements that have been reported to trigger eczema include dairy products, coffee (both caffeinated and decaffeinated), soybean products, eggs, nuts, wheat and maize (sweet corn), though food allergies may vary from person to person. However, in 2009, researchers at National Jewish Medical and Research Center found that eczema patients were especially prone to misdiagnosis of food allergies.
A study led by researchers at the University of California, San Diego School of Medicine suggests that use of oral vitamin D3 supplements bolsters production of a protective chemical normally found in the skin, and may help prevent skin infections that are a common result of atopic dermatitis, the most common form of eczema. It can be noted that the production of vitamin D3 is catalyzed by UV radiation and may influence histo -compatibility expression, correlating with both the seasonality of eczema and its relation to the immune system.
A diet rich in omega-3 (and low in omega-6) polyunsaturated fatty acids may be able to reduce symptoms.
A number of alternative therapies are used for eczema including:
Sea water: there is some anecdotal evidence that salt water baths may help some children with atopic eczema. One reason might be that seawater has antiseptic properties. The Dead Sea is popular for alleviating skin problems including eczema. The benefit of this treatment must be weighed against the extreme discomfort and burning sensations suffered as the salt water contacts raw skin.
has been used for many years as a topical treatment in the alleviation of eczema, although this could be suppressive. It was fashionable in the Victorian and Edwardian eras. However, there is currently no scientific evidence for the claim that sulfur treatment relieves eczema.
are live microorganisms taken orally, such as the Lactobacillus bacteria found in yogurt. They are not effective for treating eczema in older populations, but some research points to some strains of beneficial microorganisms having the ability to prevent the triad of allergies, eczema and asthma, although in rare cases they have a very small risk of infection in those with poor immune system response.
Traditional Chinese medicine:
According to American Academy of Dermatology, while certain blends of Chinese herbal medicines have been proven effective in controlling eczema, they have also proven toxic with severe consequences. In Chinese Medicine diagnosis, eczema is often considered a manifestation of underlying ill health. Treatment aims to improve the overall health of the individual, therefore not only resolving the eczema but improving quality of life (energy level, digestion, disease resistance, etc.). A recent study published in the British Journal of Dermatology describes improvements in quality of life and reduced need for topical corticosteroid application. Another British trial with ten different plants traditionally used in Chinese medicine for eczema treatment suggest a benefit with herbal remedy, but reviewers noted that the blinding was not maintained, leaving the results invalid.
Other remedies lacking scientific evidence include chiropractic spinal manipulation.
Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema.
In the 1980s, Swedish dermatologist Peter Noren developed a behavioural approach to the treatment of long term atopic eczema. This approach has been further developed by dermatologist Richard Staughton and psychiatrist Christopher Bridgett at the Chelsea and Westminster Hospital in London. Patients undergo a six-week monitored program involving scratch habit reversal and self-awareness of scratching levels. For long-term eczema sufferers, scratching can become habitual. Sometimes scratching becomes a reflex, resulting in scratching without conscious awareness, rather than from the feeling of itchiness itself. The habit reversal program is done in conjunction with the standard applied emollient/corticosteroid treatments so that the skin can heal. It also reduces future scratching, as well as reduces the likelihood of further flare ups. The behavioral approach can give an eczema sufferer some control over the degree of severity of eczema.
The lifetime clinician-recorded prevalence of eczema has been seen to peak in infancy, with female predominance of eczema presentations occurring during the reproductive period between fifteen and forty nine years.
Other than direct treatments of the symptoms, no cure is presently known for most types of dermatitis; even cortisone treatments and immuno-modulation may often have only minor effects on what may be a complex problem. As the condition is often related to family history of allergies (and thus heredity), it is probable that gene therapy or genetic engineering might help.
Damage from the enzymatic activity of allergens is usually prevented by the body’s own protease inhibitors, such as, LEKTI, produced from the gene SPINK5. Mutations in this gene are known to cause Netherton’s syndrome, which is a congenital erythroderma. These patients nearly always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence supports the hypothesis that skin damage from allergens may be the cause of eczema, and may provide a venue for further treatment.
Another study identified a gene that the researchers believe to be the cause of inherited eczema and some related disorders. The gene produces the protein filaggrin, the lack of which causes dry skin and impaired skin barrier function.
A recent study indicated that two specific chemicals found in the blood are connected to the itching sensations associated with eczema. The chemicals are Brain-derived neurotrophic factor (BDNF) and Substance P.
Eczema has increased dramatically in England as a study showed a forty two percent rise in diagnosis of the condition between 2001 and 2005, by which time it was estimated to affect five to seven million adults and children. A paper in the Journal of the Royal Society of Medicine says Eczema is thought to be a trigger for other allergic conditions. GP records show over nine million patients were used by researchers to assess how many people have the skin disorder.
Studies have shown that children who are breast-fed until age 4 months are less likely to get eczema.
If the child is not breast-fed, using a formula that contains processed cow milk protein (called partially hydrolyzed formula) may decrease the chances of developing eczema.
Eczema tends to run in families. Keeping the skin well-moisturized and avoiding irritants is important.
Those with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.
Can Cannabinoids Help Eczema?
The journal of Experimental Dermatology has published a review, in which the authors point out the therapeutic possibilities of using cannabinoids to treat skin diseases.
Recent evidence has shown that cannabinoid receptors, CB1 and CB2 are expressed in healthy and diseased skin. Therefore, a treatment targeting these receptors could prove very effective.
Where are the receptors in skin?
The CB1 receptor is located on nerves that run through out skin; large nerves fibers and even small nerve fibers associated with hair follicles have the receptors. Furthermore, previous work has demonstrated that human skin cells, epidermal ketinocytes, have the machinery to “synthesize, bind, and metabolize anandamide (AEA).” While the role of the endocannabinoid system in skin is a bit of a mystery, it appears to be important in skin cell maturation.
Cannabinoids and Inflammatory Skin Diseases
Cannabinoids may attenuate allergic responses. Mice lacking cannabinoid receptors experience more swelling and recruitment of immune cells than normal or wild-type mice. Blocking the CB2 receptor may also lead to a decrease in inflammation.
We all hate getting an itch, especially when it leads to intense scratching and pain. While numerous treatments are available for anti-itching regiments, none are very effective as “anti-pruritic” medicines. Thus there is a great need for new and effective medicines.
In regards to pruritus the authors discuss a study which had nearly 2500 people with atopic eczema. The patients used a cream containing the endocannabinoid N-Palmithoylethanolamide or PEA. This cream significantly decreased symptoms of eczema and was well tolerated.
Furthermore, another study of patients with uremic pruritus showed that a cream containing AEA and PEA eliminated all symptoms within three weeks, in 38.1% of patients and more than half experienced significant reductions. A treatment this effective is desperately needed. On a side note, this is the closest that AEA has ever come to being ingested for a clinical trial
Lastly, there is evidence that some cannabinoids may be able to inhibit malignant skin tumors. However, synthetic cannabinoids that are more potent than THC, have proven to be more effective in this regard, especially WIN-55,212-2 and JWH-133.
Topical Use of Cannabis
Cannabis has been used historically to treat a variety of ailments by topical application. Topical medicines are absorbed through the skin on affected targeted area, as a minimally invasive way to administer, and as a way to reduce side effects. Recent research has confirmed that cannabinoids are
effective at reducing pain at peripheral sites. Many medical marijuana patients have found benefit from using topically applied cannabis,as a way to minimize its central nervous system and psychoactive effects. Some patients prepare cannabis in alcohol extracts and apply as a rub to heal the affected body part. The medicine gets absorbed in the area that is most desirable and will have less of a chance to reach areas that are undesirable. Applying a cannabis preparation to the skin does not usually affect brain receptors, and thus has little effect on cognition or memory. It does not produce the “high” effect that has caused so much debate about marijuana as an intoxicant. Skin disorders in particular, do well with topical cannabis. Eczema, psoriasis, contact dermatitis, pruritis(itching) and even skin infections have been reported to improve with topical cannabis. Marijuana may also be used topically for stopping ( migraines, headaches or pain). Cannabis oil has a multitude of uses. It is an excellent pain reliever because it stimulates local THC and CBD receptors throughout our bodies. It also acts as an anti-inflammatory by stimulating circulation. The massage oil, good for a body rub, also takes pain and swelling away from arthritic joints. Topical alcohol rubs are ideal for arthritic joint pain or sore muscles. Salves may be used anywhere you would use a first aid ointment. Use it for cuts, scrapes, infections and dermatitis, eczema, psoriasis and bruises.
A review of the scientific literature revealed three clinical trials:
Investigating the use of cannabinoids in the treatment of pruritus.
Investigators from the University of Miami Dept. of Medicine, reported successful treatment of pruritus
with five mg. of THC. Prior to cannabinoid therapy, subjects had failed to respond to standard meds.
A decrease in pruritus and marked improvement in sleep was reported as well as a decrease in depression.
In two out of three patients, Delta 9 tetrahydrocannabinol may be an effective.alternative treatment for skin problems. Oral administration of the synthetic cannabinoid agonist HU-211 significantly reduced experimentally induced itch. In twelve subjects, investigators reported that topical application of HU-211 gave very good results.
Researchers at Poland University (Dept. of Dermatology) reported that topical application of endocannabinoid based cream reduced uremic pruritus.
Dry skin on hemodialysis patients was completely eliminated after a three week period of twice daily applications of the cannabinoid cream. Itching was significantly reduced in eighty one percent of the subjects. Encouraging preliminary results .
Clinical trials with GLA supplementation:
Gradual improvement in atoptic eczema symptoms. Hemp oil, due to GLA content, may assist in prevention and treatment of atoptic ecezema.
Orally: 20 ml. oil daily
Topical: external applications with hemp oil ointment twice daily
The anti-inflammatory properties in the hemp oil ointment gave positive results on all subjects.
Topical Cannabis (oil)
Use dry crushed cannabis. Add oil (such as hemp oil, almond oil, coconut oil, or olive oil) . Completely cover the plant material. Keep this mixture in a dark cool place for three weeks. Shake it daily. Then filter it through a coffee filter or cheesecloth. Decant to a dark colored dispensing bottle.
Topical Cannabis (salve)
Add beeswax to your cannabis infused oil. Heat until all the wax has melted (low heat). Use a double boiler. The more wax you use the thicker it will become. Approximately five teaspoons of beeswax per ounce of infused oil.
Topical Cannabis (lotion or cream)
– 24.0 oz distilled H2O
– 4.0oz strong cannabis oil or fat
– 1.2oz emusifying wax
– 1.2oz cosmetic grade stearic acid
– 1.0oz liquid vegetable glycerin (food grade)
– .3oz germaben ( a natural preservative necesarry to prevent spoilage/rancidity)
– .3oz essential oil of your preference(remember the smell your already working with and try to compliment it)
TIP: For a cooling sunburn lotion menthol crystals can be added in place of/with the essential oils
Heat all ingredients in a double boiler until melted then whisk until creamy. Add the last two ingredients and whisk thoroughly. Pour while still warm into containers. Makes approximately 32 ozs.
Topical Cannabis (salve)
Take 4 ounces of leaf marijuana and place in a large stock pot. Cover well with water and add 1.25 cups of olive oil. Bring to a boil and simmer at a low boil for 5-6 hours, adding water as needed.
Allow to cool and strain through cheese cloth, saving the liquid. Place the liquid into the refrigerator over night.
Peel the olive oil layer off the top and place into a small pot and heat over low to melt. Add some beeswax (1-2 ounces should work but experiment to get the consistency you like) and cool into a salve.
Instructions and Things You’ll Need to Make Salves and Ointments
- Vegetable oil
- Essential oils
- Glass bowl
- Saucepan (double boiler)
- Small glass jars for storage
Combine 1 oz. of beeswax and 1/2 cup of a vegetable oil (such as sweet almond, grape seed or sunflower) in a glass bowl. Place it over a small saucepan filled with water, and simmer until the wax melts. Using a double boiler keeps the wax from getting too hot on the direct heat.
Add 1 1/2 tablespoons of warm (but not hot) water to the melted beeswax, one drop at a time. Mix between drops until mixture becomes cool and thick.
Drop 20 to 30 drops of essential oils of your choice to the cream and stir gently.
Scoop mixture into clean, glass ointment jars and seal them.
Store cream for only a few months to ensure freshness.
Recommendation: Indica hybrid
1. Henry George Liddell, Robert Scott. “Ekzema”. A Greek-English Lexicon. Tufts University: Perseus.
2. MeSH Eczema
3. “eczema” at Dorland’s Medical Dictionary
4. a b Simpson CR, Newton J, Hippisley-Cox J, Sheikh A (March 2009). “Trends in the epidemiology and prescribing of medication for eczema in England”. Journal of the Royal Society of Medicine 102 (3): 108–17. doi:10.1258/jrsm.2009.080211. PMC 2746851.PMID 19297652.
5. Johannes Ring; Bernhard Przybilla; Thomas Ruzicka (2006).Handbook of atopic eczema. Birkhäuser. p. 4.ISBN 9783540231332. Retrieved 4 May 2010.
6. Johansson SG, Hourihane JO, Bousquet J, et al. (September 2001). “A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force”. Allergy 56 (9): 813–24.doi:10.1034/j.1398-9995.2001.t01-1-00001.x. PMID 11551246.
7. Bufford, JD; Gern JE (May 2005). “The hygiene hypothesis revisited”.Immunology and Allergy Clinics of North America 25 (2): 247–262.doi:10.1016/j.iac.2005.03.005. PMID 15878454.
8. Carswell F, Thompson S (1986). “Does natural sensitisation in eczema occur through the skin?”. Lancet 2 (8497): 13–5.doi:10.1016/S0140-6736(86)92560-2. PMID 2873316.
9. Henszel L, Kuzna-Grygiel W (2006). “[House dust mites in the etiology of allergic diseases]” (in Polish). Annales Academiae Medicae Stetinensis 52 (2): 123–7. PMID 17633128.
10. Atopic Dermatitis at eMedicine
11. “CDC Smallpox | Smallpox (Vaccinia) Vaccine Contraindications (Info for Clinicians)”. Emergency.cdc.gov. 2007-02-07. Retrieved 2010-02-07.
12. Hoare C, Li Wan Po A, Williams H (2000). “Systematic review of treatments for atopic eczema”. Health Technology Assessment 4(37): 1–191. PMID 11134919.
13. Atherton DJ (October 2003). “Topical corticosteroids in atopic dermatitis”. BMJ 327 (7421): 942–3.doi:10.1136/bmj.327.7421.942. PMC 259155. PMID 14576221.
14. Lee NP, Arriola ER (1999). “Topical corticosteroids: back to basics”.The Western Journal of Medicine 171 (5-6): 351–3. PMC 1308757.PMID 10639873.
15. “neomycin and polymyxin b sulfates and bacitracin zinc with hydrocortisone acetate (Neomycin sulfate and Polymyxin B Sulfate, Bacitracin zinc and Hydrocortisone Acetate) ointment — Warnings”.U.S. Food and Drug Administration.
16. Van Der Meer JB, Glazenburg EJ, Mulder PG, Eggink HF, Coenraads PJ (June 1999). “The management of moderate to severe atopic dermatitis in adults with topical fluticasone propionate. The Netherlands Adult Atopic DermatitisStudy Group”. British Journal of Dermatology 140 (6): 1114–21. PMID 10354080.
17. Bewley A; Dermatology Working, Group (May 2008). “Expert consensus: time for a change in the way we advise our patients to use topical corticosteroids”. The British Journal of Dermatology 158(5): 917–20. doi:10.1111/j.1365-2133.2008.08479.x.PMID 18294314.
18. “Atrophic patches”. College of Family Physicians of Canada.
19. “FDA Issues Public Health Advisory Informing Health Care Providers of Safety Concerns Associated with the Use of Two Eczema Drugs, Elidel and Protopic”. FDA. March 10, 2005. Archived from the original on 2007-09-17. Retrieved 2007-10-16.
20. N H Cox and Catherine H Smith (December 2002). “Advice to dermatologists re topical tacrolimus” (DOC). Therapy Guidelines Committee. British Association of Dermatologists.
21. “Pimecrolimus cream for atopic dermatitis”. Drug and Therapeutics Bulletin 41 (5): 33–6. May 2003. doi:10.1136/dtb.2003.41533.PMID 12789846.
22. “Microsoft Word – package insert and med guide June 2009.doc”(PDF). Retrieved 2011-03-27.
23. Martins, Gladys Aires; Arruda, Lucia (2004). “Tratamento sistêmico da psoríase – Parte I: metotrexato e acitretina”. Anais Brasileiros de Dermatologia 79. doi:10.1590/S0365-05962004000300002.
24. “Atopic dermatitis (eczema) – Prevention at Mayoclinic’s website”. Retrieved 2008-05-07.
25. “Daily Skin Care Essential to Control Atopic Dermatitis article atAmerican Academy of Dermatology’s EczemaNet website”. Retrieved 2009-03-24.
26. “Bathing and Moisturizing at National Eczema Association’s EASE website”. Retrieved 2008-05-07.
27. “Treating Eczema at The Eczema Society of Canada’s website”. Retrieved 2008-05-07.
28. “Water softener eczema relief hope”. BBC News. 2009-01-11. Retrieved 2009-12-19.
29. “Softened Water Eczema Trial, A clinical trial to see if water softeners help children with eczema”. Retrieved 2009-12-19.
30. Coderch L, López O, de la Maza A, Parra JL (2003). “Ceramides and skin function”. American Journal of Clinical Dermatology 4 (2): 107–29. doi:10.2165/00128071-200304020-00004. PMID 12553851.
31. Bouwstra JA, Ponec M (December 2006). “The skin barrier in healthy and diseased state”. Biochimica et Biophysica Acta 1758 (12): 2080–95. doi:10.1016/j.bbamem.2006.06.021. PMID 16945325.
32. Choi MJ, Maibach HI (2005). “Role of ceramides in barrier function of healthy and diseased skin”. American Journal of Clinical Dermatology 6 (4): 215–23. doi:10.2165/00128071-200506040-00002. PMID 16060709.
33. “New Skin-healing Chemicals”. Science Daily. August 30, 2007. Retrieved 2007-10-06.
34. Corazza M, Virgili A (May 2005). “Allergic contact dermatitis from ophthalmic products: can pre-treatment with sodium lauryl sulfate increase patch test sensitivity?”. Contact Dermatitis 52 (5): 239–41.doi:10.1111/j.0105-1873.2005.00606.x. PMID 15898995.
35. Murphy LA, White IR, Rastogi SC (May 2004). “Is hypoallergenic a credible term?”. Clinical and Experimental Dermatology 29 (3): 325–7. doi:10.1111/j.1365-2230.2004.01521.x. PMID 15115531.
36. Mihrshahi S, Marks G, Vanlaar C, Tovey E, Peat J (2002). “Predictors of high house dust mite allergen concentrations in residential homes in Sydney”. Allergy 57 (2): 137–42. doi:10.1034/j.1398-9995.2002.5720999.x. PMID 11929416.
37. Beck HI, Bjerring P, Harving H (1989). “Atopic dermatitis and the indoor climate. The effect from preventive measures”. Acta Dermato-venereologica 69 (2): 162–5. PMID 2564236.
38. Polderman MC, Wintzen M, le Cessie S, Pavel S (2005). “UVA-1 cold light therapy in the treatment of atopic dermatitis: 61 patients treated in the Leiden University Medical Center”. Photodermatology, photoimmunology & photomedicine 21 (2): 93–6. doi:10.1111/j.1600-0781.2005.00150.x. PMID 15752127.
39. Stöppler MC (31 May 2007). “Psoriasis PUVA Treatment Can Increase Melanoma Risk”. MedicineNet. Retrieved 2007-10-17.
40. Stern RS; Puva Follow Up, Study (May 2001). “The risk of melanoma in association with long-term exposure to PUVA”. Journal of the American Academy of Dermatology 44 (5): 755–61.doi:10.1067/mjd.2001.114576. PMID 11312420.
41. Kanny G (January 2005). “[Atopic dermatitis in children and food allergy: combination or causality? Should avoidance diets be initiated?]” (in French). Annales De Dermatologie et De Vénéréologie132 (Spec No 1): 1S90–103. PMID 15984300.
42. National Jewish Medical and Research Center (16 March 2009).”Food allergies commonly misdiagnosed, especially among eczema patients”. Press release. Retrieved 2009-03-20.
43. Atkins D (March 2008). “Food allergy: diagnosis and management”.Primary Care 35 (1): 119–40, vii. doi:10.1016/j.pop.2007.09.003.PMID 18206721.
44. “Oral Vitamin D May Help Prevent Some Skin Infections”. University of California, San Diego. October 6, 2008. Retrieved 2010-11-29.
45. Fleming Nic (March 27, 2008). “Omega-3 can help eczema”. London: The Daily Telegraph. Retrieved 2009-04-28., citing Koch C, Dölle S, Metzger M, et al. (April 2008). “Docosahexaenoic acid (DHA) supplementation in atopic eczema: a randomized, double-blind, controlled trial”. The British Journal of Dermatology 158 (4): 786–92.doi:10.1111/j.1365-2133.2007.08430.x. PMID 18241260.
46. “Atopic Eczema – British Association of Dermatologists”. Archived from the original on 2008-08-02. Retrieved 2011-03-27.
47. “Sulfur”. University of Maryland Medical Center. 4/1/2002. Retrieved 2007-10-15.
48. Boyle RJ, Bath-Hextall FJ, Leonardi-Bee J, Murrell DF, Tang ML (2008). Boyle, Robert John. ed. “Probiotics for treating eczema”.Cochrane Database of Systematic Reviews (Online) (4): CD006135.doi:10.1002/14651858.CD006135.pub2. PMID 18843705.
49. Flohr C, Pascoe D, Williams HC (February 2005). “Atopic dermatitis and the ‘hygiene hypothesis’: too clean to be true?”. The British Journal of Dermatology 152 (2): 202–16. doi:10.1111/j.1365-2133.2004.06436.x. PMID 15727630.
50. “Complementary Therapies”. American Academy of Dermatology. Retrieved 2008-08-01.
51. http://www.acupuncturetoday.com/archives2005/mar/03glick.html[dubious – discuss] 52. “Chinese medicine ‘eases eczema'”. BBC News. 13 March 2008.
53. Armstrong NC, Ernst E (August 1999). “The treatment of eczema with Chinese herbs: a systematic review of randomized clinical trials”.British Journal of Clinical Pharmacology 48 (2): 262–4.doi:10.1046/j.1365-2125.1999.00004.x. PMC 2014284.PMID 10417508.
54. Eldred DC, Tuchin PJ (November 1999). “Treatment of acute atopic eczema by chiropractic care. A case study”. Australasian Chiropractic & Osteopathy 8 (3): 96–101. PMC 2051093. PMID 17987197.
55. Ricci G, Patrizi A, Bellini F, Medri M (2006). “Use of textiles in atopic dermatitis: care of atopic dermatitis”. Current Problems in Dermatology 33: 127–43. doi:10.1159/000093940.PMID 16766885.
56. Bridgett, C. (2000). “Psychodermatology and Atopic Skin Disease in London 1989–1999 – Helping Patients to Help Themselves”.Dermatology and Psychosomatics / Dermatologie und Psychosomatik 1: 183. doi:10.1159/000057975.
57. Bridgett C (2004). “Psychocutaneous medicine”. Journal of cosmetic dermatology 3 (2): 116. doi:10.1111/j.1473-2130.2004.00047.x.PMID 17147570.
58. Osman M, Hansell AL, Simpson CR, Hollowell J, Helms PJ (February 2007). “Gender-specific presentations for asthma, allergic rhinitis and eczema in primary care”. Primary Care Respiratory Journal 16 (1): 28–35. doi:10.3132/pcrj.2007.00006.PMID 17297524.
59. Taylor B, Wadsworth J, Wadsworth M, Peckham C (December 1984). “Changes in the reported prevalence of childhood eczema since the 1939-45 war”. Lancet 2 (8414): 1255–7. doi:10.1016/S0140-