Eczema, or atopic dermatitis, is a pruritic, chronic, relapsing inflammatory skin disease, which has been increasing in prevalence since the 1960s; it affects up to 20% of people worldwide.[1,2] An epidemiological survey found the highest rates to be in industrialised nations, including Australia and New Zealand, and suggested the increase in prevalence is due to interactions between genetic and environmental factors. Even though eczema is seen across all ages, it is most common in children, with 50% of the cases diagnosed by the age of one.
Eczema affects between 10%-25% of children, and, of those, 30% or more will have the condition into adulthood.4,5 Infants with a family history of atopy (eczema, asthma or allergic rhinitis) have greatly increased risk of eczema compared to those without an atopic family history.
Eczema has significant morbidity and greatly affects quality of life, and may result in increased fatigue, sleep deprivation, activity restriction, social exclusion, anxiety and depression.[6,7] Up to 50% of children with eczema report negative effects on quality of life and it also adversely impacts carers and parents of affected children.
Signs and symptoms
Dry skin (xerosis) is a universal feature of eczema, along with fine scaling and skin roughness. Lesions are variable and will depend on the stage and severity of the condition. The main symptom of eczema is itching. In children, it generally affects the face and scalp around three months of age, but changes to the wrists, the back of the elbow and knee joints, and on the front of the ankles, around the age of two to three years.
The causes of eczema
Eczema is multifactorial, with environmental factors, socioeconomic issues, genetic predisposition and immune dysfunction all believed to play a role in its development and progression.[2,6] Earlier research promoted T helper cell deregulation, production of immunoglobulin E and mast cell activation as the cause of the pruritus and inflammation. Although Th-2 immunity dysfunction is a major mediator, it was not until recently that skin barrier function was discovered as being of key importance in eczema.
The skin barrier and genetic mutations
The skin is a crucial barrier between the individual and the environment, preventing excessive water loss and the entry of allergens, irritants and pathogens into the body.[5,6]
Poor skin barrier is directly linked to the onset and severity of eczema. Eczema sufferers have characteristically dry skin, even in non-lesioned areas. This is due to trans-epidermal water loss (TEWL), reduced fatty acid levels and increased levels of proteolytic enzymes.[3,4]
The outermost layer of the skin, called the stratum corneum (SC) is critical for the integrity of the skin barrier. It is made up of the cornified envelope, intercellular lipids, free fatty acids, such as ceramides, and keratin proteins bound tightly by filaggrin, a key protein in SCstructure and function.[5,6,11]
Filaggrin, shortened from filament aggregating protein, is necessary to produce natural moisturising factor (NMF), a pool of amino acids and derivatives that act as a natural humectant in the skin. NMF is required for UV protection, modulating pH levels and water retention.
The importance of filaggrin became clear in recent research, finding mutations in the filaggrin gene in up to 50% of patients with eczema and a two to three-fold increased disease risk. The discovery of these mutations in the skin was integral in highlighting skin barrier function deficiency as a major patho-mechanism in eczema.
The effects of skin barrier dysfunction
The loss of an effective skin barrier for any reason increases skin dryness, promotes altered microbial skin colonisation, changes pH levels, and allows greater permeability for pathogens and irritants. These, in turn, lead to pruritus, overgrowth of pathogenic bacteria, increased inflammatory responses, altered immune responses and the inflammatory skin lesions of ezcema.
It is also thought that sufferers have more sensitive skin than the general population and have a lowered itch threshold (possibly due to inflammatory cytokines).[2,3] This causes intense scratching, which leads to further skin barrier damage and perpetuates the ‘itch-scratch-rash’ cycle.
Effective treatments for childhood eczema
Improving the skin barrier and reducing the ‘itch-scratch-rash’ cycle is essential for treatment and prevention of eczema. Moisturisers containing ingredients that improve the epidermal barrier, reduce dryness and potential cracking, limit overgrowth of bacteria, reduce inflammatory processes and promote correct pH levels, are essential.
‘The goal of therapy is to restore the function of the epidermal barrier and to reduce skin inflammation.’
Lactobacillus brevis (DSM 17250)
Overgrowth of pathogenic skin bacteria is common in those with eczema. For example, Staphylococcus aureus has been found in approximately 90% of eczema sufferers, compared to 10% in non-sufferers. While initially thought to be benign, research now shows that it produces a toxin and takes advantage of the immunological and structural dysfunctions of eczema.[10,12] So, measures to reduce pathogenic overgrowth and recolonise the skin with protective commensal bacteria are recommended. However, oral antibiotic therapy has been found to be ineffective.[5,10,13]
In a recent randomised, placebo-controlled, double-blind study, a specific strain of lactic acid bacteria was used in an ointment formulation on dry skin for four weeks. This strain of Lactobacillus brevis, DSM 17250, was chosen because it produces small molecules capable of enhancing the growth of skin commensals, such as S. epidermidis. S. epidermidis modulates inflammatory responses after skin injury and selectively inhibits pathogenic organisms, including S. aureus.
Researchers initially tested L. brevis (DSM 17250) in an in vitro model for its ability to increase the growth of S. epidermidis. Compared to three other strains of L. brevis, the DSM 17250 strain showed the strongest growth promoting activity against nine strains of S. epidermidis. To determine the anti-inflammatory potential, they then extracted and tested the bioactive compounds of DSM 17250 and found that this bacterium had significant anti-inflammatory effects in vitro.
After testing the ointment on skin, microbial analysis showed a significantly high increase in commensal colonisation after 28 days. S. aureus was reduced from 66cfu to 3cfu by day seven in one subject who had high levels of this pathogen at baseline.
Additionally, DSM 17250 was effective in reducing skin dryness, tightness, roughness, scaling and sensitivity, and significantly reduced TEWL. An overall improvement of skin parameters was improved by about 70%, indicating stabilisation of the skin barrier function.
Daily topical treatment of DSM 17250 shaped the microbial diversity, allowing commensal bacteria to improve the integrity and function of the skin barrier.
Another relatively new topical treatment for eczema is lactoferrin (LF). A valuable therapeutic, LF may be used in eczema for its antimicrobial and anti-inflammatory effects, and for its direct action on wound healing.[14,15]
LF supports multiple biological processes in wound healing and inflammation by:
- increasing necessary pro-inflammatory cytokines in the initial wound healing process
- neutralising overabundant immune responses, including Th2 cells
- potentially correcting Th1/Th2 imbalances
- inhibition of several pro-inflammatory cytokines at other stages of the process, neutralising the immune response
- having an inhibitory effect against bacterial pathogens
- enhancing fibroblast and keratinocyte migration, leading to the formation of granulation tissue and re-epithelisation
- augmenting the synthesis of extracellular matrix components (collagen and hyaluronan).[14,15]
Chamomile tea has been used traditionally for bacterial superinfections, due to its anti-inflammatory and antibacterial properties. In a comparative bilateral study of chamomile flower extract cream, topical treatment was found to be equally as effective as 0.25% hydrocortisone, with greater efficacy than 0.75% fluocortin butyl and non-steroidal topical agents in eczema treatment.
Chamomile is rich in flavonoids, which have anti-inflammatory and mast stabilising effects, thereby reducing histamine formation and release. Eczema sufferers release higher amounts of histamine compared to non-sufferers, and this may be the reason for chamomile’s effectiveness in topical treatment of this condition.
Glycyrrhetinic acid (GA) and glycyrrhizin (GL) are major bioactive ingredients in licorice root that have also been found to be beneficial in eczema.
GL has cytoprotective, anti-inflammatory and immune regulatory effects in eczema. GA is antipruritic and anti-inflammatory, and inhibits the enzyme 11B-hydroxysteroid dehydrogenase, responsible for the conversion of cortisol to cortisone. This is important as excess glucocorticoids increase skin thinning and poor wound healing.[18,19] In a topical study, the use of GA cream was reported by subjects to improve eczema severity more than four times compared to placebo. It also led to reduced itching, greater patient satisfaction and fewer relapses.
The wound healing and anti-inflammatory capabilities of aloe vera are well documented. Its active constituents have been found to:
- increase collagen synthesis, composition and cross-linking, increasing skin elasticity
- increase hyaluronic acid and dermatan sulfate in granulation tissue of wounds
- inhibit the COX pathway and reduces prostaglandin E2 production
- cool and moisturise the skin
- have cohesive effects on superficial flaking epithelial cells and softens the skin
- have antiseptic and antibacterial properties.[20,21]
Other effective emollients
Emollients are often the front-line treatments for eczema. Emollients alone have been found to cut the risk of eczema in half in infants, increase pH levels and promote healthy bacterial diversity.[1,5] Vitamin E, almond oil and shea butter are well known for their skin emollient and healing properties, but there are also other very valuable emollients in the prevention and treatment of eczema.
In a randomised controlled trial, topical coconut oil was significantly superior in its ability to reduce S. aureus levels, with a 95% clearance rate compared to 50% in those using olive oil. Another study found coconut oil significantly improved eczema symptoms, TEWL and skin function, compared to mineral oil. The benefits of topical coconut oil in eczema is that it is both an emollient and an antibacterial.
Borage oil, rich in essential fatty acids, has also been tested in eczema. Children given undershirts coated in borage oil experienced significant improvement in redness, itching and TEWL after two weeks of treatment.
In a study testing the effectiveness of sea buckthorn oil on eczema, researchers also found this plant-based emollient to be effective on eczema severity, skin moisture content, TEWL and quality of life.
As part of its manifestation, eczema may also be due to internal imbalances, such as gut dysbiosis, nutrient deficiencies and food allergies. Therefore, therapies such as probiotics, vitamin E, vitamin D and omega 3 fatty acids may help. However, these should be recommended in conjunction with a topical application to restore local homeostasis to the skin barrier and function.
- Glatz M, Jo JH, Kennedy EA, et al. Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis. PLoS One 2018;13(2):e0192443. [Abstract]
- Lee JH, Son SW, Cho SH. A comprehensive review of the treatment of atopic eczema. All Asthm Immunol Res 2016;8(3):181-190. [Abstract]
- Katayama I, Aihara M, Ohya Y, et al. Japanese guidelines for atopic dermatitis 2017. Allergol Int 2017;66(2):230-247.[Abstract]
- Debinska A, Danielewicz H, Drabik-Chamerska A, et al. Filaggrin loss-of-function mutations as a predictor for atopic eczema, allergic sensitization and eczema-associated asthma in polish children population. Adv Clin Exp Med 2017;26(6):991-998.[Abstract]
- Kaufman AJ. Chapter 72 - atopic dermatitis. In: Rakel D (Ed). Integrative medicine, 4th ed, 2018. Vhatswood:Elsevier.[Source]
- Tollefson MM, Bruckner AL, Section On D. Atopic dermatitis: Skin-directed management. Ped 2014;134(6):e1735-44.[Abstract]
- Goddard AL, Lio PA. Alternative, complementary, and forgotten remedies for atopic dermatitis. Evid Comp Alt Med eCAM 2015;2015:676897.[Full Text]
- Sharma A, Loffeld A. The management of eczema in children. Paed Child Health 2015;25(2):54-59[Abstract]
- McLean WH. Filaggrin failure - from ichthyosis vulgaris to atopic eczema and beyond. Br J Dermatol 2016;175 Suppl 2:4-7.[Abstract]
- Vieira BL, Lim NR, Lohman ME, et al. Complementary and alternative medicine for atopic dermatitis: an evidence-based review. Am J Clin Dermatol 2016;17(6):557-581.[Abstract]
- Proksch E, Jensen J-M. Skin as an organ of protection. In: Goldsmith L, Katz S, Gilchrest B, et al., (Eds). Fitzpatrick’s dermatology in general medicine, 8th ed, 2008. New York City: The McGraw-Hill Companies.[Source]
- Chong M, Fonacier L. Treatment of eczema: corticosteroids and beyond. Clin Rev Allergy Immunol 2016;51(3):249-262.[Abstract]
- Holz C, Benning J, Schaudt M, et al. Novel bioactive from Lactobacillus brevis DSM 17250 to stimulate the growth of Staphylococcus epidermidis: a pilot study. Benef Microbes 2017;8(1):121-131.[Abstract]
- Hassoun LA, Sivamani RK. A systematic review of lactoferrin use in dermatology. Crit Rev Food Sci Nutr 2016:0.[Abstract]
- Takayama Y, Aoki R. Roles of lactoferrin on skin wound healing. Biochem Cell Biol 2012;90(3):497-503.[Abstract]
- Ross SM. An integrative approach to eczema (atopic dermatitis). Holist Nurs Pract 2003;17(1):56-62.[Abstract]
- Wang Y, Zhang Y, Peng G, et al. Glycyrrhizin ameliorates atopic dermatitis-like symptoms through inhibition of HMGB1. Int Immunopharmacol 2018;60:9-17.[Abstract]
- van Zuuren EJ, Fedorowicz Z, Christensen R, et al. Emollients and moisturisers for eczema. Cochrane Database Syst Rev 2017;2:Cd012119.[Abstract]
- Tiganescu A, Hupe M, Uchida Y, et al. Topical 11beta-hydroxysteroid dehydrogenase type 1 inhibition corrects cutaneous features of systemic glucocorticoid excess in female mice. Endocrinol 2018;159(1):547-556.[Abstract]
- Surjushe A, Vasani R, Saple DG. Aloe vera: a short review. I J Dermatol 2008;53(4):163-166[Abstract]
- Sahu PK, Giri DD, Singh R, et al. Therapeutic and medicinal uses of aloe vera: a review. Pharmacol Pharm 2013;04(08):599-610.[Abstract]
- Thumm EJ, Stoss M, Bayerl C, et al. Randomized trial to study efficacy of a 20% and 10% Hippophae rhamnoides containing creme used by patients with mild to intermediate atopic dermatitis. Aktuelle Dermatologie 2000;26(8):285-290.[Abstract]