Positive Health Online

Eczema (also known as atopic dermatitis or atopic eczema) affects many children and adults worldwide. Eczema is very common condition and increasing in prevalence, and has nearly tripled in industrialized countries during the past three decades.[1]

The word eczema comes from the Greek word “ekzein” which means “to boil.” Eczema is a dry skin condition and highly individual in terms that it varies from person to person and comes in many different forms. In mild cases, the skin is dry, scaly, red and itchy. In more severe cases there may be weeping, crusting and bleeding. Constant scratching causes the skin to split and bleed and also leaves it open to infection.[5]

Eczema affects people of all ages but is primarily seen in children. Recent prevalence estimates demonstrate that 15–30% of children are affected by the condition. Those who ‘grow out’ of their eczema during early childhood may see it recur again in later life.[2] To really understand what eczema is and what causes it, it helps to know something about the differences between healthy skin and skin affected by eczema.

Borage, also known as starflower

Our skin provides a strong, effective barrier that protects the body from infection or irritation. Skin is made up of a thin outer layer, a fairly elastic one in the middle, and a fatty layer at the deepest level. Each layer contains skin cells, water and fats, all of which help maintain and protect the condition of the skin. Healthy skin cells are plumped up with water, forming a protective barrier against damage and infection. Fats and oils in the skin help retain moisture, maintain body temperature and also prevent harmful substances or bacteria from entering our bodies.[15]

Filaggrin (filament-aggregating protein) has a key function in epidermal differentiation and barrier function, but the relative importance of the different functions of filaggrin in Eczema remains unclear. The gene FLG encodes a large insoluble polyprotein, profilaggrin, which is cleaved to produce multiple filaggrin peptides.[13] Filaggrin aggregates keratin 1, keratin 10 and other intermediate filaments within the cytoskeleton of keratinocytes [15), to bring about their compaction during cornification, a unique form of programmed cell death.[9] Filaggrin is a major component of the protein-lipid cornified cell envelope, which forms an important permeability barrier to water and inhibits the entry of microbes, allergens, and irritants [6), and may therefore play an important role in Eczema.

Skin affected by eczema is more liable to become red and inflamed on contact with substances that are known to irritate or cause an allergic reaction.[11] There are a number of different types of eczema which include:

• Atopic Eczema: The term ‘atopic’ refers to a personal and family tendency to develop eczema, asthma and/or hay fever;
• Contact Dermatitis is the most common type of work related skin disease;
• Seborrhoeic Eczema tends to affect the scalp, face, torso and flexures in both adults and children or babies;
• Discoid Eczema is very distinct with ‘coin shaped’ discs of eczema the size of a fifty pence piece;
• Gravitational Eczema, also called varicose or stasis eczema, is common later in life;
• Asteatotic Eczema, also known as “eczema cracquelée”, almost always affects people over the age of 60;
• The key characteristic of Pompholyx Eczema is blistering that is restricted to the hands and feet.[12]

Although the causes of eczema are largely unclear and treatments geared largely around restoring the barrier function of the dry skin typical of eczema, and alleviating skin inflammation with topical and systemic agents, it bears very much the hallmarks of a chronic, relapsing form of skin inflammation, with a disturbance of epidermal-barrier function, and IgE-mediated sensitization to foods and environmental allergens.[3] It is often the first step of the ‘atopic march’ that may lead to the development of allergic rhinitis and asthma.[13] Thus, early identification of risk factors and possible intervention strategies may lead to the discovery of measures that attenuate later expression of allergic diseases.

Eczema is a genetic condition based on the interaction between a number of genes and environmental factors. In most cases there will be a family history of either eczema or one of the other ‘atopic’ conditions i.e., asthma or hay fever.[3]

Eczema results from a complex interaction between the host (genetic susceptibility and skin barrier dysfunction) and environmental factors (allergens, irritants, and infectious agents). Genome-wide scans have identified several possible eczema loci on chromosomes 3q21.11, 16q, 17q25, 20p,12, 3p26.13, and most interestingly 1q21, which harbours a family of epithelium-related genes called the epidermal differentiation complex.[14] Thus, there are two predominant groups of genes that have been associated with eczema: genes encoding epidermal structural proteins and genes encoding major elements of the immune system, especially those important in allergic sensitization.[3]

In patients with early-onset eczema, IgE-mediated sensitization often occurs several weeks or months after the lesions appear, suggesting that the skin is the site of sensitization.[14] Recently, it has been proposed [3], that the natural history of eczema has three phases including a first and initial non-atopic phase in early infancy, when sensitization has not yet occurred; secondly, in 60–80% of patients, genetic predisposition results in the induction of IgE-mediated sensitization to foods and/or environmental allergens leading to eczema; and thirdly, scratching damages skin cells releasing auto-antigens and leading to IgE autoantibodies. Food and inhalant allergens, as well as microbial agents, contribute to eczema[16); however, the environmental and genetic factors that protect and contribute remain largely unclear.

Eczema is treated largely in allopathic medicine with antihistamines for severe pruritus, oral corticosteroids, antibiotics for infected eczema, and topical calcineurin inhibitors, such as pimecrolimus and tacrolimus.[3] These treatments appear to alleviate the condition only intermittently. Phytomedicine uses the following medicinal herbs for topical use in Eczema:

Calendula officinalis

Calendula officinalis flower extracts contain mainly triterpenes. Also present are oleanolic acid and its saponins calendulosides C–H, sterols, carotenoids and a sesquiterpene glycoside (arvoside A). Flavonoids (specifically flavonol glycosides including isoquercitrin, narcissin, neohesperidoside and rutin) have also been identified. Calendula officinalis is often used in externally-applied products for the treatment of inflammatory skin conditions such as in eczema, cuts, bruises, burns and scalds, as well as conjunctivitis.[4]

Blue Chamomile

Matricaria recutita

The flowerheads of German chamomile contain essential oil composed mainly of (-)-α-bisabolol. Sesquiterpenes and proazulenes (e.g. matricarin and matricin) are also present. Chamazulene (1 to 15%), another volatile oil found in German chamomile, is formed from matricin during steam distillation of the oil. Other constituents present in German chamomile include flavonoids (apigenin, luteolin, quercetin, rutin), and the natural coumarins umbelliferone and its methyl ether, heniarin. German chamomile is used internally as an anti-inflammatory agent also for many gastrointestinal disturbances and nervous disorders, the latter being an important element in the treatment of eczema. Topically, German chamomile is widely used in to counteract inflammatory skin conditions, including atopic eczema.[8]

Althea officinalis

Phytochemical investigation of the seeds of Althea officinalis L. (Malvaceae) led to the isolation of three new phytoconstituents, identified as n-hexacos-2-enyl-1,5-olide (altheahexacosanyl lactone), 2beta-hydroxycalamene (altheacalamene) and 5,6-dihydroxycoumarin-5-dodecanoate-6beta-D-glucopyranoside, along with the known phytoconstituents lauric acid, beta-sitosterol and lanosterol. Marshmallow is a very useful medicinal herb, as its soothing demulcent properties make it very effective in treating inflammations and irritations of the mucous membranes and equally the epidermis in the treatment of atopic eczema. The whole plant, but especially the root, is demulcent and highly emollient. The root can be used in an ointment for treating boils and abscesses.[17]

Glycorrhiza glabra

Licorice has a great number of active compounds of different classes that act in different ways. The most important constituents are usually considered to be the oleanane-type triterpenes, mainly glycyrrhizin (glycyrrhizic or glycyrrhizinic acid), to which it is usually standardized, and its aglycone glycyrrhetinic acid. There are also numerous phenolics and flavonoids of the chalcone and isoflavone type, and many natural coumarins such as liqcoumarin, umbelliferone, glabrocoumarones A and B, herniarin, and glycyrin. It also contains polysaccharides such as glycyrrhizan GA, and a small amount of volatile oil. The dried root and stolons of Licorice are used topically as an anti-inflammatory agent, largely due to its mineralocorticoid and oestrogenic activity, as a result of glycyrrhetinic acid, and therefore is used in the treatment of atopic eczema and other inflammatory skin conditions.[18]

Stellaria media

Chickweed contains the following phytochemicals: Saponins 4.5% majorly composed of gypsogenin; flavonoids such as: orientin, isoorrientin, vitexin, isovitexin; isovitexin 7,2"-di-O-beta-glucopyra-noside; isovitexin 7-O-beta-D-galactopyranoside-2"-O-beta-glucopyranoside; luteolin; apigenin; genistein, 6,8-2-C-vicenin-2; p-hydroxybenzoic acid; ferulic acid; caffeic acid; chlorogenic acid; saccharopine; aminoadipic acid; ascorbic acid; dehydroascorbic acid;[4) chickweed is chiefly used to treat irritated skin, being applied in the form of ointment or cream. Chickweed is used to alleviate pruritus, hence frequently added to topical eczema prescriptions for eczema and other inflammatory skin conditions. Chickweed works particularly well in combination with Matricaria recutita due to its strong anti-inflammatory properties and has proven very successful in the treatment of mild to chronic eczema. It can be applied to the affected areas throughout the day.[8]

Although topical treatment in Eczema performs a very important role, it is important not to ignore the recent NICE guidelines on the recognition and management of food allergy in children and young people, and stress the importance of the allergy-focused history.[19]

The guidelines cite eczema as one of several clinical scenarios that should encourage the clinician to take such a history into account, the rationale being that food allergy affects approximately 50% of children with severe eczema. The guidelines state that the allergy-focused history should elicit: 1) the nature of the 'food reaction' (symptoms, cause, reproducibility etc.); 2) presence or absence of an 'atopic diathesis' (personal or family history of food allergy, eczema, allergic rhinitis or asthma); and 3) a feeding history that includes recognition of failure to thrive. Failure to ask these 3 questions represents a missed opportunity to identify children with food allergy and attendant risks that include exacerbation of asthma and anaphylaxis as well as worsening eczema.[19] The blood test used to test for allergens is called a specific IgE test (formally known as the RAST test). It is used to measure the number of IgE antibodies in the blood that have been produced by the immune system in response to a suspected allergen.[6] An IgE blood allergy test is therefore invaluable to screen for food and other potential external allergens.

In sum, an allergy focused case history, as well as an IgE mediated allergy blood tests, to identify potential food or other external allergies, in combination with topical anti-inflammatory and skin barrier restoring agents, currently provide together the best possible outcome in patients suffering from Eczema.

References

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2. Biagini JM, LeMasters GK, Ryan PH, Levin L, Reponen T, Bernstein DI et al. Environmental risk factors of rhinitis in early infancy. Pediatr Allergy Immunol 17:278–284. 2006.

3. Bieber T. Atopic dermatitis. N Engl J Med 358:1483–1494. 2008.

4. Budzinski JW, Foster BC, Vandenhoek S, Arnason JT. An in vitro evaluation of human cytochrome P450 3A4 inhibition by selected commercial herbal extracts and tinctures. Phytomedicine 7: 273–82. 2000.

5. Bufford JD, Reardon CL, Li Z, Roberg KA, Dasilva D, Eggleston PA et al. Effects of dog ownership in early childhood on immune development and atopic diseases. Clin Exp Allergy 38:1635–1643. 2008.

6. Cho SH, Reponen T, Bernstein DI, Olds R, Levin L, Liu X et al. The effect of home characteristics on dust antigen concentrations and loads in homes. Sci Total Environ 371:31–43. 2006a.

7. Devitt A, Moffatt OD, Raykundalia C, Capra JD, Simmons DL, Gregory CD. Human CD14 mediates recognition and phagocytosis of apoptotic cells. Nature 392:505–509. 1998. [Not referenced within article.]

8. Ganzera M, Schneider P, Stuppner H. Inhibitory effects of the essential oil of chamomile (Matricaria recutitia L.) and its major constituents on human cytochrome P450 enzymes. Life Sci  78, 856–61. 2006.

9. Hudson TJ. Skin barrier function and allergic risk. Nat Genet 38:399–400. 2006.

10. Jeong DW, Kim YH, Kim HH, Ji HY, Yoo SD, Choi WR, Lee SM, Han C-K, Lee HS. Dose-linear pharmacokinetics of oleanolic acid after intravenous and oral administration in rats. Biopharm Drug Dispos. 28, 51–7. 2007. [Not referenced within article.]

11. LeMasters GK, Wilson K, Levin L, Biagini J, Ryan P, Lockey JE et al. High prevalence of aeroallergen sensitization among infants of atopic parents. J Pediatr 149:505–511. 2006.

12. Leung DY, Boguniewicz M, Howell MD, Nomura I, Hamid QA. New insights into atopic dermatitis. J Clin Invest 113:651–657. 2004.

13. Litonjua AA, Milton DK, Celedon JC, Ryan L, Weiss ST, Gold DR A longitudinal analysis of wheezing in young children: the independent effects of early life exposure to house dust endotoxin, allergens, and pets. J Allergy Clin Immunol 110:736–742. 2002.

14. Manolio TA, Bailey-Wilson JE, Collins FS  Genes, environment and the value of prospective cohort studies. Nat Rev Genet 7:812–820. 2006.

15. McGrath JA, Uitto J.  The filaggrin story: novel insights into skin-barrier function and disease. Trends Mol Med 14:20–27. 2008.

16. Meklin T, Haugland RA, Reponen T, Varma M, Lummus Z, Bernstein D et al. Quantitative PCR analysis of house dust can reveal abnormal mold conditions. J Environ Monit 6:615–620. 2004.

17. Rani S, Khan SA, Ali M. Phytochemical investigation of the seeds of Althea officinalis L. Department of Pharmaceutical Chemistry, Jamia Hamdard (Hamdard University), New Delhi 110062, India. 2010.

18. Paolini M, Pozzetti L, Sapone A, Cantelli-Forti G. Effect of licorice and glycyrrhizin on murine liver CYP-dependent monooxygenases. Life Sci  62, 571–82. 1998.

19. Sackeyfio A, Senthinathan A, Kandaswamy P, Barry P W, Baker M. Diagnosis and assessment of food allergy in children and young people: summary of NICE guidance. BMJ; 342: d74. 2011.