Dermatitis and your skin

Dermatitis is uncomfortable and itchy; skin becomes reddened, inflamed, dry and rough. It can sometimes crack. It can sometimes weep and it can sometimes affect a person’s entire body. The 2013-2014 annual contact dermatitis review from the North American Contact Dermatitis Group showed over 66% of patients tested had at least one clinically diagnosable reaction with a further 49% of patients having a full diagnosis of allergic contact dermatitis1.

Rates of allergic contact dermatitis are rising, however allergic dermatitis is not the only form of this inflammatory skin condition. In today’s western environment it’s important to understand the distinct forms of dermatitis alongside the best methods of avoidance and treatment. Preventing or treating a skin condition appropriately in its beginning stages can help to prevent the duration and severity of its path.

What is dermatitis?

Dermatitis is an umbrella term used to describe a range of skin conditions characterized by inflammation. Inflammation is the normal response of skin to stress. If skin is broken, damaged or cut, a person’s immune system is activated and inflammation is initiated.

Inflammation is a normal feature of the healing process, however its pathology is complex – with chemical mediators for vascular dilation as well as the creation of reactive oxygen species2. To heal, the body must neutralise bacteria and other similar entities. Skin requires the presence of oxidative chemicals to do this. When these ingredients are present for small portions of time, their benefits outweigh their negative effects. When inflammatory biomarkers are present for elongated periods of time e.g. in chronic conditions such as dermatitis, their ongoing presence causes damage.

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What are the different types of dermatitis?

Dermatitis is a wide reaching group of skin conditions, most colloquially referred to as eczema. In fact eczema is a specific type of dermatitis being accompanied by several others;

  1. Atopic dermatitis (eczema)
  2. Contact dermatitis
  3. Irritant dermatitis
  4. Seborrhoeic dermatitis
  5. Hand dermatitis
  6. Neurodermatitis
  7. Discoid eczema/nummular dermatitis
  8. Stasis dermatitis

Eczema or atopic dermatitis is a skin condition caused in part by genetic abnormality. Stress, allergy and lifestyle factors may provoke and flare the condition, however at its heart rests genetic vulnerability. Atopic dermatitis is estimated to affect around 20% of the western population3 often being accompanied by other atopic conditions such as asthma and hay fever. In the majority of cases eczema begins in the first 6 months from birth, with a much smaller 16% of cases beginning in adulthood4. Most commonly eczema presents itself on the inside of elbows and the backs of knees; however it can also affect all other parts of the body.

Contact dermatitis is conversely caused by exposure to a specific environmental substance. As reviews from the North American Contact Dermatitis Group show, this is often to ingredients found in skincare products such as commonly used preservative combinations. Contact dermatitis appears on areas of skin exposed to these allergens, resolving itself on avoidance of these ingredients. If the contact allergen remains unidentified the condition will worsen.

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Other forms of dermatitis such as seborrheic dermatitis and hand dermatitis effect specific areas of the body. In the case of seborrheic dermatitis, this is the scalp. Dandruff and seborrheic dermatitis are interchangeably used to describe a condition characterised by an increased presence of the malassezia yeast.

Neurodermatits is also distinct, being caused by a sensation of itching resulting in an itch-scratch cycle. It’s the initial urge to itch that causes the progression of neurodermatitis5.

Finally other dermatitis conditions such as discoid eczema present themselves with a specific visual pattern. In the instance of discoid eczema, this is described as oval sores.

What causes dermatitis?

The most common forms of dermatitis are atopic, irritant and contact. Atopic dermatitis is caused by a genetic mutation resulting in a reduced barrier function. When barrier function is reduced trans epidermal water loss increases and dryness follows. Skin then becomes more easily penetrable by everyday allergens, bacteria and viruses6, which in turn cause flares of the condition. Most recent research has highlighted the role or mutation of the filaggrin protein as a premeditator to atopic dermatitis. The filaggrin protein is responsible for several functions from the packing of skins keratin fibres to the creation of skins natural moisturising factor7.

Forms of dermatitis such as irritant and contact are not only worsened by exposure to an allergen or irritant, they are also caused by it. In conditions of allergic dermatitis, symptoms are provoked by sensitivity to an allergen. Allergens are ingredients having a relatively small molecular size making them ideal for permeating the skin barrier. When these ingredients enter the skin, they are seen as foreign and activate the skin’s immune response – resulting in inflammation. Contact allergy to ingredients such as sensitizers is cumulative, a person may be exposed to a substance for years without reaction at which point skins reaches its sensitization point and contact dermatitis begins.

Does dermatitis affect some skin types more than others?

Conditions such as atopic dermatitis and contact dermatitis appear to be related closely to similar atopic triad conditions – eczema, hay fever and asthma. These often also have a genetic basis. People with an atopic condition alongside a family history of the condition have an increased risk of dermatitis symptoms.

In addition, the nature of contact dermatitis places people who work in facilities where exposure to chemicals is frequent e.g. manufacture of perfumed products or where recurrent hand washing is common place e.g. hospital staff is at increased risk of dermatitis.

Can dermatitis be treated?

In conditions such as atopic dermatitis, symptoms can be treated and flares can be minimized to help control the condition into dormancy. In the case of atopic or irritant contact dermatitis, so long as the cause of reaction is avoided, symptoms can be effectively treated without recurrence.

The first line of defence in treatment for dermatosis is the use of emollient rich skincare. All forms of dermatitis share a reduced skin barrier function paving the way for allergens, irritants and sensitizers. Emollient rich skincare can help to replenish and reform a depleted skin barrier. Treatments containing urea – a skin identical ingredient found in skins natural moisturising factor have been found particularly effective for the rehydration of dermatitis prone skin8. The dry and irritated skin symptoms caused by dermatitis can often exasperate the condition, therefore rehydrating skin is also an extremely valid and important treatment path.

Can dermatitis be avoided? In cases of atopic dermatitis it is advisable to apply emollient rich skincare even when inflammatory skin lesions are not visible9. This will help to avoid recurrence of the condition. Low scent or fragrance free skincare is recommended, alongside skincare suited to sensitive skin types such as the griffin+row skincare range. Exposure to hot water should also be kept to a minimum.

The second line of defence is trigger identification. Cases of contact dermatitis are commonly provoked by ingredients in personal care products such as fragrance and hydroxyethyl methacrylate10, by ingredients found in wearable products such as nickel and wool and by environmental factors such as pollen. Many forms of dermatitis are worsened on exposure to commonly reactive allergens. Identification and avoidance helps to reduce and control flares.

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If you find the term “fragrance” or “perfume” on your skincare label, then this means that your skincare product may contain hundreds of undeclared chemicals, many of which may be known allergens. It goes without saying that at griffin+row we do not use any artificial fragrances or any other harmful chemicals in our products.

Can dermatitis be avoided? With appropriate avoidance of common allergens, irritants and sensitizers, dermatitis can be avoided and existing conditions lessened.

For extreme and prevalent cases of dermatitis, often topical steroid creams are prescribed. These products have proven effective in the treatment of acute flare-ups11, however are also often associated with steroid withdrawal symptoms. Treatment should be kept to small periods of time and application strengths should be tailored to the sensitivity of the skin.

With the many side effects of steroid creams, newly developed topical calcineurin inhibitors such as pimecrolimus and tacrolimus offer treatment with increased selectivity12. Studies show pimecrolimus has a good safety profile for a treatment length of up to 2 years13 and tacrolimus for up to 4 years14.

In severe to extreme cases of dermatitis phototherapy provides an additional treatment option. Therapy forms range from broad-band UVB to narrow-band UVB, UVA, UVA1, PUVA and Balneo-PUVA15. The beneficial effects of phototherapy are thought to be a consequence of several factors – anti-microbial effects against s.aureus a form of bacteria prolific on dermatitis affected skin, toxicity to immunocyte inflammatory cells and inhibition of langerham cell function16.

  1. North American Contact Dermatitis Group Patch Test Results 2013-2014. DeKoven JG, Warshaw EM, Belsito DV, Sasseville D, Maibach HI, Taylor JS, Marks JG, Fowler JF Jr, Mathias CG, DeLeo VA, Pratt MD, Zirwas MJ, Zug KA. Dermatitis. 2017 Jan/Feb;28(1):33-46. doi: 10.1097/DER.0000000000000225.

  2. Skin inflammation: reactive oxygen species and the role of iron. Trenam CW, Blake DR, Morris CJ. J Invest Dermatol. 1992 Dec;99(6):675-82.

  3. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP, Goudie DR, Sandilands A, Campbell LE, Smith FJ, O’Regan GM, Watson RM, Cecil JE, Bale SJ, Compton JG, DiGiovanna JJ, Fleckman P, Lewis-Jones S, Arseculeratne G, Sergeant A, Munro CS, El Houate B, McElreavey K, Halkjaer LB, Bisgaard H, Mukhopadhyay S, McLean WH. Nat Genet. 2006 Apr;38(4):441-6. Epub 2006 Mar 19.

  4. Adult-onset atopic dermatitis. Ozkaya E. J Am Acad Dermatol. 2005 Apr;52(4):579-82.

  5. Itch and Motivation to Scratch: An Investigation of the Central and Peripheral Correlates of Allergen- and Histamine-Induced Itch in Humans Siri G. Leknes, Susanna Bantick, Carolyn M. Willis, John D. Wilkinson, Richard G. Wise, Irene Tracey Journal of Neurophysiology Jan 2007, 97 (1) 415-422; DOI: 10.1152/jn.00070.2006

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

  7. The genetics of the skin barrier in eczema and other allergic disorders. Marenholz I, Esparza-Gordillo J, Lee YA. Curr Opin Allergy Clin Immunol. 2015 Oct;15(5):426-34. doi: 10.1097/ACI.0000000000000194

  8. Corneometric, sebumetric and TEWL measurements following the cleaning of atopic skin with a urea emulsion versus a detergent cleanser. Rudolph R, Kownatzki E. Contact Dermatitis. 2004 Jun;50(6):354-8.

  9. International Consensus Conference on Atopic Dermatitis II (ICCAD II): clinical update and current treatment strategies. Ellis C, Luger T, Abeck D, Allen R, Graham-Brown RA, De Prost Y, Eichenfield LF, Ferrandiz C, Giannetti A, Hanifin J, Koo JY, Leung D, Lynde C, Ring J, Ruiz-Maldonado R, Saurat JH; ICCAD II Faculty.Br J Dermatol. 2003 May;148 Suppl 63:3-10.

  10. North American Contact Dermatitis Group Patch Test Results 2013-2014. DeKoven JG, Warshaw EM, Belsito DV, Sasseville D, Maibach HI, Taylor JS, Marks JG, Fowler JF Jr, Mathias CG, DeLeo VA, Pratt MD, Zirwas MJ, Zug KA. Dermatitis. 2017 Jan/Feb;28(1):33-46. doi: 10.1097/DER.0000000000000225.

  11. Position paper on diagnosis and treatment of atopic dermatitis. Darsow U, Lübbe J, Taïeb A, Seidenari S, Wollenberg A, Calza AM, Giusti F, Ring J; European Task Force on Atopic Dermatitis. J Eur Acad Dermatol Venereol. 2005 May;19(3):286-95.

  12. Immunomodulation and safety of topical calcineurin inhibitors for the treatment of atopic dermatitis.Hultsch T, Kapp A, Spergel J. Dermatology. 2005;211(2):174-87. Review. Erratum in: Dermatology. 2005;211(3):292.

  13. Paul C, Cork M, Rossi AB, Papp KA, Barbier N, De Prost Y. Safety and tolerability of 1% pimecrolimus cream among infants: experience with 1133 patients treated for up to 2 years. Pediatrics 2006;117:118–28.

  14. Breuer K, Werfel T, Kapp A. Safety and efficacy of topical calcineurin inhibitors in the treatment of childhood atopic dermatitis. Am J Clin Dermatol 2005;6:65–77.

  15. Akdis, C. A., Akdis, M., Bieber, T., Bindslev-Jensen, C., Boguniewicz, M., Eigenmann, P., Hamid, Q., Kapp, A., Leung, D. Y. M., Lipozencic, J., Luger, T. A., Muraro, A., Novak, N., Platts-Mills, T. A. E., Rosenwasser, L., Scheynius, A., Simons, F. E. R., Spergel, J., Turjanmaa, K., Wahn, U., Weidinger, S., Werfel, T., Zuberbier, T. and the European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Group (2006), Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report. Allergy, 61: 969–987. doi:10.1111/j.1398-9995.2006.01153.x

  16. Phototherapy of atopic dermatitis. Scheinfeld NS, Tutrone WD, Weinberg JM, DeLeo VA. Clin Dermatol. 2003 May-Jun;21(3):241-8.

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