Art & science skin care
Current clinical practice in atopic dermatitis Odedra KM (2014) Current clinical practice in atopic dermatitis. Nursing Standard. 28, 49, 45-51. Date of submission: March 7 2014; date of acceptance: May 12 2014.
Abstract Atopic dermatitis affects both children and adults, and often presents in early life as itchy, dry skin primarily located on the face, trunk and limbs. There is usually a history of family or personal atopic disease and an increased blood level of the allergic antibody immunoglobulin E. The mainstays of treatment are emollients and corticosteroid ointments and/or creams. Other therapies include immunomodulators and management of any associated infections. Caring for a patient with atopic dermatitis requires skilled assessment, effective education and the ability to involve and support patients and carers in the management of this condition.
Author Katy Mara Odedra Asthma and allergy clinical nurse specialist, Imperial College Healthcare NHS Trust, St Mary’s Hospital, London. Correspondence to: [email protected]
Keywords Atopic dermatitis, atopic eczema, concordance, corticosteroids, dermatology, eczema review, emollients, immunomodulators, skin care
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ATOPIC DERMATITIS IS defined as a chronic itchy inflammatory skin disorder resulting in an eczematous rash, and it is also known as atopic eczema. The skin barrier can become leaky, resulting in penetration of microorganisms and allergens. Guidance on managing atopic dermatitis in children is provided by the National Institute for Health and Care Excellence (NICE) (2007) and in adults and children by the Scottish Intercollegiate Guidelines Network (SIGN) (2011), and skilled interventions by healthcare professionals are required to promote
adherence to treatment regimens. The usual treatment involves the use of emollients, topical corticosteroids and antibiotics, antivirals and/or antifungals for infections. Specialised treatments such as phototherapy or immunomodulators may be useful when conventional therapy is ineffective. Atopic dermatitis affects up to 20% of the population worldwide. Data from the International Study of Asthma and Allergies in Childhood demonstrated that atopic dermatitis prevalence rates have predominantly stabilised or decreased in some countries such as the UK and New Zealand, while prevalence rates have increased in other countries in Western Europe and South East Asia (Williams et al 2008). This illustrates that in contrast to other allergic conditions, it affects individuals in both developed and less developed countries (Mallol et al 1999, DaVeiga 2012). It has a significant effect on sleep and quality of life as well as socioeconomic effects such as restricted social interaction and employment. It is a complex condition caused by many factors, including genetics, environment and immunology, and results in skin barrier disruption. The mechanism of this disruption is not understood fully but involves innate and acquired immune responses. In some infants atopic dermatitis resolves with age, while others develop allergic conditions such as allergic rhinitis and asthma. Genetic predisposition to atopy – the production of immunoglobulin E (IgE) in response to environmental allergens – is a factor. Bergmann et al (1998) showed that children with atopic dermatitis are more likely to develop asthma than those without atopic dermatitis. If there is also an atopic family history, the chance of having asthma at age five years is 50% (Bergmann et al 1998).
Diagnostic criteria Diagnosis is based on clinical features. Atopic dermatitis usually presents in children under 12 months of age as an itchy skin condition that does not resolve, and is diagnosed if the presentation meets three or more of the following criteria (NICE 2007, SIGN 2011):
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Art & science skin care A history of or a visible flexural dermatitis involving the skin creases, including elbows (antecubital fossae), behind the knees (popliteal fossae), front of ankles and around neck and eyes, as well as dermatitis on the cheeks and/or extensor area, if under 18 months of age. Family or personal history of atopic conditions such as rhinitis and/or asthma. History of propensity to dry skin in the past year. Onset of signs and symptoms under the age of two years (not used if child is under four years old). Individuals with dark skin tones may present with atopic dermatitis on the extensor surfaces with a well-defined distribution and/or follicular papules in the eczematous area (Allen et al 2008).
Assessment History
The clinical history should include an assessment of the pruritic nature of the skin rash and its distribution, age of onset, effect on growth and development, duration of symptoms including nocturnal exacerbations, seasonal variation, infection, personal or family history of atopy and triggers such as irritants, foods or inhaled allergens (NICE 2007). The effect of the condition on the patient and his or her family can be assessed using validated questionnaires such as Severity Scoring of Atopic Dermatitis (SCORAD), Eczema Area and Severity Index (EASI) and Patient-Oriented Eczema Measure (POEM) (Schmitt et al 2007). These assessment tools collect holistic information on factors such as patient perception of the condition, quality of life and sleep disturbance.
there is a 70% likelihood that the individual will have atopic dermatitis (Brown and McLean 2012).
Investigations
Atopic dermatitis has no specific laboratory features that can be used for diagnosis. Up to 80% of patients show increased total and specific serum IgE levels but these levels are also high in patients with other atopic diseases (Leung 1995). Skin biopsy may be useful for ruling out other conditions such as psoriasis. This should not be undertaken lightly, particularly in children, and should be considered only where the diagnosis is in doubt. Swabs for culture may be useful if the skin looks infected (Figure 2). If contact atopic dermatitis is suspected, the patient should be referred for patch testing as recommended by the British Association of Dermatologists (BAD) (Bourke et al 2009).
Assessing severity
After evaluating clinical history, examination and investigation results, severity is assessed. This assessment varies widely and will influence the treatment plan. NICE (2007) provides a stepped care plan to assist this process (Table 1).
FIGURE 1 Flexural atopic dermatitis behind the knees
FIGURE 2 Infected atopic dermatitis on the forearm
SUPERSTOCK
The physical examination of a patient with atopic dermatitis should include assessment of the morphology, distribution and extent of skin lesions. The condition is usually symmetrical, occurring on the face, trunk and limbs, where it primarily affects the flexures such as behind the knees (Figure 1), elbows and wrists (Epstein et al 2004). Assessment of secondary infection is important because more than 90% of patients with chronic atopic dermatitis can be colonised with Staphylococcus aureus, which is associated with increased severity of atopic dermatitis (Guzik et al 2005). Observation of other symptoms such as dark circles under the eyes and recurrent conjunctivitis may suggest atopy. Signs that filaggrin – a vital protein in the epidermis with a role in skin barrier function – is lacking, are scaly skin on the limbs and abdomen called ichthyosis vulgaris, and palmar hyperlinearity. If ichthyosis vulgaris is present
ALAMY
Physical examination
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Variations in presentation
Clinical presentations of atopic dermatitis vary depending on patient age and disease severity. In infants, it often presents as scaling red puffy areas on the face with similar presentations on the trunk and arms. In childhood, the skin can be lichenified, especially on the antecubital and popliteal fossae, the neck and the face. In adults, it is similarly distributed, with the most noticeable symptoms being lichenification and excoriation. Severe cases may present in any distribution. In food allergyinduced atopic dermatitis, symptoms of red puffy areas may be immediate or occur two hours or up to 24 hours following ingestion of the trigger food. Other symptoms include urticaria, abdominal pain, vomiting, diarrhoea and wheezing. Further variations include follicular conditions and pityriasis alba (pale dry patches mostly presenting on the face). Patients who do not meet the diagnostic criteria should be evaluated for alternative conditions, such as those listed in Table 2, and treated accordingly.
Management The aims of treatment are to relieve symptoms and prevent and/or treat complications, which
necessitate provision of evidence-based information and education to the patient, and his or her parents or carers if appropriate (Gore et al 2005). Involving patients in consultations is one of the main methods of ensuring medicines adherence (NICE 2009), and at every clinical review it is important to evaluate adherence in a non-judgemental way when prescribing, dispensing and reviewing emollients and medicines. Atopic dermatitis is generally managed in the primary care setting. However, patients who do not respond to conventional treatments should be referred to secondary care as indicated in the criteria for referral on atopic eczema (NICE 2007).
Allergic trigger avoidance
Around 50% of children with moderate-to-severe atopic dermatitis experience IgE mediated food allergy, which can provoke skin symptoms up to 24 hours after ingestion of the trigger food (Eigenmann et al 1998, Werfel and Breuer 2004). Adolescents and adults may also react to foods but this is less common than in childhood. Common exclusion diets target egg and milk, and although safe in adults, dietetic supervision is specified in children to prevent growth retardation (NICE 2007).
TABLE 1 Stepped care plan for assessing the severity of atopic dermatitis Severity assessment
Features
Clear
Normal skin, no evidence of eczema.
Mild
Dry skin areas, intermittent pruritis.
Moderate
Dry skin areas, recurrent pruritis, redness with or without excoriation, and localised skin thickening.
Severe
Extensive dry skin, continuous itching, redness with or without excoriation, skin thickening, oedema, crusting, infection, skin cracks and skin colour changes.
(National Institute for Health and Care Excellence 2007)
TABLE 2 Common and rare alternative dermatological conditions to atopic dermatitis Common
Rare
Dermatitis
Allergic contact Irritant contact Nummular Seborrhoeic
Immunological conditions
Agammaglobulinaemia Hyperimmunoglobulin E syndrome Wiskott-Aldrich syndrome
Infection
Infection Herpes simplex (eczema herpeticum) Candida Staphlococcus aureus Scabies
Metabolic conditions
Phenylketonuria Essential fatty acid deficiency Acrodermatitis enteropathica (zinc deficiency)
(Graham-Brown et al 2004)
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Art & science skin care Other common foods that can trigger symptoms include soya, wheat, fish and nuts. The effects of inhaled allergens are under investigation, and some patients respond to a reduction in exposure to allergens such as house dust mites (Tan et al 1996, Ricci et al 2000). Weather changes, stress, irritants and ultraviolet sun exposure can exacerbate atopic dermatitis, and recognition of an individual’s triggers assists in avoiding exacerbations.
Emollients
Application of emollients is the usual daily treatment to help prevent exacerbations of atopic dermatitis and maintain skin barrier function. Emollients are best applied when the skin is moist and should be applied, along the line of hair growth, liberally and frequently, ideally three to four times per day, without rubbing in. Emollients should therefore be prescribed in large quantities. There are many types and brands of emollients, and the type used depends on the severity of the atopic dermatitis. For example, a lighter lotion or cream may be used for mild skin dryness and a heavier cream or ointment for moderate-to-severe skin dryness. Bath or shower emollients can also be used but only in addition to topical emollients. Use of pump dispensers or a clean spatula helps to limit spread of bacteria. Bandages and wet wraps are recommended for severely affected or persistent areas of atopic dermatitis (NICE 2007). The treatment options can be stepped up or down according to severity of symptoms (Table 3).
Topical corticosteroids
Inflammatory changes to atopic dermatitis require more than emollients to achieve efficacy. Topical corticosteroids are useful, but they are underused and/or administered ineffectively. This highlights the importance of effective education and understanding of the stepped care plan (NICE 2007). The aim is to use the lowest potency topical corticosteroid, and
therefore least systemically absorbed, at the lowest dosage that will control the individual’s symptoms of atopic dermatitis (British National Formulary (BNF) 2014). Adverse effects are unlikely if the stepped approach is used and the correct amount is applied to the affected areas only at the correct time. Side effects may include local skin atrophy (thinning) and very rarely suppression of the adrenal gland, resulting in reduced rate of growth in children. Ointments and creams are most useful because they are least likely to irritate the skin, and should be applied once or twice daily only (NICE 2007). Education on finger tip units (FTUs) is essential and written pictorial information is helpful. One FTU is from the end (nail tip) to the first crease of an adult’s finger. Two FTUs is approximately 1g of topical corticosteroid, and this will treat twice the size of an adult’s two hands. For example, a three to six-month-old infant will require 1 FTU to cover his or her face and neck while an adult will need 2.5 FTUs (National Eczema Society 2008). Practical information on the number of FTUs to use depending on the area of the body and age is provided in Table 4.
Immunomodulators
Immunomodulators, or drugs affecting the immune response, are topical calcineurin inhibitors, such as tacrolimus, which is licensed for short-term use in the management of atopic dermatitis in patients aged two years and older where topical corticosteroids have not achieved control or adverse side effects have been encountered (NICE 2007, SIGN 2011). Tacrolimus acts by inactivating T cells and other inflammatory cells through inhibition of calcineurin (BNF 2014). Tacrolimus and other topical calcineurin inhibitors are advantageous compared with topical corticosteroids because they can suppress itching and inflammation and do not lead to skin atrophy. The main problem is tolerating the immediate
TABLE 3 Treatment options for atopic dermatitis based on severity of symptoms Clear skin Treatment is stepped up or down according to physical severity.
Emollients (body, face and neck).
Mild atopic dermatitis Emollients Mild topical corticosteroids as required (body, face and neck).
Moderate atopic dermatitis Emollients Moderate topical corticosteroids (body or severe flares on face and neck). Tacrolimus (body) Mild topical corticosteroids (face and neck) Topical calcineurin inhibitors (face and neck) Bandages
Severe atopic dermatitis Emollients Potent topical corticosteroids (body) Tacrolimus Bandages Phototherapy Systemic therapy (body, face and neck)
(Adapted from the National Institute for Health and Care Excellence 2007)
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TABLE 4 Finger tip unit (FTU) measurement for topical corticosteroid application in different age groups Recommended FTU application by age group Area of skin requiring treatment Front of chest and abdomen Back and buttocks
3-6 months
1-2 years old
3-5 years old
6-10 years old
Adult
1
1.5
1.5
2
7
1
1.5
2
2.5
7
Face and neck
1.5
2
3
4.5
2.5
Arm and hand
1
2
3
3.5
4
1.5
3
3.5
5
8
Leg and foot
(Adapted from the National Eczema Society 2008)
stinging on application. This agent should not be used if the skin appears infected because it can hinder normal immune response.
Treatment of infection
Infected atopic dermatitis should be treated based on the results of a wound swab. Infection with S. aureus can aggravate atopic dermatitis by producing toxins that activate T cells to release cytokines, which increase inflammation. Physical indicators that are suggestive are pustules, crusting and weeping discharge. Treatment with appropriate antibiotics and long-term use of antiseptics with emollients in the bath may reduce bacterial colonisation. Eczema herpeticum may require admission to hospital for systemic antiviral therapy since life-threatening dissemination has been reported, but this may be avoided through early recognition and treatment (Novelli et al 1988, Aronson et al 2011).
Phototherapy
Phototherapy should be considered for severe atopic dermatitis only. UVA and UVB exposure reduces cytokine production and increases thickening of the skin, which augments the expression of filaggrin (Tintle et al 2011). However, phototherapy should be initiated only with specialist dermatological supervision (NICE 2007). A similar type of treatment, psoralen plus ultraviolet light therapy (PUVA), makes the skin more sensitive to UV light and therefore improves the effectiveness of phototherapy (NICE 2007). There is little information about the long-term side effects of phototherapy, although it is regarded as a valuable and relatively safe option in the treatment of atopic dermatitis (Walker and Jacobe 2011).
Systemic treatments
Only a specialist dermatologist should commence a patient on systemic immunosuppressive therapies such as azathioprine, ciclosporin, methotrexate and oral corticosteroids. A systematic review concluded
that the use of ciclosporin in the short term is efficacious, while azathioprine and methotrexate are regarded as second and third-line treatments because of weak evidence and overall limited efficacy (Roekevisch et al 2014). The monoclonal antibody omalizumab (anti-IgE antibody) is not licenced for treatment of atopic dermatitis, although studies have demonstrated benefit in some patients (Babu et al 2013, Hotze et al 2014), and therefore omalizumab may be considered for use on a case-by-case basis.
Antihistamine use
The cause of itching in patients with atopic dermatitis is generally not the release of histamine but is much more complicated. It is thought to involve particular nerve fibres that may be activated by inflammatory cells and/or signalling molecules including interleukins and eosinophils in the skin (Darsow et al 2014). Therefore, it could be argued that antihistamines are of limited value in relieving itch in atopic dermatitis. This cannot be refuted or supported after a recent systematic review could not find, because of ethical issues raised, any randomised controlled trials using antihistamines as monotherapy (Apfelbacher et al 2013). However, nocturnal itch can respond to a sedating antihistamine such as hydroxyzine and chlorphenamine mainly as a result of sedative effects (Apfelbacher et al 2013).
Complementary and emerging therapies
In vitro studies have shown that increasing filaggrin levels in the skin decrease atopic dermatitis, and there are trials ongoing in Dundee (Brown and McLean 2012). There are many markers within specific chromosomal regions that have been linked to atopic dermatitis and asthma but as yet genetic studies have not resulted in appropriate therapies. Complementary therapies such as homeopathy, food supplementation, massage and hypnotherapy may be useful in reducing the habitual scratching, but the efficacy of these therapies is anecdotal.
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Art & science skin care As with all allergic diseases, the question arises as to whether atopic dermatitis can be prevented. A systematic review of eczema prevention concluded there is no clear evidence to show that efforts to prevent eczema are effective and therefore novel approaches are required (Foisy et al 2011). Barrier Enhancement for Eczema Prevention was a study set up in Nottingham on the premise that early skin barrier protection can stop and/or delay the onset of both atopic and non-atopic dermatitis (Williams 2012). The data were presented at the 2012 British Society of Allergy and Clinical Immunology conference but are not yet published. Early skin barrier protection shows promising results and may help prevent the development of sensitisation and halt the development and progression of allergic disease.
Role of the nurse Careful education, monitoring and support provided by the nurse are essential for patients with atopic dermatitis, together with maintenance on appropriate therapy and prompt treatment for flares and infections. Identifying potential triggers is important (Box 1), and subsequent avoidance advice can be provided by the nurse.
Awareness of the effect of atopic dermatitis on quality of life including sleep, psychosocial wellbeing and leisure of the patient and carers should be recognised and understood. Lack of concordance with therapy is the main cause of treatment failure. Effective management of the condition therefore relies on establishing therapeutic relationships between the healthcare professional, patients and carers to ensure patient
BOX 1 Triggers for atopic dermatitis Animal dander (pets). Clothing – woollens, tight fitting. Foods. Hormonal changes in women. House dust mites. Infection and skin bacteria. Pollens. Pollution. Soaps, detergents, toiletries, perfumes. Stress, itch scratch cycle, and long fingernails where dirt and bacteria can be harboured and skin easily damaged. Temperature (extremes of hot/cold, sweat). (Adapted from NHS Choices 2014)
References Allen HB, Jones NP, Bowen SE (2008) Lichenoid and other clinical presentations of atopic dermatitis in an inner city practice. Journal of the American Academy of Dermatology. 58, 3, 503-504. Apfelbacher CJ, van Zuuren EJ, Fedorowicz Z, Jupiter A, Matterne U, Weisshaar E (2013) Oral H1 antihistamines as monotherapy for eczema. Cochrane Database of Systematic Reviews. Issue 2, No. CD007770. Aronson PL, Yan AC, Mittal MK, Mohamad Z, Shah SS (2011) Delayed acyclovir and outcomes of children hospitalized with eczema herpeticum. Pediatrics. 128, 6, 1161-1167. Babu KS, Polosa R, Morjaria JB (2013) Anti-IgE – emerging opportunities for omalizumab. Expert Opinion on Biological Therapy. 13, 5, 765-777.
Bergmann RL, Edenharter G, Bergmann KE et al (1998) Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clinical and Experimental Allergy. 28, 8, 965-970. Bourke J, Coulson I, English J (2009) Guidelines for the management of contact dermatitis: an update. British Journal of Dermatology. 160, 5, 946-954. British National Formulary (2014) British National Formulary No. 67. British Medical Association and Royal Pharmaceutical Society of Great Britain, London. Brown SJ, McLean WHI (2012) One remarkable molecule: filaggrin. Journal of Investigative Dermatology. 132, 3 Pt 2, 751-762. Darsow U, Raap U, Ständer S (2014) Chapter 3. Atopic dermatitis. www.ncbi.nlm.nih.gov/
books/NBK200925 (Last accessed: July 14 2014.) DaVeiga SP (2012) Epidemiology of atopic dermatitis: a review. Allergy and Asthma Proceedings. 33, 3, 227-234. Eigenmann PA, Sicherer SH, Borkowski TA, Cohen BA, Sampson HA (1998) Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics. 101, 3, E8. Epstein O, Perkin GD, Cookson J, de Bono DP, Solomons N, Robins A (2004) Clinical Examination. Third edition. Mosby, Edinburgh. Foisy M, Boyle RJ, Chalmers JR, Simpson EL, Williams HC (2011) Overview of reviews. The prevention of eczema in infants and children: an overview of Cochrane and non-Cochrane reviews. Evidence-Based Child Health. 6, 5, 1322-1339.
Gore C, Johnson RJ, Caress AL, Woodcock A, Custovic A (2005) The information needs and preferred roles in treatment decision-making of parents caring for infants with atopic dermatitis: a qualitative study. Allergy. 60, 7, 938-943. Graham-Brown R, Savin J, Milner J (2004) In Clinical Practice Series: Dermatology. Churchill Livingstone. Guzik TJ, Bzowska M, Kasprowicz A et al (2005) Persistent skin colonization with Staphylococcus aureus in atopic dermatitis: relationship to clinical and immunological parameters. Clinical and Experimental Allergy. 35, 4, 448-455. Hotze M, Baurecht H, Rodríguez E et al (2014) Increased efficacy of omalizumab in atopic dermatitis patients with wild-type filaggrin status and higher serum levels of
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concordance and accurate monitoring of treatment response. This means involving patients and/or carers in the decision-making process by, for example, explaining the side effects of treatment and reassuring patients and/or carers that the benefits of treatment significantly outweigh potential side effects. Adapting the treatment plan to make it more cosmetically acceptable, for example using oil-based ointments at night and water-based creams during the day, is essential to promote concordance. Providing an individualised self-management plan that details information on how much ointment and/or cream to use, how to apply it and a stepped approach to management is valuable. This should be provided in combination with a verbal explanation and practical demonstration on the application of topical creams and ointments. As the quality of available information varies, it is helpful to guide patients to resources such as www.patient.co.uk and NHS Choices (www.nhs.uk), support groups and patient guidance and/or information sheets from the National Eczema Society and BAD. These are valuable resources for the nurse in combination with national guidelines from BAD, SIGN and NICE.
phosphatidylcholines. Allergy. 69, 1, 132-135. Leung DY (1995) Atopic dermatitis: the skin as a window into the pathogenesis of chronic allergic diseases. Journal of Allergy and Clinical Immunology. 96, 3, 302-318. Mallol J, Asher I, Williams H, Clayton T, Beasley R (1999) ISAAC findings in children aged 13-14 years – an overview. Allergy and Clinical Immunology International. 11, 176-182. National Eczema Society (2008) Factsheet: Topical Steroids. www. eczema.org/documents/153 (Last accessed: July 14 2014.) National Institute for Health and Care Excellence (2007) Atopic Eczema in Children. Clinical guideline No. 57. NICE, London. National Institute for Health and
Conclusion The burden of chronic disease in healthcare services is increasing. Atopic dermatitis is a common and complex condition which requires skilled assessment, education and individualised treatment that maximises effectiveness and respects patient choice. Nurses can provide a holistic approach to its long-term management, ensuring concordance with treatment regimen and accurate monitoring of treatment response. Knowledge of the therapies available is vital alongside developments in different treatment modalities and trials of preventive therapies that offer hopeful advances for the future NS
GLOSSARY Atopic Genetic predisposition to develop allergies. Dander Hair and skin shed from mammals that contain allergen particles. Excoriation Skin abrasion. Immunomodulators An agent that enhances or lessens immune response. Lichenification Thickening of the epidermal layer of the skin. Palmar hyperlinearity Pronounced skin creases in the palm of the hand. Papules Solid raised spot on the skin less than 1cm in diameter. Pruritis Severe itch, often caused by allergy and infection. Rhinoconjunctivitis Inflammation and irritation of the nasal membranes and conjunctiva often referred to as hay fever. Urticaria Raised bumpy, itchy, red rash also known as hives. It often presents in response to an allergen.
Care Excellence (2009) Medicines Adherence. Involving Patients in Decisions About Prescribed Medicines and Supporting Adherence. Clinical guideline No. 76. NICE, London.
Immunology. 133, 2, 429-438.
NHS Choices (2014) Eczema: 7 Tips to Stop the Itch. tinyurl.com/op6wqzf (Last accessed July 14 2014.)
Schmitt J, Langan S, Williams HC; European Dermato-Epidemiology Network (2007) What are the best outcome measurements for atopic eczema? A systematic review. Journal of Allergy and Clinical Immunology. 120, 6, 1389-1398.
Novelli VM, Atherton DJ, Marshall WC (1988) Eczema herpeticum. Clinical and Laboratory features. Clinical Pediatrics. 27, 5, 231-233.
Scottish Intercollegiate Guidelines Network (2011) Management of Atopic Eczema in Primary Care. National clinical guideline No. 125. SIGN, Edinburgh.
Ricci G, Patrizi A, Specchia F et al (2000) Effect of house dust mite avoidance measures in children with atopic dermatitis. British Journal of Dermatology. 143, 2, 379-384.
Tan BB, Weald D, Strickland I, Friedmann PS (1996) Double-blind controlled trial of effect of house dust mite allergen avoidance on atopic dermatitis. The Lancet. 347, 8993, 15-18.
Roekevisch E, Spuls PI, Kuester D, Limpens J, Schmitt J (2014) Efficacy and safety of systemic treatments for moderate-to-severe atopic dermatitis: a systematic review. Journal of Allergy and Clinical
Tintle S, Shemer A, Suárez-Fariñas M et al (2011) Reversal of atopic dermatitis with narrow-band UVB phototherapy and biomarkers for therapeutic response. Journal of
Allergy and Clinical Immunology. 128, 3, 583-593. Walker D, Jacobe H (2011) Phototherapy in the age of biologics. Seminars in Cutaneous Medicine and Surgery. 30, 4, 190-198. Werfel T, Breuer K (2004) Role of food allergy in atopic dermatitis. Current Opinion in Allergy and Clinical Immunology. 4, 5, 379-385. Wiliams H (2012) BEEP Study Findings. Oral presentation at the British Society of Allergy and Clinical Immunology (BSACI) Conference. July 2-4, Nottingham. Williams H, Stewart A, von Mutius E, Cookson W, Anderson HR; International Study of Asthma and Allergies in Childhood (ISAAC) Phase One and Three Study Groups (2008) Is eczema really on the increase worldwide? Journal of Allergy and Clinical Immunology. 121, 4, 947-954.
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Current clinical practice in atopic dermatitis Odedra KM (2014) Current clinical practice in atopic dermatitis. Nursing Standard. 28, 49, 45-51. Date of submission: March 7 2014; date of acceptance: May 12 2014.
Abstract Atopic dermatitis affects both children and adults, and often presents in early life as itchy, dry skin primarily located on the face, trunk and limbs. There is usually a history of family or personal atopic disease and an increased blood level of the allergic antibody immunoglobulin E. The mainstays of treatment are emollients and corticosteroid ointments and/or creams. Other therapies include immunomodulators and management of any associated infections. Caring for a patient with atopic dermatitis requires skilled assessment, effective education and the ability to involve and support patients and carers in the management of this condition.
Author Katy Mara Odedra Asthma and allergy clinical nurse specialist, Imperial College Healthcare NHS Trust, St Mary’s Hospital, London. Correspondence to: [email protected]
Keywords Atopic dermatitis, atopic eczema, concordance, corticosteroids, dermatology, eczema review, emollients, immunomodulators, skin care
Review All articles are subject to external double-blind peer review and checked for plagiarism using automated software.
Online For related articles visit the archive and search using the keywords above. Guidelines on writing for publication are available at: rcnpublishing.com/r/author-guidelines
ATOPIC DERMATITIS IS defined as a chronic itchy inflammatory skin disorder resulting in an eczematous rash, and it is also known as atopic eczema. The skin barrier can become leaky, resulting in penetration of microorganisms and allergens. Guidance on managing atopic dermatitis in children is provided by the National Institute for Health and Care Excellence (NICE) (2007) and in adults and children by the Scottish Intercollegiate Guidelines Network (SIGN) (2011), and skilled interventions by healthcare professionals are required to promote
adherence to treatment regimens. The usual treatment involves the use of emollients, topical corticosteroids and antibiotics, antivirals and/or antifungals for infections. Specialised treatments such as phototherapy or immunomodulators may be useful when conventional therapy is ineffective. Atopic dermatitis affects up to 20% of the population worldwide. Data from the International Study of Asthma and Allergies in Childhood demonstrated that atopic dermatitis prevalence rates have predominantly stabilised or decreased in some countries such as the UK and New Zealand, while prevalence rates have increased in other countries in Western Europe and South East Asia (Williams et al 2008). This illustrates that in contrast to other allergic conditions, it affects individuals in both developed and less developed countries (Mallol et al 1999, DaVeiga 2012). It has a significant effect on sleep and quality of life as well as socioeconomic effects such as restricted social interaction and employment. It is a complex condition caused by many factors, including genetics, environment and immunology, and results in skin barrier disruption. The mechanism of this disruption is not understood fully but involves innate and acquired immune responses. In some infants atopic dermatitis resolves with age, while others develop allergic conditions such as allergic rhinitis and asthma. Genetic predisposition to atopy – the production of immunoglobulin E (IgE) in response to environmental allergens – is a factor. Bergmann et al (1998) showed that children with atopic dermatitis are more likely to develop asthma than those without atopic dermatitis. If there is also an atopic family history, the chance of having asthma at age five years is 50% (Bergmann et al 1998).
Diagnostic criteria Diagnosis is based on clinical features. Atopic dermatitis usually presents in children under 12 months of age as an itchy skin condition that does not resolve, and is diagnosed if the presentation meets three or more of the following criteria (NICE 2007, SIGN 2011):
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Art & science skin care A history of or a visible flexural dermatitis involving the skin creases, including elbows (antecubital fossae), behind the knees (popliteal fossae), front of ankles and around neck and eyes, as well as dermatitis on the cheeks and/or extensor area, if under 18 months of age. Family or personal history of atopic conditions such as rhinitis and/or asthma. History of propensity to dry skin in the past year. Onset of signs and symptoms under the age of two years (not used if child is under four years old). Individuals with dark skin tones may present with atopic dermatitis on the extensor surfaces with a well-defined distribution and/or follicular papules in the eczematous area (Allen et al 2008).
Assessment History
The clinical history should include an assessment of the pruritic nature of the skin rash and its distribution, age of onset, effect on growth and development, duration of symptoms including nocturnal exacerbations, seasonal variation, infection, personal or family history of atopy and triggers such as irritants, foods or inhaled allergens (NICE 2007). The effect of the condition on the patient and his or her family can be assessed using validated questionnaires such as Severity Scoring of Atopic Dermatitis (SCORAD), Eczema Area and Severity Index (EASI) and Patient-Oriented Eczema Measure (POEM) (Schmitt et al 2007). These assessment tools collect holistic information on factors such as patient perception of the condition, quality of life and sleep disturbance.
there is a 70% likelihood that the individual will have atopic dermatitis (Brown and McLean 2012).
Investigations
Atopic dermatitis has no specific laboratory features that can be used for diagnosis. Up to 80% of patients show increased total and specific serum IgE levels but these levels are also high in patients with other atopic diseases (Leung 1995). Skin biopsy may be useful for ruling out other conditions such as psoriasis. This should not be undertaken lightly, particularly in children, and should be considered only where the diagnosis is in doubt. Swabs for culture may be useful if the skin looks infected (Figure 2). If contact atopic dermatitis is suspected, the patient should be referred for patch testing as recommended by the British Association of Dermatologists (BAD) (Bourke et al 2009).
Assessing severity
After evaluating clinical history, examination and investigation results, severity is assessed. This assessment varies widely and will influence the treatment plan. NICE (2007) provides a stepped care plan to assist this process (Table 1).
FIGURE 1 Flexural atopic dermatitis behind the knees
FIGURE 2 Infected atopic dermatitis on the forearm
SUPERSTOCK
The physical examination of a patient with atopic dermatitis should include assessment of the morphology, distribution and extent of skin lesions. The condition is usually symmetrical, occurring on the face, trunk and limbs, where it primarily affects the flexures such as behind the knees (Figure 1), elbows and wrists (Epstein et al 2004). Assessment of secondary infection is important because more than 90% of patients with chronic atopic dermatitis can be colonised with Staphylococcus aureus, which is associated with increased severity of atopic dermatitis (Guzik et al 2005). Observation of other symptoms such as dark circles under the eyes and recurrent conjunctivitis may suggest atopy. Signs that filaggrin – a vital protein in the epidermis with a role in skin barrier function – is lacking, are scaly skin on the limbs and abdomen called ichthyosis vulgaris, and palmar hyperlinearity. If ichthyosis vulgaris is present
ALAMY
Physical examination
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Variations in presentation
Clinical presentations of atopic dermatitis vary depending on patient age and disease severity. In infants, it often presents as scaling red puffy areas on the face with similar presentations on the trunk and arms. In childhood, the skin can be lichenified, especially on the antecubital and popliteal fossae, the neck and the face. In adults, it is similarly distributed, with the most noticeable symptoms being lichenification and excoriation. Severe cases may present in any distribution. In food allergyinduced atopic dermatitis, symptoms of red puffy areas may be immediate or occur two hours or up to 24 hours following ingestion of the trigger food. Other symptoms include urticaria, abdominal pain, vomiting, diarrhoea and wheezing. Further variations include follicular conditions and pityriasis alba (pale dry patches mostly presenting on the face). Patients who do not meet the diagnostic criteria should be evaluated for alternative conditions, such as those listed in Table 2, and treated accordingly.
Management The aims of treatment are to relieve symptoms and prevent and/or treat complications, which
necessitate provision of evidence-based information and education to the patient, and his or her parents or carers if appropriate (Gore et al 2005). Involving patients in consultations is one of the main methods of ensuring medicines adherence (NICE 2009), and at every clinical review it is important to evaluate adherence in a non-judgemental way when prescribing, dispensing and reviewing emollients and medicines. Atopic dermatitis is generally managed in the primary care setting. However, patients who do not respond to conventional treatments should be referred to secondary care as indicated in the criteria for referral on atopic eczema (NICE 2007).
Allergic trigger avoidance
Around 50% of children with moderate-to-severe atopic dermatitis experience IgE mediated food allergy, which can provoke skin symptoms up to 24 hours after ingestion of the trigger food (Eigenmann et al 1998, Werfel and Breuer 2004). Adolescents and adults may also react to foods but this is less common than in childhood. Common exclusion diets target egg and milk, and although safe in adults, dietetic supervision is specified in children to prevent growth retardation (NICE 2007).
TABLE 1 Stepped care plan for assessing the severity of atopic dermatitis Severity assessment
Features
Clear
Normal skin, no evidence of eczema.
Mild
Dry skin areas, intermittent pruritis.
Moderate
Dry skin areas, recurrent pruritis, redness with or without excoriation, and localised skin thickening.
Severe
Extensive dry skin, continuous itching, redness with or without excoriation, skin thickening, oedema, crusting, infection, skin cracks and skin colour changes.
(National Institute for Health and Care Excellence 2007)
TABLE 2 Common and rare alternative dermatological conditions to atopic dermatitis Common
Rare
Dermatitis
Allergic contact Irritant contact Nummular Seborrhoeic
Immunological conditions
Agammaglobulinaemia Hyperimmunoglobulin E syndrome Wiskott-Aldrich syndrome
Infection
Infection Herpes simplex (eczema herpeticum) Candida Staphlococcus aureus Scabies
Metabolic conditions
Phenylketonuria Essential fatty acid deficiency Acrodermatitis enteropathica (zinc deficiency)
(Graham-Brown et al 2004)
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Art & science skin care Other common foods that can trigger symptoms include soya, wheat, fish and nuts. The effects of inhaled allergens are under investigation, and some patients respond to a reduction in exposure to allergens such as house dust mites (Tan et al 1996, Ricci et al 2000). Weather changes, stress, irritants and ultraviolet sun exposure can exacerbate atopic dermatitis, and recognition of an individual’s triggers assists in avoiding exacerbations.
Emollients
Application of emollients is the usual daily treatment to help prevent exacerbations of atopic dermatitis and maintain skin barrier function. Emollients are best applied when the skin is moist and should be applied, along the line of hair growth, liberally and frequently, ideally three to four times per day, without rubbing in. Emollients should therefore be prescribed in large quantities. There are many types and brands of emollients, and the type used depends on the severity of the atopic dermatitis. For example, a lighter lotion or cream may be used for mild skin dryness and a heavier cream or ointment for moderate-to-severe skin dryness. Bath or shower emollients can also be used but only in addition to topical emollients. Use of pump dispensers or a clean spatula helps to limit spread of bacteria. Bandages and wet wraps are recommended for severely affected or persistent areas of atopic dermatitis (NICE 2007). The treatment options can be stepped up or down according to severity of symptoms (Table 3).
Topical corticosteroids
Inflammatory changes to atopic dermatitis require more than emollients to achieve efficacy. Topical corticosteroids are useful, but they are underused and/or administered ineffectively. This highlights the importance of effective education and understanding of the stepped care plan (NICE 2007). The aim is to use the lowest potency topical corticosteroid, and
therefore least systemically absorbed, at the lowest dosage that will control the individual’s symptoms of atopic dermatitis (British National Formulary (BNF) 2014). Adverse effects are unlikely if the stepped approach is used and the correct amount is applied to the affected areas only at the correct time. Side effects may include local skin atrophy (thinning) and very rarely suppression of the adrenal gland, resulting in reduced rate of growth in children. Ointments and creams are most useful because they are least likely to irritate the skin, and should be applied once or twice daily only (NICE 2007). Education on finger tip units (FTUs) is essential and written pictorial information is helpful. One FTU is from the end (nail tip) to the first crease of an adult’s finger. Two FTUs is approximately 1g of topical corticosteroid, and this will treat twice the size of an adult’s two hands. For example, a three to six-month-old infant will require 1 FTU to cover his or her face and neck while an adult will need 2.5 FTUs (National Eczema Society 2008). Practical information on the number of FTUs to use depending on the area of the body and age is provided in Table 4.
Immunomodulators
Immunomodulators, or drugs affecting the immune response, are topical calcineurin inhibitors, such as tacrolimus, which is licensed for short-term use in the management of atopic dermatitis in patients aged two years and older where topical corticosteroids have not achieved control or adverse side effects have been encountered (NICE 2007, SIGN 2011). Tacrolimus acts by inactivating T cells and other inflammatory cells through inhibition of calcineurin (BNF 2014). Tacrolimus and other topical calcineurin inhibitors are advantageous compared with topical corticosteroids because they can suppress itching and inflammation and do not lead to skin atrophy. The main problem is tolerating the immediate
TABLE 3 Treatment options for atopic dermatitis based on severity of symptoms Clear skin Treatment is stepped up or down according to physical severity.
Emollients (body, face and neck).
Mild atopic dermatitis Emollients Mild topical corticosteroids as required (body, face and neck).
Moderate atopic dermatitis Emollients Moderate topical corticosteroids (body or severe flares on face and neck). Tacrolimus (body) Mild topical corticosteroids (face and neck) Topical calcineurin inhibitors (face and neck) Bandages
Severe atopic dermatitis Emollients Potent topical corticosteroids (body) Tacrolimus Bandages Phototherapy Systemic therapy (body, face and neck)
(Adapted from the National Institute for Health and Care Excellence 2007)
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TABLE 4 Finger tip unit (FTU) measurement for topical corticosteroid application in different age groups Recommended FTU application by age group Area of skin requiring treatment Front of chest and abdomen Back and buttocks
3-6 months
1-2 years old
3-5 years old
6-10 years old
Adult
1
1.5
1.5
2
7
1
1.5
2
2.5
7
Face and neck
1.5
2
3
4.5
2.5
Arm and hand
1
2
3
3.5
4
1.5
3
3.5
5
8
Leg and foot
(Adapted from the National Eczema Society 2008)
stinging on application. This agent should not be used if the skin appears infected because it can hinder normal immune response.
Treatment of infection
Infected atopic dermatitis should be treated based on the results of a wound swab. Infection with S. aureus can aggravate atopic dermatitis by producing toxins that activate T cells to release cytokines, which increase inflammation. Physical indicators that are suggestive are pustules, crusting and weeping discharge. Treatment with appropriate antibiotics and long-term use of antiseptics with emollients in the bath may reduce bacterial colonisation. Eczema herpeticum may require admission to hospital for systemic antiviral therapy since life-threatening dissemination has been reported, but this may be avoided through early recognition and treatment (Novelli et al 1988, Aronson et al 2011).
Phototherapy
Phototherapy should be considered for severe atopic dermatitis only. UVA and UVB exposure reduces cytokine production and increases thickening of the skin, which augments the expression of filaggrin (Tintle et al 2011). However, phototherapy should be initiated only with specialist dermatological supervision (NICE 2007). A similar type of treatment, psoralen plus ultraviolet light therapy (PUVA), makes the skin more sensitive to UV light and therefore improves the effectiveness of phototherapy (NICE 2007). There is little information about the long-term side effects of phototherapy, although it is regarded as a valuable and relatively safe option in the treatment of atopic dermatitis (Walker and Jacobe 2011).
Systemic treatments
Only a specialist dermatologist should commence a patient on systemic immunosuppressive therapies such as azathioprine, ciclosporin, methotrexate and oral corticosteroids. A systematic review concluded
that the use of ciclosporin in the short term is efficacious, while azathioprine and methotrexate are regarded as second and third-line treatments because of weak evidence and overall limited efficacy (Roekevisch et al 2014). The monoclonal antibody omalizumab (anti-IgE antibody) is not licenced for treatment of atopic dermatitis, although studies have demonstrated benefit in some patients (Babu et al 2013, Hotze et al 2014), and therefore omalizumab may be considered for use on a case-by-case basis.
Antihistamine use
The cause of itching in patients with atopic dermatitis is generally not the release of histamine but is much more complicated. It is thought to involve particular nerve fibres that may be activated by inflammatory cells and/or signalling molecules including interleukins and eosinophils in the skin (Darsow et al 2014). Therefore, it could be argued that antihistamines are of limited value in relieving itch in atopic dermatitis. This cannot be refuted or supported after a recent systematic review could not find, because of ethical issues raised, any randomised controlled trials using antihistamines as monotherapy (Apfelbacher et al 2013). However, nocturnal itch can respond to a sedating antihistamine such as hydroxyzine and chlorphenamine mainly as a result of sedative effects (Apfelbacher et al 2013).
Complementary and emerging therapies
In vitro studies have shown that increasing filaggrin levels in the skin decrease atopic dermatitis, and there are trials ongoing in Dundee (Brown and McLean 2012). There are many markers within specific chromosomal regions that have been linked to atopic dermatitis and asthma but as yet genetic studies have not resulted in appropriate therapies. Complementary therapies such as homeopathy, food supplementation, massage and hypnotherapy may be useful in reducing the habitual scratching, but the efficacy of these therapies is anecdotal.
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Art & science skin care As with all allergic diseases, the question arises as to whether atopic dermatitis can be prevented. A systematic review of eczema prevention concluded there is no clear evidence to show that efforts to prevent eczema are effective and therefore novel approaches are required (Foisy et al 2011). Barrier Enhancement for Eczema Prevention was a study set up in Nottingham on the premise that early skin barrier protection can stop and/or delay the onset of both atopic and non-atopic dermatitis (Williams 2012). The data were presented at the 2012 British Society of Allergy and Clinical Immunology conference but are not yet published. Early skin barrier protection shows promising results and may help prevent the development of sensitisation and halt the development and progression of allergic disease.
Role of the nurse Careful education, monitoring and support provided by the nurse are essential for patients with atopic dermatitis, together with maintenance on appropriate therapy and prompt treatment for flares and infections. Identifying potential triggers is important (Box 1), and subsequent avoidance advice can be provided by the nurse.
Awareness of the effect of atopic dermatitis on quality of life including sleep, psychosocial wellbeing and leisure of the patient and carers should be recognised and understood. Lack of concordance with therapy is the main cause of treatment failure. Effective management of the condition therefore relies on establishing therapeutic relationships between the healthcare professional, patients and carers to ensure patient
BOX 1 Triggers for atopic dermatitis Animal dander (pets). Clothing – woollens, tight fitting. Foods. Hormonal changes in women. House dust mites. Infection and skin bacteria. Pollens. Pollution. Soaps, detergents, toiletries, perfumes. Stress, itch scratch cycle, and long fingernails where dirt and bacteria can be harboured and skin easily damaged. Temperature (extremes of hot/cold, sweat). (Adapted from NHS Choices 2014)
References Allen HB, Jones NP, Bowen SE (2008) Lichenoid and other clinical presentations of atopic dermatitis in an inner city practice. Journal of the American Academy of Dermatology. 58, 3, 503-504. Apfelbacher CJ, van Zuuren EJ, Fedorowicz Z, Jupiter A, Matterne U, Weisshaar E (2013) Oral H1 antihistamines as monotherapy for eczema. Cochrane Database of Systematic Reviews. Issue 2, No. CD007770. Aronson PL, Yan AC, Mittal MK, Mohamad Z, Shah SS (2011) Delayed acyclovir and outcomes of children hospitalized with eczema herpeticum. Pediatrics. 128, 6, 1161-1167. Babu KS, Polosa R, Morjaria JB (2013) Anti-IgE – emerging opportunities for omalizumab. Expert Opinion on Biological Therapy. 13, 5, 765-777.
Bergmann RL, Edenharter G, Bergmann KE et al (1998) Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clinical and Experimental Allergy. 28, 8, 965-970. Bourke J, Coulson I, English J (2009) Guidelines for the management of contact dermatitis: an update. British Journal of Dermatology. 160, 5, 946-954. British National Formulary (2014) British National Formulary No. 67. British Medical Association and Royal Pharmaceutical Society of Great Britain, London. Brown SJ, McLean WHI (2012) One remarkable molecule: filaggrin. Journal of Investigative Dermatology. 132, 3 Pt 2, 751-762. Darsow U, Raap U, Ständer S (2014) Chapter 3. Atopic dermatitis. www.ncbi.nlm.nih.gov/
books/NBK200925 (Last accessed: July 14 2014.) DaVeiga SP (2012) Epidemiology of atopic dermatitis: a review. Allergy and Asthma Proceedings. 33, 3, 227-234. Eigenmann PA, Sicherer SH, Borkowski TA, Cohen BA, Sampson HA (1998) Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics. 101, 3, E8. Epstein O, Perkin GD, Cookson J, de Bono DP, Solomons N, Robins A (2004) Clinical Examination. Third edition. Mosby, Edinburgh. Foisy M, Boyle RJ, Chalmers JR, Simpson EL, Williams HC (2011) Overview of reviews. The prevention of eczema in infants and children: an overview of Cochrane and non-Cochrane reviews. Evidence-Based Child Health. 6, 5, 1322-1339.
Gore C, Johnson RJ, Caress AL, Woodcock A, Custovic A (2005) The information needs and preferred roles in treatment decision-making of parents caring for infants with atopic dermatitis: a qualitative study. Allergy. 60, 7, 938-943. Graham-Brown R, Savin J, Milner J (2004) In Clinical Practice Series: Dermatology. Churchill Livingstone. Guzik TJ, Bzowska M, Kasprowicz A et al (2005) Persistent skin colonization with Staphylococcus aureus in atopic dermatitis: relationship to clinical and immunological parameters. Clinical and Experimental Allergy. 35, 4, 448-455. Hotze M, Baurecht H, Rodríguez E et al (2014) Increased efficacy of omalizumab in atopic dermatitis patients with wild-type filaggrin status and higher serum levels of
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concordance and accurate monitoring of treatment response. This means involving patients and/or carers in the decision-making process by, for example, explaining the side effects of treatment and reassuring patients and/or carers that the benefits of treatment significantly outweigh potential side effects. Adapting the treatment plan to make it more cosmetically acceptable, for example using oil-based ointments at night and water-based creams during the day, is essential to promote concordance. Providing an individualised self-management plan that details information on how much ointment and/or cream to use, how to apply it and a stepped approach to management is valuable. This should be provided in combination with a verbal explanation and practical demonstration on the application of topical creams and ointments. As the quality of available information varies, it is helpful to guide patients to resources such as www.patient.co.uk and NHS Choices (www.nhs.uk), support groups and patient guidance and/or information sheets from the National Eczema Society and BAD. These are valuable resources for the nurse in combination with national guidelines from BAD, SIGN and NICE.
phosphatidylcholines. Allergy. 69, 1, 132-135. Leung DY (1995) Atopic dermatitis: the skin as a window into the pathogenesis of chronic allergic diseases. Journal of Allergy and Clinical Immunology. 96, 3, 302-318. Mallol J, Asher I, Williams H, Clayton T, Beasley R (1999) ISAAC findings in children aged 13-14 years – an overview. Allergy and Clinical Immunology International. 11, 176-182. National Eczema Society (2008) Factsheet: Topical Steroids. www. eczema.org/documents/153 (Last accessed: July 14 2014.) National Institute for Health and Care Excellence (2007) Atopic Eczema in Children. Clinical guideline No. 57. NICE, London. National Institute for Health and
Conclusion The burden of chronic disease in healthcare services is increasing. Atopic dermatitis is a common and complex condition which requires skilled assessment, education and individualised treatment that maximises effectiveness and respects patient choice. Nurses can provide a holistic approach to its long-term management, ensuring concordance with treatment regimen and accurate monitoring of treatment response. Knowledge of the therapies available is vital alongside developments in different treatment modalities and trials of preventive therapies that offer hopeful advances for the future NS
GLOSSARY Atopic Genetic predisposition to develop allergies. Dander Hair and skin shed from mammals that contain allergen particles. Excoriation Skin abrasion. Immunomodulators An agent that enhances or lessens immune response. Lichenification Thickening of the epidermal layer of the skin. Palmar hyperlinearity Pronounced skin creases in the palm of the hand. Papules Solid raised spot on the skin less than 1cm in diameter. Pruritis Severe itch, often caused by allergy and infection. Rhinoconjunctivitis Inflammation and irritation of the nasal membranes and conjunctiva often referred to as hay fever. Urticaria Raised bumpy, itchy, red rash also known as hives. It often presents in response to an allergen.
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Tintle S, Shemer A, Suárez-Fariñas M et al (2011) Reversal of atopic dermatitis with narrow-band UVB phototherapy and biomarkers for therapeutic response. Journal of
Allergy and Clinical Immunology. 128, 3, 583-593. Walker D, Jacobe H (2011) Phototherapy in the age of biologics. Seminars in Cutaneous Medicine and Surgery. 30, 4, 190-198. Werfel T, Breuer K (2004) Role of food allergy in atopic dermatitis. Current Opinion in Allergy and Clinical Immunology. 4, 5, 379-385. Wiliams H (2012) BEEP Study Findings. Oral presentation at the British Society of Allergy and Clinical Immunology (BSACI) Conference. July 2-4, Nottingham. Williams H, Stewart A, von Mutius E, Cookson W, Anderson HR; International Study of Asthma and Allergies in Childhood (ISAAC) Phase One and Three Study Groups (2008) Is eczema really on the increase worldwide? Journal of Allergy and Clinical Immunology. 121, 4, 947-954.
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