Eczema and psoriasis

57 Eczema and psoriasis






Eczema


The terms ‘eczema’ and ‘dermatitis’ may be used interchangeably and describe the same clinical and histological entity. Eczema is an itchy erythematous (red) eruption consisting of ill-defined erythematous patches or papules. The skin surface is usually scaly and as time progresses, constant scratching leads to thickened, ‘lichenified’ skin.



Pathology and clinical features


Acute eczema is an inflammatory process leading to oedema in the epidermis. The oedema is seen histologically in the epidermis as ‘spongiosis’. Oedema manifests as fluid that collects into tiny blisters which may then coalesce. This is seen histologically as intraepidermal vesicles and clinically as pompholyx blisters on thicker palmar and plantar skin, and as excoriated, ruptured crusted vesicles elsewhere. Tightly packed keratinocyte cells in the epidermis usually prevent transepidermal fluid loss and the entry of pathogens. This barrier function of the skin is lost in eczema. A schematic diagram demonstrating the normal skin epidermis and the effects on the barrier function during an acute eczema flare is shown in Fig. 57.1.



In the chronic form of eczema, prolonged rubbing and scratching results in a thickened epidermis and an increase in the upper horny cell layer of keratin, termed hyperkeratosis. Clinically, the skin appears thick, leathery, scaly and ‘lichenified’ with exaggerated skin markings, like tree bark (Fig. 57.2). Both acute and chronic stages are accompanied by a heavy chronic inflammatory cell infiltration of the dermis and epidermis. The main consequent symptom of these pathological processes is itch. The dictum of ‘if it’s not itchy, it’s not eczema’ holds true.




Clinical types



Atopic eczema


Atopic eczema is the commonest skin disorder of childhood, affecting between 10% and 20% of school age children in the UK. The aetiology is a combination of genetic, environmental and immunological factors.


The term ‘atopy’ describes an exaggerated propensity to form IgE to common allergens. In later life, approximately half of eczema patients will develop associated atopic disorders such as asthma and allergic rhinitis. The molecular pathology in atopic eczema is complex. The epidermal Langerhans cells have high-affinity IgE receptors through which the T-helper cells (Th2 and Th1) release cytokines and mediate skin inflammation.


Atopic eczema is diagnosed clinically and the criteria for definition include chronic itchy skin with three or more of the following: a history of flexural involvement of the skin creases, visible flexural involvement, dry skin, other atopic disease or onset within the first 2 years of life. The clinical course and distribution change through puberty and adulthood. In infants, common areas affected are face, neck and nappy area. Through childhood, flexural sites such as folds of the elbows and backs of the knees are classically involved (see Fig. 57.3). Symptoms usually improve with age and approximately 60% have resolution of symptoms by the age of 16.





Contact dermatitis


Contact dermatitis is classified as either allergic contact dermatitis (ACD) or irritant contact dermatitis (ICD).



Allergic contact dermatitis


ACD is a delayed type IV hypersensitivity reaction that develops in response to an antigen to which the host immune system has been previously sensitised. As a consequence, symptoms rarely develop on first exposure to the stimulus and may only manifest months or years later following repeated re-exposure.


Many common compounds can lead to ACD. The most common compounds implicated are:








Diagnosis relies heavily on a detailed patient history as well as recognising the pattern and distribution of the eczematous rash. Although the signs are usually localised to the area exposed to the allergen, secondary generalised eczema may develop.


The standard confirmatory investigation is patch testing and is used to differentiate allergic from ICD. This involves application of a standard, with or without a specialised range of compounds, to the patient’s back over 72 h. This is followed by examination for a cutaneous reaction at day 2 and day 4. Identification of relevant compounds allows the patient to avoid the substance in the future, and this will hopefully reduce symptoms. Common areas of the body affected by ACD, with corresponding probable sensitisers, are listed in Table 57.1.


Table 57.1 Common locations for allergic contact dermatitis and possible sensitisers





















Location Possible sensitising agents
Periorbital Airborne allergens, nail polish, contact lens solution
Umbilicus Nickel hypersensitivity to belt/jean button
Neck Antiseptic in soap, cosmetics
Hairline PPD in hair dye, hair perming solution
Hands Latex or rubber accelerators in gloves, nickel, fragrances, protein contact dermatitis in food preparation, irritant contact dermatitis due to water

PPD, p-phenylediamine.



Irritant contact dermatitis


This is the most common form of occupational dermatitis and the commonest cause of hand eczema (Fig. 57.5). Unlike ACD, ICD is not immunologically mediated. The mechanism involves disruption of the epidermal permeability barrier and a direct cytotoxic effect depending on the irritant. Patients with pre-existing epidermal barrier dysfunction such as atopic eczema are at higher risk. The occupation of the individual may also be a risk factor, especially those working as builders, hairdressers, gardeners, healthcare workers and chefs. Irritants include detergents, oils, water, inorganic acids, alcohols and plastics. Preventative skin care is key and this includes the use of barriers such as emollients or cotton gloves in addition to avoiding suspected irritants.








Treatment


First-line treatment of eczema should include an emollient and soap substitute for washing. Topical steroids are used for anti-inflammatory effect. Systemic treatments for adult atopic eczema include oral prednisolone, ciclosporin and azathioprine. If there is a secondary bacterial infection, then this should be treated with oral antibiotics. The antibiotic(s) should be chosen based on sensitivity determined by wound swab.




Topical corticosteroids


Topical steroids act as anti-inflammatory agents and are extremely useful and important in managing eczema. In recent years, the public have veered from overuse of topical steroids causing long-lasting side effects, to high levels of anxiety regarding possible side effects concerning their use. This can commonly lead to under treatment in children. Therefore, patient/carer education regarding appropriate topical steroid use is a crucial part of eczema management.


Topical steroids are classified into four main groups according to potency: mild, moderately potent, potent and very potent (Table 57.2). The choice of topical steroid is dependent on the site and severity of skin disease. Potent and very potent steroids should be avoided on delicate sites such as the face, genitals and flexures. The periorbital region should be treated with caution due to the thin skin increasing the likelihood of absorption and risk of cataracts or glaucoma. Treatment should be reviewed regularly and tailored accordingly. It is also important to remember that any form of occlusion will increase the absorption of steroid applied.



Side effects are mainly local and include striae (stretch marks), telangiectasia (visible dilated small blood vessels), epidermal thinning, purpura (bruising), acne and perioral dermatitis. Lower frequency side effects include poor wound healing, spread or worsening of untreated infections and hypertrichosis. Hypopigmentation is a temporary side effect of long-term topical steroid use and is frequently exploited in illegal ‘skin bleaching’ agents. Rarely, adrenal suppression or Cushing’s syndrome due to systemic absorption may occur.


Local and systemic side effects are extremely rare with appropriate use and duration of topical steroid treatment. Patients should be advised to spread preparations thinly either once or twice daily. The recommended amount used can be quantified using a fingertip unit (Fig. 57.7). The quantity in this unit is sufficient to cover an area the size of two adult palms. Table 57.3 details the quantities for application to different sites required for twice-daily treatment for 1 week.








Calcineurin inhibitors


The past decade saw the introduction of topical calcineurin inhibitors for the treatment of chronic eczema. These non-steroid immunomodulators inhibit calcineurin phosphatase which is important in T-lymphocyte activation. The main side effect is burning or stinging on initial application, but this usually improves after a few days. Although a theoretical risk of increased malignancy exists with these agents, studies have not shown an association between exposure to topical calcineurin inhibitors and increased rates of cutaneous malignancy. Calcineurin inhibitors should not be used on infected skin and are generally not very useful in severely inflamed eczematous skin. Their greatest value appears to be in maintenance therapy.


Tacrolimus ointment (Protopic®) is a calcineurin inhibitor derived from the oral transplant medicine FK506. The 0.1% and 0.03% preparations are indicated in the treatment of moderate to severe atopic dermatitis in adults and children over the age of 2 years. Tacrolimus is now also used in clinical practice as a second-line agent for other steroid responsive dermatoses.


Pimecrolimus 1% cream (Elidel®) is indicated for short-term or intermittent long-term use in mild to moderate atopic dermatitis. Studies have shown that it is effective, well tolerated and has minimal adverse effects in the long-term control of eczema in children aged over 2 years (Langley et al., 2008). Furthermore, this has resulted in the reduced use of topical steroids leading to a lower risk of steroid-induced side effects (Kapp et al., 2002).







Systemic therapies








Phototherapy


Phototherapy can be effective in select cases of atopic dermatitis. Narrow-band UVB is the therapy of choice (Gambichler et al., 2005; Meduri et al., 2007). The potential side effects of all types of phototherapy include burning, premature ageing and a small increased risk of skin cancer. A small proportion of patients have photosensitive eczema, and this should be determined by taking a detailed patient history before prescribing phototherapy treatment. A treatment course requires a patient to attend two or three times a week for at least 6 weeks.



Dietary supplements


Current evidence suggests that probiotics are not an effective treatment for eczema and may carry a small risk of adverse events such as infection and small bowel ischaemia. There is no evidence for use of evening primrose oil. The use of Chinese herbal medications in atopic eczema is under close scrutiny, and conflicting results have been obtained. Liver function should be monitored as hepatitis is a known side effect of some Chinese herbal medicines.


Interactions with drugs used in the treatment of eczema and psoriasis are shown in Table 57.4.


Table 57.4 Interactions with drugs used in the treatment of eczema and psoriasis
















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Jun 18, 2016 | Posted by in PHARMACY | Comments Off on Eczema and psoriasis

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  Interacting drug Outcome
Methotrexate Aspirin Increased plasma concentration and toxicity of methotrexate
NSAIDs Increased plasma concentration and toxicity of methotrexate
Probenecid