Numerous studies suggest that the prevalence of AD is increasing in South Africa. From 1995 to 2002, increases were reported for adolescents (13- to 14-years) in Cape Town for self-identified symptoms of AD (15.5%–26.2%) and physician-diagnosed AD (9.6%–16.7%).3
AD is more common in urban than rural settings in South Africa. For example, in Cape Town, a prevalence of 23.5% was reported in children between one- to three years, compared to 1.8% in the rural Eastern Cape.3
Impact on quality of life
While many cases of AD are mild and can be managed with simple topical treatment, up to 50% of AD cases are moderate-severe, which negatively impact patients quality of life (QoL) as a result of constant itching, loss of sleep, pain (see the article on page 50 on the management of painful skin conditions), and social isolation due to low self-esteem.1
AD has been shown to be associated with psychiatric disorders (depression and anxiety) and suicidality as a result of constant itching and discomfort, disfigurement, and perceived social stigmatisation. In addition, poor sleep related to AD may increase the risk of psychiatric disorders.4
Schonmann et al found that among the 526 808 patients with AD included in their study, AD was associated with increased incidence of new depression (14%) and anxiety (17%). They observed a stronger effect of AD on depression with increasing severity compared with no AD: mild (10%), moderate (19%) and severe (26%).4
In addition, they found that AD was more strongly associated with depression and anxiety in those aged 40 to 59 years (compared with younger and older age groups) and were more prevalent in men than in women.4
Presentation and diagnosis of AD
The cardinal symptom of AD is itching, which can be debilitating as shown above. Clinical findings are characterised by ill-defined, papular erythema and fine-scale. Chronic eczema results in thickening and increased scaling of the skin (lichenification).1
Generalised dry skin (xerosis and/or ichthyosis vulgaris) is typical in more extensive cases. Depending on the severity and chronicity of the disease, skin findings may also include exudate, vesicles, fissures, lichenification and excoriations.1
Silverberg et al found that AD lesion distribution differed based on ethnicity and age. In patients with dark skin, the erythema is often not visible. Instead, the scaling or thickening from lichenification may be more prominent with hyper- or hypopigmentation.1,5
The most common sites of skin lesions include the popliteal fossae, lower legs, dorsal feet, and antecubital fossae, but in patients with darker skin, lesions on the trunk were significantly more common.5
Age ≥60 years was associated with significantly lower proportions of active lesions on the face and scalp, and a significantly higher proportion of lesions on the buttocks or genitals.5
Although AD is associated with allergic conditions, it is not an allergy per se. Rather, AD inflammation is mediated by T cell activation in the skin where the antigenic targets for activation are likely to be numerous in any one individual.1
IgE is considered to play little in the role of mediating skin inflammation, yet, in individuals with AD, IgE allergies are more common and account for the association with allergic rhinitis, food allergy and asthma.1
Induction of IgE responses in AD is thought to be a consequence of increased allergen exposure through broken skin in the setting of a cutaneous drive towards the initiation of Th2 responses (which subsequently induce B cell class switching to IgE production).1
Therefore demonstration of allergic responses (measurement of specific immunoglobulin [Ig] E) are not required to make a diagnosis, according to Plant and Ardern-Jones.1
Managing AD
The overall goals of treatment for AD are to reduce the signs and symptoms of disease, induce disease remission and improve the quality of life of both patients and their caregivers.3
Regular application of topical emollients alongside treatment with topical corticosteroids (TCSs) or calcineurin inhibitors (TCIs) forms the foundation of treatment of all AD. Concerns regarding the safety of TCSs as first-line therapy for treating AD flares have led to poor treatment adherence and subsequent worsening of disease control and quality of life.1,6
Safety concerns include skin thinning and retardation of growth and development. These concerns are thought to mainly originate from what is now considered to be inappropriate use, such as using potent TCS on the face or continual long-term use.6
Strategies recommended to minimise exposure to TCS, and hence the risk of adverse events, include reducing the frequency of application to once daily during treatment of an inflammatory episode, or TCS used for two consecutive days a week (sometimes referred to as ‘weekend therapy’) as a strategy to prevent flares.6
TCIs are known as steroid-sparing options and were approved in the early 2000s for the treatment of AD. TCIs such as tacrolimus ointment (0.03% and 0.1%) and pimecrolimus cream (1%), are recommended treatment options in contemporary management guidelines.1
Management of all patients with AD
Step 1: For all patients
- Avoid irritants
- Avoid soaps/shower gels/bubble baths
- Use emollients to wash
- Repair barrier
- Emollients are regularly applied even when AD control is good
- For more active disease use ointment formulations
- Treat inflammation (itch)
- Topical CSs: Ladder of potency use least potent possible
- Topical CIs: Use as steroid-sparing agents and prevention
Step 2: If all topical treatment fails
- Phototherapy
- Systemic immunosuppression (methotrexate, ciclosporin, azathioprine, mycophenolate mofetil)
Step 3: If classical immunosuppressant treatment fails
- Dupilumab
The 2020 South African algorithm for the treatment of AD in paediatric patients recommends:3
1. TCIs as first-line treatment for patients with AD in sensitive body areas, patients with steroid-induced atrophy and patients who have current long-term uninterrupted TCS use.
2. Pimecrolimus and tacrolimus are indicated for the treatment of mild-to-moderate and moderate-to-severe AD, respectively.
3. For mild–acute AD flares in paediatric patients, we recommend low or moderate potency TCSs once daily or pimecrolimus twice daily until clear.
4. For moderate AE flares, patients may use appropriate strength TCSs, either once or twice daily or a TCI twice daily.
5. If a TCI is selected as first-line therapy and the acute flare is not controlled, a short (7–14 days) course of TCS may achieve control, which can then be gradually reduced or switched to a TCI to maintain results.
6. A TCI twice daily for mild-to-moderate AD flares is recommended in children and sensitive body areas. In the European AD guidelines, pimecrolimus is recommended as the treatment of choice for facial lesions and children. The treatment should be applied twice daily from the first appearance of signs and symptoms until complete resolution.
7. For the management of severe disease flares, moderate or potent TCSs are recommended.
8. In the European AD guidelines, pimecrolimus is recommended for facial lesions and for children, and both pimecrolimus and tacrolimus for long-term maintenance treatment.
9. For patients with four or more acute flares per year, proactive maintenance treatment. This is a combination of long-term, low-dose anti-inflammatory treatment (TCIs or TCSs of the appropriate strength) two and three times weekly, applied to areas of skin previously affected by AD, together with the liberal use of emollients over the entire body.
10. Alternatively, intermittent therapy with TCI may be recommended which involves the resumption of treatment at the very first signs of a new flare, that is, pruritus.
11. The duration of maintenance therapy is determined on an individual basis. Discontinuation may be attempted by slowly decreasing the frequency of application and closely monitoring the results.
Diagnostic criteria of AD in children
In order to qualify as a case of AD, the child must have:
- An itchy skin condition (or parental report of scratching or rubbing in a child)
Plus three or more of the following:
- Onset <2-years (not used if child is <4-years)
- History of skin crease involvement (including cheeks in children 10-years)
- History of a generally dry skin
- Personal history of other atopic disease (or history of any atopic disease in a first-degree relative in children <4-years)
- Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children <4-years).
REFERENCES:
1. Plant A and Ardern-Jones MR. Advances in atopic dermatitis. Clin Med (Lond), 2021.
2. Suaini NHA, Tan CPT, Loo EXL and Tham EH. Global differences in atopic dermatitis. Paed Allger Immunol, 2021.
3. Kannenberg SM, Karabus S, Visser WI, et al. Paediatric atopic eczema (atopic dermatitis) in South Africa: A practical algorithm for the management of mild-to-moderate disease in daily clinical practice. SAFP, 2020.
4. Schonmann Y, Mansfield KE, Hayes JF, et al. Atopic Eczema in Adulthood and Risk of Depression and Anxiety: A Population-Based Cohort Study. J Allergy Clin Immunol Pract, 2020.
5. Silverberg JI, Margolis DJ, Boguniewicz M, et al. Distribution of atopic dermatitis lesions in United States adults. JEADV, 2019.
6. Axon E, Chalmers JR, Sante M, et al. Safety of topical corticosteroids in atopic eczema: an umbrella review. BMJ Open, 2021.
