This eruption is seborrhoeic dermatitis. It is more common among men and typically
affects the sebum-rich areas of the face, scalp and chest. The pathophysiology of seborrhoeic
dermatitis is incompletely understood, however. It is linked with Malassezia yeast,
complement activation and abnormalities of T-cell immunity. It may worsen in individuals
infected with HIV or affected by Parkinson’s disease.
The condition usually begins around puberty with a peak of incidence between 25 and
40 years of age. An infantile form of seborrhoeic dermatitis may manifest as cradle cap
(Fig. 4.2), facial greasy scaly dermatitis, napkin dermatitis and, rarely, as an erythroderma.
In predisposed individuals seborrhoeic dermatitis usually recurs. Treatment is aimed,
therefore, at reducing morbidity and preventing flares. Treatment aims are two-fold:
reducing the yeast burden as a secondary preventative measure, and switching off the
resultant secondary dermatitis when it occurs. Although topical corticosteroids may
improve appearances of the dermatitis in the short term, they are thought to hasten recurrences
and may foster dependence due to a ‘rebound effect’ and are usually discouraged.
The use of a ketoconazole shampoo, with frequent washing and prolonged lathering often
improves associated dandruff and may improve the facial involvement by depletion of
Malassezia. Use of ketoconazole shampoo as a face wash can be irritating, but if tolerated
may improve erythema and scaling. Ketoconazole or miconazole cream, calcineurin
inhibitors in combination with antiseptic emollient washes are recommended. For severe
or refractory seborrhoeic dermatitis systemic itraconazole as a short course or ‘pulsed’
(one week per month) is highly effective at reducing the yeast burden.
The diagnosis is pompholyx or dyshidrotic eczema, the symmetrical and diffuse clear vesicles
over the palmar aspect of the hands associated with pruritus are highly suggestive
and the diagnosis is based on clinical features. Other differential diagnoses to consider
include contact dermatitis (irritant or allergic), friction blisters (e.g. epidermolysis bullosa
simplex), herpes simplex infection, and palmoplantar pustular psoriasis.
Atopy appears to be a predisposing factor for pompholyx. There are several potential
triggers of pompholyx including stress and as an ‘id reaction’ to a distant dermatophyte
infection. In this case the features of interdigital maceration associated with inflammatory
pustules and vesicles on the instep are suggestive of inflammatory tinea pedis.
Investigations should include scrapings from the feet (interdigital spaces and affected
areas over the plantar aspects) and hands for mycological tests (direct microscopy and
culture). In this case, scrapings from the feet demonstrated hyphae and spores on direct
microscopy with subsequent culture confirming the presence of the zoophilic organism
Trichophyton mentagrophytes var. mentagrophytes. There was no fungal infection of the
hands.
Treatment of a pompholyx ‘id reaction’ involves treatment of the tinea pedis as well as
treatment of the pompholyx itself. Inflammatory tinea pedis is usually managed with systemic
antifungal therapy (itraconzole, terbinafine or fluconazole). Infected scales can be
present on clothing or within footwear, so frequent laundering is recommended. Draining
the larger bullae with a sterile needle will reduce the discomfort. Compresses or soaks
with dilute potassium permanganate help to dry the vesicles and prevent secondary bacterial
infection. Potent or superpotent topical corticosteroids are the mainstay of therapy.
In the short term a combination preparation of topical corticosteroids and antibacterial
agent is useful. Occasionally, systemic steroids are required