This pattern of eczema commonly affects the sides of the fingers, palms, the toes or soles of the feet. Irritant vesicles are the initial feature, though with more serious attacks bullae may be seen.
The patients are usually in their twenties or thirties when they develop the disease. A previous history of atopy is not elicited in the majority of patients . Endogenous factors that trigger this type of eczema are not known. The role of dietary nickel provoking the disease in nickel-sensitive patients is controversial. Attacks may occur frequently and at regular intervals. This condition should not be confused with the irritant vesicles found on fingers of normal individuals in hot weather.



Drying and bacteriostatic solutions such as potassium permanganate 0.01% are used daily until weeping is controlled. Potent topical corticosteroids containing antibiotics or antiseptics may be necessary to control severe attacks, e.g. betamethasone valerate 0.1% cream with neomycin or fluocinolone acetonide 0.025% cream with c1ioquinol.
Systemic treatment with steroids, e.g. i.m. Synacthen, given at regular intervals over weeks or even months, or prednisolone by mouth in doses of between 10 and 15 mg daily, may be necessary to break the frequency of attacks and heal the skin.

Discoid or nummular eczema

This type of disease occurs mainly in the middle-aged or elderly with no previous history of skin disease. Papules and coin-shaped raised lesions associated with extreme itching occur on the limbs, most commonly on the lower leg; they may merge to form plaques. Annular patchesmay appear in association with other patterns of eczema  during early life. The cause is unknown but bacterial antigens have been implicated. Eczematous lesions on the legs are sometimes due to venous incompetence (see p. 629).


Occlusive bandages containing zinc paste or ichthammol may help to alleviate itching and prevent incessant scratching. Impregnated steroid tape containing flurandrenolone 0.0125% may produce the same effect; intralesional triamcinolone or local potent topical corricosteroids improve the condition of the skin and give relieffrom itching. The disease often improves when the patient  retires from work.

Exogenous eczema

Exogenous eczema can be divided into primary irritantdermatitis and true contact dermatitis associated with a  cell-mediated immune response.

Primary irritant dermatitis

This is essentially a degreasing of the skin with a subsequent water loss followed by dryness, fissuring and cracking. It can occur both at work and in the home. Industrial solvents that remove greasy coatings covering metal components in industry can with equal efficiency remove surface lipids from the skin if they are not handled with care.
Those working in the home are also at risk; the changes in the skin occur in parallel with the extent of immersion of the hands in water. Initially the skin beneath a ring is often involved, as neat detergent or soap powder tends to lodge there and erode the skin. This spreads to the thin skin on the sides of the fingers, the webs and the backs of the hands; the palms are only affected in more severe and chronic disease. A similar type of disease may be seen in other occupations with the use of cleaning and detergent solutions, such as bar work and hairdressing. Asteatotic eczema or eczema craquele This is a condition often seen in long-stay elderly hospital patients. Dryness of the skin is more evident with ageing.
The condition is made worse by excessive washing with soap. The eczema can result in a ‘crocodile skin’ appearance that is most noticeable on the lower limbs. This condition may also be seen in hypothyroidism.
Although the skin may appear inflamed, the use of emollients and creams or soap substitutes has the greatest beneficial effect and topical corticosteroids are often unnecessary.

Allergic contact dermatitis

This is a good example of cell-mediated immune disease or type IV reaction. T lymphocytes are sensitized to the antigen, some time after the irst contact. Small-molecular-weight substances passing through the skin need to be linked to skin proteins (haptens) in order to sensitize. Langerhans’ cells in the dermis present the antigen to lymphocytes. The sensitivity lasts for life.


An unusual pattern of rash with clear-cut demarcation or odd-shaped areas of erythema and scaling should arouse suspicion and in combination with a careful history indicate a cause. All areas of the skin may be involved, but the back is the most convenient site for testing. The suspected allergen is then placed in contact with the skin as a patch test. If the causative agent cannot be clearly defined, e.g. in hand eczema, then a range of known everyday antigens are tested, including materials such as rubber, nickel and medicaments. Positive readings will need to be interpreted with caution and may not have an obvious relevance when considering the patient’s history or occupation.

If the major distribution of an eruption appears to involve exposed skin, then photo-patch testing may be required. Two identical sets of likely allergens are placed on the back; one set is exposed to long-wave UV (UVA) light, with the second non-exposed set acting as a control.


Remove the known irritant or allergen if this is possible. Steroid creams are helpful for short periods when the disease is severe. Antipruritic agents may be necessary for symptomatic relief of itching.
Miscellaneous Exfoliative dermatitis (erythroderma) In this condition the entire skin is erythematous, oedemato us and scaly. The disease is rare and can be idiopathic (without a preceding skin condition) or can follow dermatitis, psoriasis or other skin disease. It can also be a reaction to many drugs, e.g. sulphonamides, sulphonylureas, gold. It is also an occasional feature of systemic disorders, particularly the lymphomas, so that a skin biopsy may be necessary. MANAGEMENT. Body fluid loss can be considerable and the patient needs intensive medical care; systemic steroid therapy is often necessary.


This chronic skin disease is seen most commonly as erythematous well-demarcated silvery scaled plaques over extensor surfaces such as the elbows and knees, and in the scalp. In this common pattern the onset of the disease is unusual before 15 years of age, and the initial presentationmay occur in old age. Psoriasis occurs throughout the world; in the temperate zones 2% of the population are affected. It is less common in some races with pigmented skins. Characteristically there are periods of activity and remission that are often impossible to predict.
Arthropathy occurs in association with the skin disease in about 8-10% of individuals. Pathogenetic factors tha  link the two conditions are not clear, through abnormal vascular changes are seen in both.


Genetic factors

The mode of inheritance of the disease is not known but certain HLA markers are recognized. HLA-B13, B16, B17 and DR7 are all associated with an increased relative risk and HLA-CW6 has an increased risk up to seven times hat of the general population. The B loci occupy an area adjacent to the gene that expresses CW6. HLA-B27 is seenin up to 90% of individuals with ankylosing spondylitis and in 70% of individuals who develop a similar spinal arthropathy with psoriasis.


The role of infection as an exacerbating factor is suggested by the following observations: IN CHILDREN OR YOUNG ADULTS, superficial small patterned lesions of guttate psoriasis may appear overthe trunk and limbs 10-14 days following a throat  infection with f3-haemolytic streptococci, and up to 75% of these individuals have the HLA-CW6 marker or DR7.
PATIENTS WITH REITER’S SYNDROME (see p.396) may develop skin lesions that are identical to those seen in psoriasis. Reiter’s disease can occur after dysentery or after venereal contact, again suggesting an infective aetiology that might induce psoriasis.
PATIENTS WITH HIV INFECTION do not have an increased incidence of psoriasis. However, patients with a low CD4 T-cell count may experience severe psoriasis (often of a pustular pattern) and unusually,
different patterns of the condition may occur in the same individual.
• Emotional trauma
Emotional trauma can trigger psoriasis: for example, a child followed through to adolescence may be seen to have an exacerbation of the disease with the stress of  chool examinations. Patients can also develop a reactive psychological state owing to the severity of their skindisease.

Mechanical trauma 

Repeated trauma to the skin over the elbows and knees as part of everyday activity may explain the common involvement of these sites with psoriasis. In sedentary occupations, e.g. in chauffeurs, there may be intractable disease over the lumbosacral region. Scratching the skin  when the disease is in an active phase may induce lesionsalong the line of trauma-the isomorphic response or  Koebner phenomenon. Irritant types of psoriasis such as that affecting the scalp may be made worse by scratching. Drugs
Lithium carbonate may induce intractable psoriasis. This agent inhibits adenylate cyclase activity, which may alter  epidermal cell kinetics. The f3-receptor antagonists such as propranolol may exacerbate psoriasis through similar mechanisms.


The pathogenesis is unclear but a number of factors play a role.
EPIDERMAL CELL PROLIFERATION is seen in both the lesions and the uninvolved skin of psoriatics. There is a shortening of the epidermal cell-cycle time and an increase in the number of proliferative cells in the
growth fraction of the epidermis. DIVISION is normally limited to the basal layer in normal skin but may extend over several layers within psoriatic plaques. Polyamines are known to be important in regulating cellular proliferation, and the levels of these substances and of their rate-limiting enzyme, ornithine decarboxylase, are elevated in
ARACHIDONIC ACID LEVELS are greatly elevated in both uninvolved and lesional skin. Many stimuli that affect the cell membrane may cause a release of phospholipase and arachidonic acid and a number of inflammatory mediators are formed from arachidonic ac id via the lipoxygenase pathway (see Fig. 12.30). The major initial metabolite in the lipoxygenase pathway is 5-hydroperoxyeicosatetraenoic acid (5-HPETE). This is the precursor of a family of peptido-hydroxyeicosatetraenoic acids, including the leukotrienes, that can alter enzyme pathways that control cell kinetics. Leukotrienes also have marked chemoattractant properties.
LEUKOTRIENE B. (LTB.) levels are elevated in lesional skin and the injection of this substance causes an increase in polymorphonuclear infiltration. Polymorphonuclear cell infiltration of the epidermis and the
formation of Munro microabscesses are an important pathological feature in this disease. A variety of immune factors may also attract polymorphonuclear leucocytes; these include immune complexes and complement fragments.

HUMORAL AND CELLULAR ABNORMALITIES have been demonstrated in psoriasis, including elevated IgA and alteration of T-cell function. The relative lack of sensitization to the common sensitizer dinitrochlorobenzene (DNCB) in patients with psoriasis supports the concept of an altered cell-mediated immune response in this disease.

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