This allergic reaction of the skin occurs to a substance which comes in contact with the surface of the skin. The antigens responsible for this type of dermatitis are simple chemical compounds present in the substances to which the patient is exposed during his daily activities.
Clothes, shoes and jewellery, lipsticks, hair dyes, local application, plants juices of vegetables and fruits or chemicals and tools employed in industries, factories and other professional activities are few of man substances that might cause this poblem.
Sometimes, components of plants or other agents suspended in the air can sensitise an individual and cause contact dermatitis without the patient being aware of a direct contact.
Clinically, the lesions consist of a dermatitic reaction which may be acute, subactue, or chronic, depending upon the nature of the antigenic substance and the degree of hypersensitivity of the individual.
As a general rule, volatile substances or liquid antigens produce an acute reaction which consists of severe itching, oedema, erythema, papules and papulo-vesicles, while solid antigens tend to produce a subacute reaction consisting of itchy erythematous and scaly areas.
On the palms and soles, this reaction usually consists of erythema and fissures. The dermatitic reaction is always limited to the areas of skin which come in contact with the antigen.
The best clue to the causative agent, lies in the distribution of the lesions on the body.
Most important thing to do is to prevent further exposures of the patient to the causative agent.
Treatment of the acute attack consists of local compresses with saline or potassium permanganate, followed by local applications of a corticosteroid ointment with or without antibiotics.
For itching, oral antihistamine tablets a short course of systemic corticosteroids may be helpful in providing quick relief.
After the clinical manifestations have subsided and the systemic corticosteroids have been withdrawn, the patient should be subjected to patch test with the substances suspected to be responsible for his contact dermatitis to confirm the actual cause.
If it is not possible to avoid further exposures to the agent, the patient should be advised to use physical barriers or barrier creams which when applied on the skin, prevent the causative agent from entering the skin.
The barrier creams have to be applied at least two or three times a day on the skin areas which are likely to be exposed to the causative agent.
Whenever the skin area is washed or wiped, application of the barrier cream should be repeated.
Atopic Dermatitis – Clinical Features
Atopic dermatitis is allergic disorder of the skin where the patient inherits an increased tendency of getting sensitized to various antigens in his environment.
This tendency is inherited as a polygenic recessive character and several relations of the patient also often suffer from one of the atopic disorders like asthma, urticaria, atopic dermatitis and allergic rhinitis.
Most patients also have other immunologic abnormalities such as
- Depression of cell-mediated immunity
- Absence of IgA antibodies
- Defective phagocytic function of leucocytes and monocytes
- High levels of IgE.
Atopic dermatitis patients have
- An increased tendency for vaso-constriction manifesting as a pallor on the skin especially the face
- White dermographism
- Delayed blanch phenomenon
- Vasoconstrictor response following injections of histamine and cholinergic drugs.
During infancy the disease is called infantile eczema and consist of severely itchy, erythematous, papular or papulo-vesicular lesions which appear bilaterally on the cheeks and spread to other parts of the body. Severe cases may have exudation and massive crusting.
The first lesions may appear at as early an age as two months and continue to appear recurrently during the first two years of life.
Some cases may recover completely for the rest of their life, while others may progress to the childhood type of atopic dermatitis.
In the childhood dermatitis, the lesions are predominantly situated in the cubital and the popliteal fossae and consist of severely itchy, erythematous papules with some lichenification.
The skin at this stage tends to become dry, and there is no exudation.
These lesions may show remissions and relapses and as the age advances.
During the adult stage they tend to become more and more dry and lichenified and may also involve the face, the neck and the trunk. In severe cases, the whole skin may become lichenified.
Aggravations of the clinical condition are caused by exposures to the antigens to which the patient is sensitive.
These may include any of the foods, pollen, fungi, insects, parasites and bacteria. In infants, it is usually the food antigens which are responsible for the aggravations, while in adults it may be any of the other antigens.
In addition, the immunologic abnormalities make the patient more prone to develop widespread and extensive lesions of viral infections such as warts, molluscum contagiosum and herpes, and also recurrent pyoderma.