Allergic contact eczema named also allergic contact dermatitis (Latin: contact dermatitis, contact eczema) develops after a direct contact with an allergen. Clinically, two types of disease can be distinguished: an acute type (Latin: contact dermatitis acuta, eczema acutum) and a chronic type (contact dermatitis chronic, eczema chronicum) (1).

Most of the allergens evoking the disease are characterized by a low molecular weight (lower than 1000 daltons). Contact allergens are haptens, which acquire a full antigenic capacity only after binding themselves with protein in the skin. From the clinical point of view, an important factor of developing a contact allergy is a fully preserved correct function of the epidermal barrier. Mechanical damages of the epidermis, maceration, dryness, inflammation are the causes of increased hapten penetration into the skin. Occlusive bandages are factors facilitating the penetration.

Allergic contact dermatitis is a result from type IV hypersensitivity according to Gell and Coombs classification. Its development consists of two phases: induction and release. During the induction phase haptens bind in the extravascular space with serum proteins creating an immunological complex, which is then presented by the Langerhans cells to Th1 lymphocytes in the surrounding lymph glands. This presentation occurs with the participation of the MHC histocompatibility antigens of the II class. This leads to the formation of the specific memory Th1 lymphocytes for the presented haptens. During the next contact with a given allergen, after at least 24-48 hours, the release phase starts, which activates the specific memory Th1 lymphocytes producing the proinflammatory cytokines, such as IL-2, IFN-γ and TNF-α (2). The released cytokines are responsible for the activation and migration of the allergic reaction cells including cytotoxic lymphocytes, macrophages and neutrophiles. Keratinocytes also take part in this reaction. Keratinocytes have ICAM-1 adhesive molecules on their surface, which are ligands for the LFA-1 cell receptors of leucocytes. Keratinocytes not only present MHC class II antigens on their surface and produce Il-1 and TNF-α, but also stimulate the inflammatory reaction (3, 4). The release of inflammation mediators and the activation of allergic reaction cells induce epidermal spongiosis and the development of local inflammation. After some time the effector phase is placated by the Treg 1 lymphocytes, which produce Il-10 (5). The antibodies do not play any role in the reaction initiation, which distinguishes contact allergy from other types of allergic reactions.

Oversensitivity to allergens depend on many overlapping factors. On one hand, skin inflammation may cause the development of contact oversensitivity to different antigens. On the other hand, the intolerance of some factors correlates with polyvalent contact allergy shown in patch tests. According to some authors, contact allergy to three or more antigens defines the contact allergy polyvalence. Genetic factors affect this phenomenon (6).

Glucocorticosteroids are drugs commonly used in treating patients suffering from eczema. Synthetic derivatives of adrenal cortex glucocorticosteroids comprise a group of drugs having antiphlogistic, antiproliferative, antiallergic and immunosuppressive properties. Thanks to these properties they constituted a turning point in treating many diseases. They are now being the most often used drugs both in external application, as well as systemically.

Adrenal cortex produces hormones, whose mother substance is cyklopentanoperhydrofenantren, named steroid system. Their traditional name is glucocorticosteroids (gcs), because at first only their effect on glucose transformation was noticed. Thomas Addison described the clinical symptoms of adrenal cortex failure for the first time in 1855. Only in the years 1940-1948 chemical structure was determined. The method of cortisone synthesis was elaborated by an American biochemist Edward Kendall in 1948. In 1949 an American rheumatologist Hench used the synthetically produced cortisone to treat a patient with a rheumatoid joint inflammation (7). It was a 29-year old women immobilized due to intense pains. Two injections of the new drug managed to restore her physical fitness. This spectacular health improvement experienced by her went down to history as a “cortisone miracle”.

In 1950 Edward Kendall, Tadeusz Reichstein and Philip Showalter Hench received a Nobel prize in medicine for their discovery of chemical structure and the function of adrenal cortex hormones and their application in treating rheumatic diseases. For the first time hydrocortisone was used locally for skin diseases treatment in 1952 by Sulzberger and Witten (8). Professor Howard Maibach jokes that the history of dermatopharmacology can be divided into two periods: BC (before corticoids) and AC (after corticoids) (9).

Corticosteroid receptors are located intracellular. They are cytoplasmatic receptors, from which results the concept of their two stages function (two steps model). The first step is creating an active hormone/ /receptor complex, then transferring it to the nucleus and binding with the nuclear chromatin (10). The binding of an active steroid/receptor complex with DNA induces lipocortin-1 synthesis. It is an inflammatory protein from the group of annexines. Lipocortins bind with phospholipids of the cell membranes, disabling A phospholypase to release arachidonic acid from them. As a result, the lipid inflammatory mediators production track breaks (prostaglandin, leukotriene). Glucokorticosteroids restrain the induction of nitric oxide (iNOS) decreasing the inflammatory mediator synthesis this way (11). They also decrease the amount and the activity of mast cells in the skin (12). The most recent studies prove that the active steroid/receptor complex can directly restrain transcriptive factors. The consequence of this process is a reduced expression of adhesive molecules, which blocks the leucocytes migration to the inflammation focus. Also, the proinflammatory cytokines (Il-1, Il-2, Il-6, TFNa) activity and the amount of their receptors decreases.

Gcs currently used in treatment are synthetic derivatives of the adrenal cortex hormones. In comparison to natural compounds they have a stronger anti-inflammatory and immunosuppressive function and produce less unwanted symptoms. For many years the allergy to corticosteroids has been negated, which was caused by their anti-inflammatory properties, which mask the symptoms of contact allergy. The first case of contact allergy to hydrocortisone was recorded in Copenhagen in 1958. Then, 20.000 patients were tested and 0,3% of them had positive results. In Poland, first tests with hydrocortisone were carried out in the years 1980-1981. All of them gave negative results. The first positive results were obtained in 1988 in the Warsaw Dermatological Clinic. The allergy to hydrocortisone was diagnosed in 1% of patients (13).