Pathogenesis and properties of urticaria
The urticaria is a frequent entity which affects around twenty percent of the population in general. It constitutes a syndrome characterized for the emergence of hives and pruritus, the papules and edematous plaques are transitory, they are resolved in less than twenty four hours and are localized in any part of the body. If the cutaneous compromise takes place at a superficial level the lesions are known as hives which are pale, erythematosus and pruritic; if the condition affects the deepest layers of the dermis, the subcutaneous cellular tissue or the submucosal tissue the lesions are known as angioedema being more associated to pain than to pruritus and it mainly compromises lips, eyelids, genitals and tongue.
If the time of duration of the condition exceeds the six weeks it is considered as chronic, in more than forty percent of the cases with an evolution of more than six months it has been described the persistence of hives for even more than ten years. The chronic urticaria is mainly present on adults and it is twice common on women than on men and in seventy percent of the cases, the cause cannot be determined, therefore in those cases the condition is considered as a chronic idiopathic urticaria.
The urticaria has a spectrum of causes and clinical presentations. A series of factors has been attributed to this condition on its pathogenesis; among them recently the urticaria has been associated to the presence of antigens releasers of histamine which can be found on fifty percent of the cases which in the past had an “unknown” cause and on which cases the condition was tagged as autoimmune.
In the daily dermatological practice there are cases of chronic urticaria where the therapeutic handling turns out to be difficult sometimes, since the cause for the condition cannot be specified.
The urticaria is caused by the degranulation of cutaneous mast cells and basophils. The degranulation releases powerful vasoactive mediators which induce the vasodilatation and an increment of capillary permeability which is translated in erythema and the formation of a hive. The pruritus and pain are caused by intense sensory nerve stimulation. The most important vasoactive mediator is the histamine; there are other inflammatory mediators like leukotrienes, arachidonic acid metabolites, serotonin, D2 prostaglandin, heparin, platelet activating factor, acetyl choline, C3 anaphylatoxins, codeine, kinins and neuromediators that are released by cutaneous nerve endings.
It is not clear yet which is the event that triggers the degranulation on skin or the mechanisms of control that come from the degranulation of mast cells in other tissues. Local factors that include heat and pressure can stimulate the vasodilatation and the vasopermeability which can help in the extravascular passage of proteins that are relatively big, including antibodies, in the dermis to a concentration big enough to trigger degranulation.
The degranulation is attributed to immunological causes, non immunological and idiopathic. One of the principal factors that induce the degranulation of mast cells on chronic urticaria are antigens.