Actinic prurigo: an allergy to sunlight

The Actinic prurigo corresponds to a less frequent photodermatoses but which is more common during childhood. Some consider this condition as a variant of solar polymorphic eruption, but the clinical manifestations are very different. The etiology for this condition is unknown. It is easy to observe that this condition has a restricted ethnic distribution: it can be found on America and it is almost exclusive for Amerindians and their descendants. This condition has not been reported on individuals of African origin, and just a few reports have been found on United Kingdom.

An approach to try to elucidate the pathogeny of the actinic prurigo is to investigate if the proteins of the Major Complex of Histocompatibility (MCH); which are responsible for presenting the antigens for the initiation of immune response and which are associated to many conditions, are implicated in the development of this pathology.

The typing of MCH in patients of different communities has provided information about the alleles that are associated to this condition in different races and ethnic groups. These associations suggest in some way that the alleles may express and condition an immune response to an antigen induced by light and trigger a chronic reaction on skin.

Another type of approach to the study of the actinic prurigo is the study of cells and molecules implied on the emergence of lesions on skin. On recent years have been described protein molecules which control cellular migration, known as molecules of adherence. These proteins can be found on capillary and vascular endothelium and in extracellular matrices which have their ligands or counterparties on the different types of leukocytes. Their expression depends on the state of the activation and maturation of the cell.

The migration of circulating lymphocytes to specific tissues like skin is directed by the interaction of these cells with the vascular endothelium through the molecules of adhesion, being determinant in inflammatory process like in chronic dermatoses on which an increment of the ELAM-1 molecule has been incremented. It has been made an analysis of the different components of the immune system that are present on lesions on the skin of a patient affected by actinic prurigo using monoclonal antibodies.

The actinic prurigo begins on the first decade of life and is characterized for being perennial with more severity during summer and spring. It is not clear the relation between the exposition to sunlight and the emergence of the condition on the anamnesis; family incidence is frequent. Lesions initially consist in pruritic, erythematous and edematous nodules or papules.

After that a chronic prurigo is developed on exposed areas as in non exposed areas with nodules and plaques that are frequently crusted and excoriated, associated to eczematization. The typical compromise is facial (especially from cheeks, the tip of the nose and part of the lower lip) and of the distal end of the limbs, in more severe cases the sacral and the gluteal are also compromised. It can be accompanied by conjunctivitis.