Actinic prurigo: a case-control study of risk factors

Abstract

Background: Actinic prurigo (AP) is an idiopathic photodermatosis that usually onsets during childhood and predominates in women. It is characterized by the symmetrical involvement of sun-exposed areas of the skin, lips, and conjunctiva.

Objectives: This study aimed to analyze the risk factors associated with AP using a case-control design.

Methods: All patients diagnosed with AP during 1990-2006 at Dr. Manuel Gea González General Hospital in Mexico City were included. Respective controls were recruited. Race, demographic, geographic, socioeconomic, environmental, clinical, and nutritional risk factors were assessed.

Results: A total of 132 persons were enrolled. These included 44 cases and two control groups comprising, respectively, dermatology and non-dermatology outpatients without AP or any autoimmune disease. Distribution by gender, age, place of birth, place of residence, and economic status did not differ significantly among the three groups. A total of 256 variables were analyzed. Only 19 variables were found to be statistically significant (P < 0.05). These were: use of a boiler; use of firewood; car ownership; use of earthenware; mixed material housing; socioeconomic level 1; sun exposure; use of soap; lemon consumption; use of moisturizing hair cream; living with pets in the house; living with farm animals; age; having a family member with AP; having had surgery; having had trauma; having been hospitalized; use of oral medication; and use of herbal medication. Of 40 macro- and micronutrients analyzed, 11 were found to have statistically significant effects (P < 0.05).

Conclusions: Multiple epidemiologic, geographic, clinical, and immunologic factors are involved in the etiology of AP. This study proposes a clear line for research directed at specific risk factors that refer to an individual's clinical, allergic, health, and socioeconomic status. Further study should also investigate the etiologic role of diet in AP and the molecular mechanisms behind the development of AP to establish whether AP is caused by exposure to polycyclic aromatic hydrocarbons.