Algunos aspectos de la prevención primaria y secundaria en alergia y asma / Strategies for primary and secondary prevention of asthma and allergy

Existe un aumento en la prevalencia de las enfermedades alérgicas y el asma. Dicho incremento es más notable en la población urbana de los países occidentales más industrializados. Enfermedades como el eczema atópico, la alergia a alimentos, la rinoconjuntivitis alérgica y el asma bronquial, entre otras, además de generar costos millonarios a los distintos estados, afectan notablemente la calidad de vida de la población que las padece, reflejándose en un gran ausentismo escolar y laboral entre otros aspectos. Las enfermedades alérgicas y el asma surgen de la interacción de factores genéticos y factores ambientales. Dicha interacción que provocará la sensibilización atópica y posteriormente el desarrollo de las distintas enfermedades, comienza en la vida fetal intrauterina, siendo clave el primer, y tal vez el segundo año de vida. Se describen diversas estrategias de prevención primaria para evitar la sensibilización, entre las que se destacan, el control ambiental para evitar o disminuir el contacto a diversos aeroalérgenos interiores, la manipulación en la dieta fomentando lactancia materna exclusiva hasta los 4 a 6 meses, utilizando en niños de riesgo fórmulas hidrolizadas como suplemento, evitar el tabaquismo en la embarazada y el pasivo en los niños pequeños. Entre las estrategias en la prevención secundaria, es decir, el evitar el desarrollo de una enfermedad alérgica después de la sensibilización, se destaca nuevamente el control ambiental (se mencionan distintos consejos de la OMS), la inmunoterapia con alérgenos y la farmacoterapia (antihistamínicos). Por último, se mencionan la influencia de la polución ambiental y el potencial papel de la terapia génica.

There has been an increase in the prevalence of asthma and allergic diseases, more notably in urban population of western developed countries diseases such as atopic eczema, food allergy, allergic rhinoconjunctivitis and bronchial asthma, among other, not only generate millionaire costs to the different states, but also considerably affect the quality of life of the population suffering them, which is reflected in a great work and school absence, among other aspects. Allergic diseases and asthma develop from the interaction between genes and environment. Such an interaction will cause allergic sensitization and lately the development of different diseases. It starts in fetal life and becomes more important in the first, and perhaps second, year of life. Different strategies for primary prevention are described to avoid atopic sensitization, such as allergen avoidance of indoor allergens, diet manipulation to avoid cow's milk protein with exclusive breast feeding until four to six months of life; use of hydrolyzed milk formulae as a replacement for or supplement to breast-feeding, late introduction of solid food, avoidance of active smoking among pregnant women and passive smoking in children. Among other strategies for secondary prevention, this is to avoid the development of an allergic disease after sensitization has occurred, again allergen avoidance is mentioned (with advice measures by WHO), allergen immunotherapy and medication (antihistamines). At last, the influence of air pollution and the potential use of gene therapy are also considered.

Dust-mites: effect on lipid peroxidation.

BACKGROUND: Dust-mites are present in our homes, feed on dead exfoliated skin and other organic material. It is also known that oxidative stress may lead to cellular damage that can be confirmed by markers of cellular disruption. Oxidative stress in various infective processes has been documented. We investigated whether house dust-mites cause oxidative stress in patients. METHODS: Products of lipid peroxidation in erythrocytes and lymphocytes were assessed by measuring malondialdehyde concentration. RESULTS: Our results showed that patients who had a positive skin test for dust-mite antigens and had dust-mites present in their houses (dust-mite positive) had increased erythrocyte malondialdehyde levels (62.39 [18.56] nmol/g-Hb) compared with those who were skin test positive, dust-mite negative (45.45 [10.82]) or skin test negative, dust-mite negative (42.20 [5.68]). They also had significantly higher levels of lymphocyte malondialdehyde (4.22 [0.55] nmol/g-protein) compared with those who were skin test positive, dust-mite negative (3.46 [0.29]) or skin test negative, dust-mite negative (1.25 [0.31]; p <0.05). However, there was no statistically significant difference between the malondialdehyde levels of dust-mite negative/skin test positive and dust-mite negative/skin test negative patients. CONCLUSION: Increased malondialdehyde activity in lymphocytes and erythrocytes in the dust-mite positive/skin test positive group shows the presence of the oxidative stress in patients with dust-mite infestation.