Anafilaxia oral por alimentos contaminados por ácaros: (síndrome de las panquecas) / Oral anaphylaxis by mite contaminated food: (the pancake syndrome)

La anafilaxia oral por ácaros es un nuevo síndrome caracterizado por síntomas alérgicos graves que se presentan en individuos alérgicos rápidamente después de la ingestion de alimentos confeccionados con harinas de trigo contaminadas con ácaros. Este síndrome más común en ambientes tropicales, es desencadenado más frecuentemente por panquecas y por ello ha sido designado "el síndrome de las panquecas". Se postula que los alergenos responsables son alergenos termorresistentes ya que los alimentos cocinados son capaces de inducir los síntomas. Una variedad del síndrome puede presentarse durante el ejercicio físico (anafilaxia inducida por ejercicio asociada a la ingestión de polvo con ácaros). Se recomienda conservar las harinas de trigo en el refrigerador para prevenir la proliferación de los ácaros y la aparición del cuadro clínico.

Oral mite anaphylaxis is a new syndrome characterized by severe allergic symptoms occurring in allergic patients immediately after the intake of foods made with mite-contaminated wheat flour. This syndrome, which is more common in tropical environments, is triggered more aften by pancakes and for that reason it has been designated "the pancake syndrome". Since cooked foods are able to induce the symptoms, it has been suggested that thermoresistant allergens are involved. A variety of this syndrome can occur during physical exercise (dust mite-ingestion associated exercise induced anaphylaxis). In order to prevent mite proliferation and the production of the clinical picture it is recommended to store wheat flours in the refrigerator.

Major house dust mite allergen, Der p I, activates phospholipase D in human peripheral blood mononuclear cells from allergic patients: involvement of protein kinase C

The major house-dust-mite allergen, Der p I, stimulates the phospholipase D (PLD) in peripheral blood mononuclear cells (PBMC) from allergic patients with maximal responses after 30 min exposure. At 30 min, Der p I stimulated PLD activity by 1.4-fold in mild, 1.6-fold in moderate and 2-fold in severe allergic patients over control values (p < 0.05). When the cells were pretreated for 24 h with phorbol myristate acetate to down-regulate protein kinase C (PKC), PLD stimulation by Der p I was largely abolished. These results indicate that in PBMC from allergic patients, Der p I can stimulate PLD activity, and that PKC activation is involved in this stimulation.