Pollen-food allergy syndrome and lipid transfer protein syndrome: Clinical relevance

Abstract

The role of an allergist in recognizing the pollen-food allergy syndrome (PFAS) and lipid transfer protein syndrome (LTPS) is essential. LTPS differs from PFAS by having a different family of panallergens and clinical characteristics. Both are complex syndromes posing diagnostic and therapeutic challenges. Many cross-reactive allergen components are involved, such as plant panallergens profilins, PR-10 proteins (Bet v 1 homologous), and lipid transfer proteins (LTP). PFAS results from cross-reactivity between pollen-specific immunoglobulin E (IgE) and homologous proteins found in fruits and vegetables. In most cases, grass pollen is responsible for profilin hypersensitivity. But, tree and weed pollen may also act as primary sensitizers, depending on geographical differences. Nonspecific LTP (nsLTP) is ubiquitous in terrestrial plants and can induce systemic allergic severe reactions. Peach (Pru P 3) is the primary sensitizer for LTP-driven allergy, and its clinical relevance is considered the prototypic marker for LTPS. nsLTPs have been identified as a major allergen in tree and weed plants. A second critical point is the diagnosis of LTPS associated with cofactors such as exercise, alcohol, antacids, and NSAIDS, that can promote severe reactions. Skin Prick Test (SPT) with Peach extracts that have been highly enriched for Pru p 3 with very low content of other allergens for LTPS, is suggestive of LTPS. For PFAS, positive SPT with profilin-enriched date palm pollen and watermelon extract shows sensitivity and specificity that is very close to that of the recombinant grass pollen profilin. The present review address differences between the PFAS from LTP syndrome with particular attention to the clinical impact on cross-reactivity or cross-sensitization to pollens.