Precision Medicine in Atopic Diseases

Antonella Cianferoni; Isabella Annesi-Maesano

Disclosures

Curr Opin Allergy Clin Immunol. 2019;19(6):654-664. 

In This Article

Abstract and Introduction

Abstract

Purpose of review: To analyze the status of precision medicine in atopic diseases.

Recent findings: Atopic diseases are increasingly recognized as heterogeneous in nature and they can be quite different in severity, response to therapy, triggers, genetic back ground, ancestral risk and type of inflammation. This significant variability in the landscape of atopic diseases is not reflected in the common treatment guidelines that follow 'one fits all' approach for their management. Such an approach is largely based on minimal 'phenotype' elements, such as severity of disease and response to therapy and does not reflect the information accumulate in the last 20 years about particular pathogenic pathways (endotypes) leading to disease (phenotypes) based on biomolecular analysis of the single individuals. Accumulating data have defined asthma allergic rhinitis, food allergy based on their endotypes and clinically relevant phenotypes. In general, atopic diseases can be largely classified as high or low Th2 inflammatory status, which may explain the severity and response to therapy.

Summary: Precision medicine is aiming to use known endotype phenotype to guide specific individualized treatment. The work aimed in deep characterization of diseases to guide the disease management is crucial in light of the availability of ever more precise treatment able to target specific pathways.

Introduction

Atopic diseases, such as atopic dermatitis, asthma, allergic rhino-conjunctivitis and food allergy, are among the most common chronic diseases in westernized developed societies. They represent diverse inflammatory conditions[1] characterized by significant complexity, with multiple genetic and environmental factors interlinked through an inherited tendency to produce immunoglobulin E (IgE) antibodies in response to small amounts of commonly tolerated proteins known as allergens and non-IgE-associated mechanisms.[2] These diseases generally begin very early in life and can persist into adult life.[3] As in patients with other chronic diseases, they often occur in the same individuals (multimorbidity) more often than expected by chance.[4]

Treatment of atopic diseases is based on global highly publicized guidelines that characterize patient groups largely on minimal 'phenotype' elements, such as severity of disease and response to therapy (i.e. topical steroid and other anti-inflammatory therapies).[5–9] This 'one fits all' approach is being challenged by an increased recognition that atopic diseases are a heterogeneous in nature and they can be quite different in severity, natural history, response to therapy, triggers, genetic back ground, ancestral risk, environmental risk factors and type of inflammation.[10–17] This significant variability has been confirmed by the information obtained with biomolecular analysis accumulated in the last 20 years about particular pathogenic pathways (endotypes) leading to disease (phenotypes).[18,19] On the basis of such knowledge, highly selective drugs targeting specific pathways are being developed and in the near future, the current management of atopic diseases will become obsolete replaced by 'precision medicine' when the knowledge of 'phenotype' and 'endotype' of a patients will guide a truly individualized treatment. This progress has stimulated interest in applying systems biology approaches to biomedical research and efforts to create a personalized, predictive, preventive, and participatory (P4) medicine are increasing worldwide.[20]

This review will analyze the status of precision medicine in atopic diseases.

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