Phenotyping the heterogeneity of chronic obstructive pulmonary disease

Abstract

COPD (chronic obstructive pulmonary disease) is a heterogeneous disease associated with significant morbidity and mortality. Current diagnostic criteria based on the presence of fixed airflow obstruction and symptoms do not integrate the complex pathological changes occurring within lung, do not define different airway inflammatory patterns, nor do they define different physiological changes or differences in structure as can be defined by imaging. Over recent years, there has been interest in describing this heterogeneity and using this information to subgroup patients into COPD phenotypes. Most approaches to phenotyping have considered disease at a single scale and have not integrated information from different scales (e.g. organ-whole person, tissue-organ, cell-tissue and gene-cell) of disease to provide multi-dimensional phenotypes. Integration of disease biology with clinical expression is critical to improve understanding of this disease. When combined with biostatistical modelling, this information may lead to identification of new drug targets, new end points for clinical trials and targeted treatment for subgroups of COPD patients. It is hoped this will ultimately improve COPD outcomes and represent a move towards personalised medicine. In the present review, we will consider these aspects of multi-dimensional phenotyping in more detail.

Socioeconomic impact of asthma, chronic obstructive pulmonary disease and asthma-COPD overlap syndrome

“…Asthma and chronic obstructive pulmonary disease (COPD) are major airway diseases and have unique distinctive features (2). However, clinicians often encounter patients presenting overlapping symptoms of both diseases.…”

Bringing Stability to the Chronic Obstructive Pulmonary Disease Patient: Clinical and Pharmacological Considerations for Frequent Exacerbators

“…As mentioned above, eosinophilia has become a major target for precision medicine in COPD since the identification of eosinophilic endotype. [124] [125] [126] In addition to using LABA/ICS in this subgroup, various TH2 cytokines involved in eosinophilic pathways are now being evaluated as potential therapeutic targets in these patients. Interleukin-5 (IL-5) is a candidate cytokine as it regulates differentiation, proliferation, survival, and activation of eosinophils.…”

Asthma-COPD overlap szindróma

“…A köpet neutrofilszáma összefüggést mutatott a súlyosabb asthmafenotípusokkal, amelyek magas dózi-sú inhalációs vagy orális kortikoszteroidhasználat ellené-re is több egészségügyi kezeléssel és csökkent légzés-funkciós értékekkel párosultak [27]. A másik fontos megfigyelés, hogy a COPD-betegek 20-40%-ánál a kö-pet eozinfilszintje emelkedett [28], illetve 15-40%-ban a sejtek jelen voltak a bronchoalveolaris lavage és tüdőszö-veti mintákban is [29]. COPD-ben a köpet eozinofilszá-mának csökkenése összefüggést mutatott az 1 másod-perc alatti erőltetett kilégzési volumen (FEV 1 ) enyhe, illetve a betegségspecifikus kérdőívek eredményeinek javulásával bronchodilatator adását követően [30].…”