Estudo do envelhecimento na Doença Pulmonar Obstrutiva Crônica: aspectos imunes e endócrinos

Abstract

ABSTRACT Considered a disease associated with aging, Chronic Obstructive Pulmonary Disease (COPD) presents airflow limitation associated with chronic lung inflammation involving changes in the respiratory and systemic systems. Risk factors such as smoking, inhalation of harmful gases, and genetic mutations can influence the development of the disease. COPD results from the complex interaction between genetic and environmental factors over time. Both COPD and the aging process share similar mechanisms of immunosenescence. These changes are thought to result in an "accelerated aging" process in COPD patients. The immunosenescence found in COPD is related to the clinical course of the disease, associated with worsening gas exchange, pulmonary hyperinflation, and increased risk of mortality. Pulmonary function testing is a valuable tool in identifying patients at risk of developing COPD. A specific subtype of this disease is known as spirometry with impaired preserved relationship (PRISm). The interference of endocrine aging was identified in individuals with COPD by analyzing DHEA-S (dehydroepiandrosterone sulfate) levels and GH (growth hormone). Accelerated lung, immune, and endocrine aging in the disease are often discussed individually in the literature. Studies that assess how relaxing these systems are require renewed attention, given that COPD is not limited to repercussions only at the local level. The objective of this study was to evaluate the clinical, endocrine, and immunological profile in individuals diagnosed with COPD, as well as in individuals with risk factors for the development of the disease, in addition to reviewing the aspect of immunosenescence in COPD. This study presents a systematic review addressing immunosenescence changes in COPD and discussing their clinical repercussions. In addition, an original article presents the immunoendocrine profile of individuals with COPD and PRISm, as well as the influence of these hormones on lung function and immunological markers.