Asthma medication adherence, control, and psychological symptoms: a cross-sectional study.

BACKGROUND: Nonadherence to therapies and psychological disorders are associated with poor asthma control. This study aims to assess the prevalence of anxiety and depressive symptoms, asthma control, and adherence to inhalers and to investigate whether there is an association of anxiety and depressive symptoms with adherence to inhalers and asthma control. METHODS: We measured anxiety and depressive symptoms using the Hospital Anxiety and Depression Scale in patients with asthma. Asthma Control Test and the 10-Item Test of Adherence to Inhalers Scale were used to assess levels of asthma control adherence to inhalers, respectively. Univariate and multivariate regression models assessed the associations of anxiety and depressive symptoms with adherence to inhalers and asthma control. RESULTS: A total of 287 patients completed the study, of whom 72% were female. The mean ± SD age and body mass index of our study population were 44 ± 13 years and 29 ± 7.2 kg/m2, respectively. Poor adherence to inhaler use was highly prevalent (49.8%; 95% CI: 43.8 to 55.7). The prevalence of anxiety, depression and poor asthma control was 27.2% (95% CI: 22.1 to 32.7), 20.9% (95% CI: 16.3 to 26.1), and 22.7% (95% CI: 17.9 to 27.9), respectively. We found a negative relationship between asthma control and anxiety, and depressive symptoms (adjusted ß: -0.25; 95% CI: -0.36 to -0.14; p < 0.001 and adjusted ß: -0.29; 95% CI: -0.40 to -0.18; p < 0.001, respectively). A negative relationship was also observed between adherence to inhalers and anxiety and depressive symptoms (adjusted ß: -0.34; 95% CI: -0.46 to -0.22; p < 0.001 and adjusted ß: -0.36; 95% CI: - 0.48 to - 0.24; p < 0.001, respectively). CONCLUSIONS: The high prevalence of uncontrolled asthma symptoms and poor adherence to inhalers and their impact on anxiety and depression levels among patients with asthma point to the need for early screening for psychological symptoms and recognition of nonadherence as part of asthma assessment and management plan in primary care in Saudi Arabia to avoid further worsening of asthma symptoms. Further studies are needed to explore the effectiveness of specific psychoeducational interventions and investigate the long-term impact of early psychological symptom detection on asthma outcomes.

Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.

Pulmonary hypertension (PH) due to chronic obstructive pulmonary disease (COPD) is classified as Group 3 PH, with no current proven targeted therapies. Studies suggest that cigarette smoke, the most risk factor for COPD can cause vascular remodelling and eventually PH as a result of dysfunction and proliferation of pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs). In addition, hypoxia is a known driver of pulmonary vascular remodelling in COPD, and it is also thought that the presence of hypoxia in patients with COPD may further exaggerate cigarette smoke-induced vascular remodelling; however, the underlying cause is not fully understood. Three main pathways (prostanoids, nitric oxide and endothelin) are currently used as a therapeutic target for the treatment of patients with different groups of PH. However, drugs targeting these three pathways are not approved for patients with COPD-associated PH due to lack of evidence. Thus, this review aims to shed light on the role of impaired prostanoids, nitric oxide and endothelin pathways in cigarette smoke- and hypoxia-induced pulmonary vascular remodelling and also discusses the potential of using these pathways as therapeutic target for patients with PH secondary to COPD.

Inhaled therapies targeting prostacyclin pathway in pulmonary hypertension due to COPD: systematic review.

Background: Pulmonary hypertension due to chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) is classified as group 3 pulmonary hypertension. Inhaled treprostinil, a prostaglandin I2 analogue also known as prostacyclin, has recently been approved as a first drug for patients with pulmonary hypertension secondary to ILD. However, due to a lack of evidence, no therapies are currently approved for those with COPD-associated pulmonary hypertension. Thus, this systematic review aims to summarise the current evidence to assess the impact of inhaled prostaglandin I2 analogue use on the pulmonary hemodynamics, exercise function, lung function, and gas exchange in patients with pulmonary hypertension due to COPD. Methods: We systematically searched the electronic databases of Medline, Embase, Scopus and Cochrane from inception to 1 February 2023. Studies of adult patients with a confirmed diagnosis of COPD-associated pulmonary hypertension who received inhaled drugs targeting the prostacyclin pathway were included in the systematic review. Case reports, systematic reviews, conference abstracts with no full text, non-full-text articles, non-English manuscripts and book chapters were excluded from this systematic review. A risk-of-bias assessment was carried out for the studies included in this review, using two different Cochrane risk-of-bias tools for randomised and non-randomised clinical trials. Results: A total of four studies met our inclusion criteria and were included in this systematic review. The results of one prospective clinical trial showed an improvement in the pulmonary hemodynamics (e.g., cardiac index, cardiac output and mean pulmonary artery pressure) in response to inhaled prostacyclin use in patients with pulmonary hypertension secondary to COPD. However, the severity of dyspnoea, lung function, exercise capacity and gas exchange were not affected when inhaled prostacyclin was used for patients with COPD-related pulmonary hypertension. Conclusion: This systematic review demonstrated that although inhaled prostacyclin does not seem to improve COPD-related outcomes (e.g., lung function and exercise capacity), short-term use of inhaled prostacyclin has the potential to reduce mean pulmonary artery pressure and pulmonary vascular resistance without impairing ventilation-perfusion mismatch. Further studies with larger sample sizes are warranted. Systematic review registration: CRD42022372803, https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=372803.