Lee Y, et al. Allergy Asthma Immunol Res. 2019 May;11(3):394-405. https://doi.org/10.4168/aair.2019.11.3.394

Jung HY, et al. Allergy Asthma Immunol Res. 2019 Jan;11(1):90-103. https://doi.org/10.4168/aair.2019.11.1.90

Lee JH, et al. Yonsei Med J. 2019 Jun;60(6):570-577. https://doi.org/10.3349/ymj.2019.60.6.570

Introduction: Inhaled corticosteroids (ICSs) are recommended for patients with frequent exacerbation of chronic obstructive pulmonary disease (COPD). However, accumulating evidence has indicated the risk of pneumonia from the use of ICS. This study aimed to investigate the association between ICS and pneumonia in the real-world clinical setting. Methods: A retrospective cohort study was performed using nationwide population data from the Korea National Health Insurance Service. Subjects who had a new diagnosis of COPD and who received inhaled bronchodilators without a diagnosis of pneumonia before the initiation of bronchodilators were identified. Subjects were followed up until their first diagnosis of pneumonia. The risk of pneumonia in ICS users was compared to that in non-ICS users. Results: A total of 87,594 subjects were identified and 1:1 matched to 22,161 ICS users and non-ICS users. More ICS users were diagnosed with pneumonia compared to non-ICS users (33.73% versus 24.51%, P< 0.0001). The incidence rate per 100,000 person-years was 8904.98 for ICS users and 6206.79 for non-ICS users. The hazard ratio (HR) of pneumonia for ICS users was 1.62 (95% CI 1.54– 1.70). The HR of subjects prescribed with the lowest ICS cumulative dose was 1.35 (1.27– 1.43). The HR increased to 1.51 (1.42– 1.60), 1.96 (1.85– 2.09), and 2.03 (1.89– 2.18) as the cumulative dose increased. Pneumonia was strongly associated with fluticasone propionate (1.79 (1.70– 1.89)) and fluticasone furoate (1.80 (1.61– 2.01)) use, compared to the use of other types of ICS. Conclusion: ICS increases the risk of pneumonia in patients with COPD. Hence, ICS should be carefully prescribed in patients with risk factors for pneumonia while considering the cumulative doses and subtypes of ICS.

Background: Adenosine deaminase (ADA) activity is typically elevated in patients with tuberculous pleural effusion (TPE), but low ADA has occasionally been reported in patients with TPE. The characteristics of these patients are not well-known, and erroneous exclusion of the possibility of TPE can result in a delayed diagnosis. This study investigated the characteristics of patients with TPE who had low ADA activity.Methods: We retrospectively reviewed patients with microbiologically or pathologically confirmed TPE between 2012 to 2018 in a tertiary hospital in South Korea. Patients were categorised into two groups: high ADA (≥40 IU/L) and low ADA (< 40 IU/L). Clinical characteristics and Sequential Organ Failure Assessment (SOFA) scores were compared between groups.Results: A total of 192 patients with TPE were included; 36 (18.8%) had ADA < 40 IU/L with a mean ADA activity level of 20.9 (±9.2) IU/L. Patients with low ADA were older (75.3 vs. 62.0 years,p < 0.001) and had a lower mean lymphocyte percentage (47.6% vs. 69.9%,p < 0.001) than patients with high ADA. Patients in the low ADA group had a significantly higher mean SOFA score (2.31 vs. 0.68,p < 0.001), and patients with organ dysfunction were significantly more common in the low ADA group (p < 0.001). Patients with 2 or ≥ 3 organ dysfunctions constituted 19.4 and 13.9% of the patients in the low ADA group, whereas they constituted 7.1 and 1.3% of the patients in the high ADA group (p < 0.001). Multivariate logistic regression analyses showed that older age (odds ratio = 1.030, 95% confidence interval 1.002–1.060,p = 0.038) and a higher SOFA score (odds ratio = 1.598, 95% confidence interval 1.239–2.060,p < 0.001) were significantly associated with low ADA activity in patients with TPE.Conclusions: ADA activity can be low in patients with TPE who are elderly, critically ill, and exhibit multiorgan failure. Low ADA activity cannot completely exclude the diagnosis of TPE, and physicians should exercise caution when interpreting pleural fluid exams.

Lee JH, et al. Allergy Asthma Immunol Res. 2024 Mar;16(2):168-178. https://doi.org/10.4168/aair.2024.16.2.168