In this study, we have assessed the COPD’s influence on the severity of clinical and CT characteristics of COVID-19-associated pneumonia. The hospitalization rate of our patients with COPD and COVID-19 infection was relatively low, only 76 out of 281 patients, 50 of which demonstrated CT spectrum of COVID-19-associated pneumonia. This echoes the reports on the relatively low hospitalization rates of the patients with COVID-19 infection in other countries, average 2–12% [1, 11, 26,27,28]. Also, as per the summary of the Global Initiative for Chronic Obstructive Lung Disease’s 2022, patients with COPD are not at greatly increased risk of infection with SARS-CoV-2 [29].
Our COPD group had a higher mean age and larger male fraction compared to the non-COPD group. This is concordant with demographic data observed by Wu F. et al. and Turan O. et al., with the reported male fraction of 79–83% and mean age of 70–71 years in COPD- vs. 55–56 years for the non-COPD group [30, 31].
The severity of COVID-19 infection and outcomes are reported to be worse in the patients with COPD due to increased expression of angiotensin-converting enzyme-2 receptors (ACE-2 receptors) in the airways and other organs, especially in the presence of diabetes, cardiovascular disease, and obesity [19]. COPD is believed to be an independent factor for respiratory failure in COVID-19 infection given chronic airway dysfunction and increased potential of virus binding [19]. However, hypoxia level, in-hospital mortality, and intensive care unit (ICU) admission rate are heterogeneously reported in the literature. For example, Gemicioglu B. et al. demonstrated a high SpO2 level of 92.57 ± 7.1% in COPD patients with COVID-19 infection [32]. At the same time, Aalinezhad M. et al. has concluded that COPD was linked to more profound hypoxemia in patients with COVID-19-associated pneumonia (89.83 ± 8.02) [33]. Lee et al. in the nationwide retrospective study in South Korea has shown an increased rate of ICU admission, mechanical ventilation and all-cause mortality in the COPD group [34]. In our study, we have found no statistically significant difference in the level of SpO2, hospital length of stay or in-hospital mortality between COPD and non-COPD groups. Our observations are concordant with those by Turan O. et al. who demonstrated a mortality rate of 13.2% vs. 7.% and hospitalization length of 10.06 ± 4.04 days vs. 11.05 ± 5.42 days in COPD- vs. non-COPD group, respectively [31]. Similarly, COPD was not a significant risk factor for increased in-hospital mortality in comparison with non-COPD patients in several other studies [31, 35, 36]. On the contrary, Guan WJ et al. and Lee et al. identified that COPD as a risk factor for ICU admission assisted ventilation and mortality, which remained significant even after the adjustments for age and smoking [16, 34]. Gerayeli FV et al. reported increased odds of hospitalization (OR = 4.23, 95% CI 3.65–4.90), ICU admission (OR = 1.35, 95% CI 1.02–1.78), and mortality (OR = 2.47, 95% CI 2.18–2.79), accompanied by the results of Sanchez-Ramirez DC et al. on higher odds of worse outcomes (OR = 5.8; 95% CI: 3.9–8.5) in patients with COPD [37, 38].
Such varieties in the course of the disease and outcomes between the studies might be multifactorial, and at least partially explained by the unique genetic profile (including expression of ACE-2 receptors), ethnicity and geography, as well as comorbidities, treatment variations, criteria for ICU admission, and mechanical ventilation modes. For instance, a tendency to therapeutic rather than prophylactic anti-coagulation in our country (not published data), even with a milder course of the disease, might have resisted the effects of endothelial cell dysfunction and coagulopathy previously reported in COVID-19 infection [34]. Moreover, severe course of the disease and associated diffuse alveolar damage by CT criteria was rare in our study (2% in COPD- and 2.6% in non-COPD group). Finally, a relatively small number of the included patients and methodology might have impacted our results too.
In regards to the major comorbidities, diabetes mellitus and cardiovascular diseases were observed at the same rate in both groups. This is concordant with other studies [16, 27, 34,]. For example, Marron RM et al. showed increased rates of ischemic heart disease, congestive heart failure and stroke among all the patients with COPD, with no obvious difference in the admission rates in comparison with the patients without COPD [39].
We have observed that dyspnea at rest, dry cough and fever ≥ 38.0 °C were the most common symptoms on admission in both groups. Guan WJ et al. and Zhang J et al. have demonstrated a similar rate of mild fever (88.0% vs.79.5%) and cough (70.2% vs. 61.8%) in both groups, respectively [16, 40]. Similarly, Goyal P. et al. concluded that cough (79.4%), fever (77.1%) and dyspnea (56.5%) were the most common clinical findings regardless of the COPD status [28].
Our laboratory values showed lower ALC and higher leukocyte, including ANC and NLR in patients with COPD. Similar results are demonstrated by Gemicioglu B. et al., lower ALC (1.42 ± 0.77 × 109/L), higher WBC (10.6 ± 5.2 × 109/L) and ANC (7.94 ± 4.18 × 109/L), with the median level of NLR 8.09 ± 7.25 [32]. In contrast, Basin S. et al. observed no significant differences in the level of leukocytes and lymphocytes in patients with COPD vs. control group (6.4 × 109/L vs. 6.5 × 109/L and 1.0 vs. 0.9 × 109/L, respectively) [41]. Such heterogeneities in the results might be due to differences in the severity of the disease among included patients in different studies. In our study, only 1 patient from COPD group and 2 patients from non-COPD group had diffuse alveolar damage.
None of our CT findings differ statistically between COPD and non-COPD groups. However, the patients with COPD were more likely to have milder CT severity score, especially CT1 (less than 25% of lung involvement) category, less likely to have bilateral and central localization of GGO, right lower lobe and left lung involvement, as well as a “crazy-paving” pattern. “Reversed halo” sign was not present in the patients with COPD. In regards to the severity score, our results are concordant with those by Basin S. et al. [41]. In detail, the referenced study reported CT1 category of 63.1% vs. 42.4%; CT2 category, 26.2% vs. 40.2%; CT3 category, 9.2% vs. 15.0%; CT4 category (more than 75%), 1.5% vs. 3.3% in COPD vs. non-COPD group, respectively. CT-based severity score of less than 25% of lung involvement (CT1 category) in patients with COPD was the most common in his study, similar to ours. We have found a positive correlation between CT severity score and in-hospital mortality in patients with hypoxia regardless COPD status, with the most significant mortality rate among the patients under CT severity score of 4 (more than 75% of lung involvement). However, we had only 4 patients with CT 4 category in COPD group vs. 30 patients without COPD.
There is a number of limitations in our study. First, spirometry data in the patients with CT findings compatible with COPD are not available. Second, the cohort of the patients with COPD is relatively small, i.e., only 50 patients. Moreover, a small number of the patients included in non-COPD group did report a smoking history but did not have findings of COPD by CT criteria. Third, we did not longitudinal evaluation of the disease severity by CT. Also, inflammatory cytokine levels that might influence the disease severity and outcome were not done at our hospital. However, we did include conventional laboratory values that are known to correlate with the severity of the disease and outcome. Overall, we believe that our results do contribute to the existing literature on clinical and imaging characterization of the patients with COVID-19 infection and suggest that older age, male gender, CT-based severity score, and hypoxia correlate with the clinical severity and in-hospital mortality regardless of COPD status.