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Clinical Investigations: INFECTIOUS DISEASE |

Pneumonic vs Nonpneumonic Acute Exacerbations of COPD*

David Lieberman, MD; Devora Lieberman, MD; Yevgenia Gelfer, MD; Raiesa Varshavsky, MD; Bella Dvoskin, MD, PhD; Maija Leinonen, PhD; Maureen G. Friedman, PhD
Author and Funding Information

*From the Pulmonary Unit (Dr. Lieberman), and Division of Internal Medicine (Drs. Lieberman, Gelfer, and Varshavsky), Soroka University Medical Center, the Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel; The National Public Health Institute (Dr. Leinonen), Oulu, Finland; and the Department of Virology (Drs. Dvoskin and Friedman), the Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Correspondence to: David Lieberman, MD, Pulmonary Unit, Soroka Medical Center, Beer-Sheva, Israel 84101; e-mail: Lieberma@bgumail.bgu.ac.il



Chest. 2002;122(4):1264-1270. doi:10.1378/chest.122.4.1264
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Study objective: To describe and compare the background, clinical manifestations, disease course, and infectious etiologies of pneumonic acute exacerbations (PNAE) vs nonpneumonic acute exacerbations (NPAE) of COPD.

Design: A prospective, observational study.

Setting: A tertiary university medical center in southern Israel.

Patients: Twenty-three hospitalizations for PNAE and 217 hospitalizations for NPAE were included in the study. Paired sera were obtained for each of the hospitalizations and were tested serologically for 12 pathogens. Only a significant change in antibody titers or levels was considered diagnostic.

Results: No significant differences were found between the two groups for any of the parameters related to COPD or comorbidity. The clinical type of the exacerbation was not significantly different between the groups. Compared to NPAE, patients with PNAE had lower Po2 values at hospital admission (p = 0.004) but higher rates of abrupt onset (p = 0.005), ICU admissions (p = 0.006), invasive mechanical ventilation (p = 0.01), mortality (p = 0.007), and longer hospital stay (p = 0.001). In 22 PNAE hospitalizations (96%) and in 153 NPAE hospitalizations (71%), at least one infectious etiology was identified (p = 0.001). Mixed infection was found in 13 patients with PNAE (59%) and in 59 patients with NPAE (39%; not significant [NS]). Viral etiology was identified in 18 patients with PNAE (78%) compared with 99 patients with NPAE (46%; p = 0.003). Pneumococcal etiology was found in 10 patients with PNAE (43%) and in 38 patients with NPAE (18%; p = 0.006). An atypical etiology was identified in 8 patients with PNAE (35%) and 64 patients with NPAE (30%; NS).

Conclusions: Community-acquired pneumonia is common among patients hospitalized for an acute exacerbation of COPD and is generally manifested by more severe clinical and laboratory parameters. In PNAE, compared to NPAE, viral and pneumococcal etiologies are more common, but the rate of atypical pathogens is similar. The therapeutic significance of these findings should be investigated further.


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