Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used to alleviate symptoms during community-acquired pneumonia (CAP), while neither clinical data nor guidelines encourage this use. Experimental data suggest that NSAIDs impair neutrophil intrinsic functions, their recruitment to the inflammatory site, and the resolution of inflammatory processes after acute pulmonary bacterial challenge. During CAP, numerous observational data collected in hospitalized children, hospitalized adults, and adults admitted to intensive care units (ICUs) support a strong association between pre-hospital NSAID exposure and a delayed hospital referral, a delayed administration of antibiotic therapy, and the occurrence of pleuropulmonary complications, even in the only study that has accounted for a protopathic bias. Other endpoints have been described including a longer duration of antibiotic therapy and a greater hospital length of stay. In all adult series, patients exposed to NSAIDs were younger and had fewer comorbidities. The mechanisms by which NSAID use would entail a complicated course in pneumonia still remain uncertain. The temporal hypothesis and the immunological hypothesis are the two main emerging hypotheses. Current data strongly support an association between NSAID intake during the outpatient treatment of CAP and a complicated course. This should encourage experts and scientific societies to strongly advise against the use of NSAIDs in the management of lower respiratory tract infections.
Highlights
Community-acquired pneumonia (CAP) is a frequent disease, with an annual incidence rate ranging from 1.6 to 9 cases per 1000 inhabitants in Western Europe [1,2]
non-steroidal anti-inflammatory drugs (NSAIDs) users had a higher risk of pleuropulmonary complications (3.8%) in comparison with both former users (2.4%) and non-users (2.3%) (adjusted rate ratio 1.81; 95% confidence interval (CI), 1.60–2.05)
During CAP, numerous observational data collected in hospitalized children [45,46,49,50,53], hospitalized adults [51,52,54], and intensive care units (ICUs) adults [47,48] supported a strong association between pre-hospital NSAID exposure and (i) a delayed hospital referral, (ii) a delayed administration of antibiotic therapy, and (iii) the occurrence of pleuropulmonary complications, even in the only study that accounted for a protopathic bias [50]
Summary
The pivotal role of COX in the resolution of inflammation, especially inducible COX-2, has been described during the last decade. It has been demonstrated that first-phase COX-2-induced eicosanoids promote a shift to anti-inflammatory lipids, which deliver a stop signal [33,34]. This lipid mediator class switching highlights the dual role of COX-2 in the inflammatory response: amplifying the initial acute phase, and acting for resolution. This dual role has been described in animal studies. In a carrageenan-induced model of pleurisy in rats, both the selective inhibition of COX-2 and the dual inhibition of COX-1/COX-2 limited exudate volume and inflammatory cell recruitment within pleura at 2 h, but exacerbated pleural inflammation at 48 h [36]
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