Could Nonsteroidal Antiinflammatory Drugs (NSAIDs) Enhance the Progression of Bacterial Infections to Toxic Shock Syndrome?

Anecdotal reports suggest an association between the use of nonsteroidal antiinflammatory drugs (NSAIDs) and the progression of invasive group A streptococcal infections to shock and multiorgan failure. There is a biochemical rationale that could support this theory. Though NSAIDs are frequently use...

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Bibliographic Details
Published in:Clinical infectious diseases 1995-10, Vol.21 (4), p.977-980
Main Author: STEVENS, D. L
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents, Non-Steroidal - adverse effects
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Biological and medical sciences
Cytokines
Cytokines - drug effects
Cytokines - metabolism
Disease Progression
Drug toxicity and drugs side effects treatment
Endotoxins
Fever
Humans
Hypothesis
Infections
Medical sciences
Miscellaneous (drug allergy, mutagens, teratogens...)
Nonsteroidal antiinflammatory agents
Pain
Pharmacology. Drug treatments
Prostaglandins
Shock, Septic - chemically induced
Shock, Septic - immunology
Staphylococcal Infections - complications
Staphylococcal Infections - drug therapy
Staphylococcal Infections - immunology
Staphylococcus
Staphylococcus aureus - isolation & purification
Streptococcal Infections - complications
Streptococcal Infections - drug therapy
Streptococcal Infections - immunology
Streptococcus pyogenes
Streptococcus pyogenes - isolation & purification
Toxicity
Tumor Necrosis Factor-alpha - drug effects
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factors
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Description
Summary:Anecdotal reports suggest an association between the use of nonsteroidal antiinflammatory drugs (NSAIDs) and the progression of invasive group A streptococcal infections to shock and multiorgan failure. There is a biochemical rationale that could support this theory. Though NSAIDs are frequently used to relieve pain or reduce fever, they also attenuate granulocyte functions such as chemotaxis, phagocytosis, and bacterial killing. In addition, findings in recent studies involving human volunteers injected with endotoxin suggest that pretreatment with NSAIDs enhances production of tumor necrosis factor, which leads to higher blood levels of this cytokine, probably by preventing feedback inhibition by prostaglandin E2. Thus, NSAIDs may contribute to the sudden onset of shock, organ failure, and aggressive infection by inhibiting neutrophil function, augmenting cytokine production, and attenuating the cardinal manifestations of inflammation.
ISSN:1058-4838
1537-6591
DOI:10.1093/clinids/21.4.977