Chest
Volume 104, Issue 2, August 1993, Pages 389-392
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Clinical Investigation
Hydrocortisone and Tumor Necrosis Factor in Severe Community-Acquired Pneumonia: A Randomized Controlled Study

https://doi.org/10.1378/chest.104.2.389Get rights and content

Background

Community-acquired pneumonia is a major cause of death in third world countries. Antimicrobial therapy may have little impact on the natural history of patients with severe pneumonia. We hypothesized that the intrapulmonary production of tumor necrosis factor-α (TNF-α) may be responsible for the progressive lung injury and shock commonly seen in patients with severe pneumonia after commencing antibiotic therapy.

Aim

To investigate the effects of a single bolus of hydrocortisone on the clinical course and serum TNF-α levels of patients with severe community-acquired pneumonia.

Design

Randomized placebo-controlled study.

Setting

Multidisciplinary ICU of a tertiary care teaching hospital.

Patients and methods

Patients with three or more British Thoracic Society criteria of severe pneumonia were studied. Patients were randomized to receive either a single dose of hydrocortisone (10 mg/kg) or placebo 30 min prior to commencing antibiotic therapy. Patients were treated with cefotaxime and other antibiotics as clinically indicated. Blood for TNF-α was taken at the time of hospital admission and repeated 2, 6, and 12 h after starting antibiotic therapy.

Results

Thirty patients were studied: 16 received placebo and 14 received hydrocortisone. The patients who received placebo tended to be sicker than the patients who received hydrocortisone. The baseline TNF-α value was 989±374 pg/ml in the placebo group and 827± 394 pg/ml in the hydrocortisone group. In both groups of patients, the TNF-α levels did not change significantly with time. There was no correlation between the TNF-α levels and the APACHE II score, lung injury score, or outcome. The only variable that predicted outcome was the APACHE II score.

Conclusion

Bactericidal antibiotics do not increase serum TNF-α levels in patients with severe pneumonia. Hydrocortisone given prior to antibiotic treatment had no effect on the serum TNF-α levels or the clinical course of patients with severe community-acquired pneumonia.

Section snippets

Methods

This study was conducted in the ICU of a tertiary care teaching hospital. The study was approved hv the Institutional Review Board for research involving human subjects. Informed consent was obtained from all patients.

Patients with community-acquired pneumonia admitted to the medical admissions ward with three or more of the following criteria (British Thoracic Society criteria of severe pneumonia) were identified and admitted to the ICU prior to the commencement of antibiotic therapy:4 (1)

Results

Thirty patients were entered into the study: 16 received placebo and 14 received hydrocortisone. The admission characteristics of the two groups are listed in Table 1. The patients who received placebo tended to be sicker than the hydrocortisone group; however, only the WBC count was significantly different between the two groups.

Serum TNF-α levels were elevated in all the patients studied. The serial TNF levels are listed in Table 2. There was no difference in the TNF-α levels between the

Discussion

In this study, we have documented that patients with severe community-acquired pneumonia have high baseline levels of serum TNF-α that are unaffected by bactericidal antibiotics and remain stable when followed for up to 12 h. Furthermore, the serum TNF-α levels were unaffected by treatment with low-dose hydrocortisone. In addition, we were unable to demonstrate a relationship between the serum TNF-α level and illness severity as measured by the APACHE II score, lung injury score, or patient

Conclusion

The use of bactericidal antibiotics in patients with severe pneumonia was not associated with an increase in serum TNF-α levels. Furthermore, hydrocortisone given at the time of commencing antibiotic treatment had no effect on the serum TNF-α levels or the clinical course of patients with severe community-acquired pneumonia.

ACKNOWLEDGMENT

The authors acknowledge the technical assistance of Avril Mer, Dip, Medical Tech.

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    Manuscript received October 20; revision accepted December 14.

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