Pulmonary infiltrates in patients receiving long-term glucocorticoid treatment: etiology, prognostic factors, and associated inflammatory response.
BACKGROUND
Glucocorticoid treatment alters immunoregulatory defense mechanisms and may therefore favor the development of different pulmonary infections.


METHODS
The etiology, prognostic factors, and associated inflammatory response of pulmonary infiltrates in 33 patients receiving long-term glucocorticoid treatment (LTGCT) were prospectively evaluated.


RESULTS
Aspergillus spp (n = 9, 31%) and Staphylococcus spp (n = 6, 21%) were the most common causative agents. Using different diagnostic techniques, we obtained a specific diagnosis in 28 of 33 episodes (85%) of pulmonary infiltrates. Bronchoscopic techniques provided the diagnosis in 64% of the cases. Crude mortality was 45%. Variables associated with mortality were as follows: age > 64 years, bilateral radiographic involvement, delay in diagnosis, inappropriate empirical treatment, Simplified Acute Physiology Score (SAPS) II > or = 25, and requirement for mechanical ventilation (MV). SAPS II > or = 25 (odds ratio [OR], 16; 95% confidence interval, 1 to 260) and MV requirement (OR, 50; 95% confidence interval, 2 to 360) were also significant on multivariate analysis. Pulmonary infections were associated with an increase in the concentration of relevant inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 both in serum and BAL. This local and systemic inflammatory response was attenuated when compared with the response observed in patients with pulmonary infections but without glucocorticoid treatment or receiving glucocorticoids for a short period of time (< 9 days).


CONCLUSIONS
Pulmonary infiltrates in patients receiving LTGCT are often caused by fungi and Gram-positive cocci, and are associated with attenuated local and systemic inflammatory response. Although in most cases, sputum cultures and bronchoscopic techniques are diagnostic, the associated mortality is high, particularly in those requiring MV.
Agustí
Carlos
C
Servei de Pneumologia, Institut Clínic de Pneumologia i Cirurgía Toràcica, Barcelona, Spain.
Rañó
Ana
A
Filella
Xavier
X
González
Juliá
J
Moreno
Asunción
A
Xaubet
Antoni
A
Torres
Antoni
A
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001228:Aspergillosis / Q000139:chemically induced* / Q000276:immunology / Q000401:mortality; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002177:Candidiasis / Q000139:chemically induced* / Q000276:immunology / Q000401:mortality; D003240:Connective Tissue Diseases / Q000188:drug therapy / Q000276:immunology; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects*; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008134:Long-Term Care; D008171:Lung Diseases / Q000139:chemically induced* / Q000276:immunology / Q000401:mortality; D008297:Male; D008875:Middle Aged; D018410:Pneumonia, Bacterial / Q000139:chemically induced* / Q000276:immunology / Q000401:mortality; D011023:Pneumonia, Staphylococcal / Q000139:chemically induced* / Q000276:immunology / Q000401:mortality; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000276:immunology; D012307:Risk Factors; D015996:Survival Rate; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D005938:Glucocorticoids; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha