Inflammation - A new therapeutic target in pneumonia

Inflammation is a hallmark of pneumonia. Therefore, managing inflammation is an attractive adjunct to targeted antibiotic therapy, mainly in severe pneumonia. Recent investigations indicate that glucocorticoids given in physiological doses (from 10-fold to 100-fold less than doses administered in the past) could be of benefit. We could also manage inflammation by administering or influencing cytokines. A major concern is that drugs designed to target a single cytokine or receptor could prove ineffective due to the redundancy of signaling pathways involved. This may require selection of drugs with broad activity or the targeting of molecules common to inflammatory signaling pathways. Drugs affecting multiple molecules or key inflammatory pathway intermediates could be more effective, but their use will need to be weighed against the risk of impairing innate immunity. Indirect approaches to manage inflammation, such as neutralizing cytotoxic substances in the lung (e.g., inhibiting, neutralizing and eliminating endotoxin), could be used in combination with other approaches. Ideally, potential treatment of life-threatening bacterial pneumonia will combine immunoadjuvant and conventional antibiotic therapy, although intense clinical research with immunotherapy has not yet yielded a successful treatment adjunct. We believe that compounds capable of stimulating early host defense and microbial clearance, but not the later phases of inflammatory tissue injury associated with sepsis, may be advantageous. Copyright © 2005 S. Karger AG, Basel

The Time Course of Pulmonary Function Tests in COPD Patients with Different Levels of Blood Eosinophils

Only very few studies have investigated the influence of eosinophils on the functional progression of COPD. We aimed at retrospectively analyzing the trend of pulmonary function tests over time in patients with COPD according to two baseline blood eosinophil cell count strata (<2% [EOS−] and ≥2% [EOS+]). We used the last 9-year data present in the database of our outpatient clinic and selected only those who had two blood counts that would guarantee the stability of the value of eosinophils and serial spirometry for 4 consecutive years. The analysis of the time course of the spirometric variables analysed showed differences in FEV1 and FVC decline between the subjects of the EOS− group and those of the EOS+ group. The integrated evaluation of our results suggests that the different level of blood eosinophils in the two groups may have influenced independently the time course of the pulmonary function tests and identify two subgroups of subjects with specific disease characteristics: the hyperinflator and the rapid decliner, respectively