If we look at studies using other outcomes than long-term change in lung function and exacerbations, a somewhat mixed picture emerges, and it is not obvious whether it helps us to clarify the position of ICS. Several short-term studies have been published looking at the effect of ICS on various surrogate markers, supposedly reflecting ongoing inflammation. Importantly, studies of cell types and mediators from bronchoalveolar lavage fluid have shown clear differences between asthma and COPD [21,22], and the choice of inflammatory markers is therefore crucial. It would be outside the scope of this chapter to summarize findings in this area; some studies have been interpreted as showing an effect of ICS on relevant measures, whereas others have been interpreted as negative.
Perhaps the most interesting findings come from a recent non-controlled study from Canada. Sin and Tu  used a pharmacoepidemiological set-up to study the effects of inhaled corticosteroids in elderly patients discharged from hospital with a diagnosis of COPD. Their register linkage study included more than 22000 patients, and they were able to show a statistically significant 10% reduction in the 1-year risk of readmission or death. After controlling for markers of disease severity, the beneficial effect may be even larger, up to 25%. This study, which will inevitably be criticized for being uncontrolled, may show the true impact of the reduction in exacerbations shown in ISOLDE and LHSII. Its approach of looking at patients immediately after a hospitali-zation for COPD may provide us with an insight into a more optimal time for study inclusion than the one usually chosen .
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.