We appreciate the thoughtful comments by Hoeper and Welte on our article in CHEST (August 2006)1 demonstrating that elevated pulmonary artery pressure in COPD is associated with increases in C-reactive protein (CRP) and tumor necrosis factor (TNF)-α levels. We fully agree that there are several limitations to our study that were discussed in depth in the original article.1Importantly, in view of the cross-sectional character of the data, our results should be considered as hypotheses generating. Indeed, Sin and Man2underline that it is a challenge for the COPD research community to determine, through well-designed clinical and animal studies, the validity of the hypothesis that systemic inflammation may be involved in the pathogenesis of pulmonary hypertension. Hoeper and Welte provide us with interesting observations of no increases of interleukin (IL)-1, IL-6, or TNF-α in patients with idiopathic pulmonary arterial hypertension compared to healthy individuals. However, TNF-α but not IL-1 and IL-6 were increased in patients with pulmonary arterial hypertension associated with connective tissue disease. These data do not contradict our results in any way. First, we have studied a different population of patients; second, Hoeper and Welte did not assess serum CRP in their study. Importantly, our main result was that Pao2 and log-CRP levels were the only two significant predictors of systolic pulmonary artery pressure. This finding is meaningful especially in the light of recently published studies indicating that CRP levels correlate with 6-min walk distance3 and, in addition, relate to mortality in COPD patients.4 Nevertheless, valuable data of Hoeper and Welte emphasize the need to publish also negative results in scientific journals. Only by doing so can the scientific community gain a complex picture of the studied medical field.