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Hannover Medical School, Hannover, Germany
Correspondence to: Marius M. Hoeper, MD, Hannover Medical School, Department of Respiratory Medicine, 30623 Hannover, Germany; e-mail: hoeper.marius{at}mh-hannover.de
To the Editor:
We wish to raise two issues regarding the article by Joppa et al1 (August 2006), who reported that elevated serum levels of C-reactive protein and tumor necrosis factor (TNF)-
are associated with the development of pulmonary hypertension (PH) in patients with COPD. First, we doubt that the observed differences in C-reactive protein and TNF- levels observed in COPD patients with and without PH were meaningful, given the small sample sizes, the wide overlaps, and the fact that the diagnosis of PH was based solely on echocardiography, a method that has a poor accuracy in detecting PH in patients with lung disease.2
Second, the role of inflammation in PH remains controversial. The authors refer to a article by Humbert et al,3 who reported elevated serum concentrations of interleukin (IL)-1 and IL-6, but not TNF-, in 29 patients with idiopathic pulmonary arterial hypertension (IPAH). This article3 is often quoted to support the hypothesis that systemic inflammation plays a role in pulmonary arterial hypertension (PAH). However, to the best of our knowledge, these findings have never been confirmed in larger populations of PAH patients. We measured serum concentrations of TNF- , IL-1, and IL-6 in 53 patients with IPAH, 17 patients with PAH associated with connective tissue disease (APAH), and 25 healthy individuals. This study was approved by the local ethics committee, and all patients gave written informed consent. As shown in Figure 1
, none of these cytokines was elevated in patients with IPAH; patients with APAH, however, had significantly elevated serum levels of TNF- but not of IL-1 and IL-6.
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Footnotes
The authors have no conflicts of interest to disclose.
The authors have no conflicts of interest to disclose.
References
L. Pasteur Teaching Hospital, Kosice, Slovakia
Correspondence to: Ruzena Tkacova, MD, PhD, L. Pasteur Teaching Hospital, P. J. Safarik University, Rastislavova 43, Kosice, 041 90, Slovakia; e-mail: rtkacova{at}central.medic.upjs.sk
To the Editor:
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)- levels. We fully agree that there are several limitations to our study that were discussed in depth in the original article.1 Importantly, in view of the cross-sectional character of the data, our results should be considered as hypotheses generating. Indeed, Sin and Man2 underline 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- in patients with idiopathic pulmonary arterial hypertension compared to healthy individuals. However, TNF- 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.
References
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