Why polycythemia in copd

Secondary polycythemia in chronic obstructive pulmonary disease: prevalence and risk factors. BMC Pulm Med. Show More. Login Register. Enjoying our content? Thanks for visiting Pulmonology Advisor. If you wish to read unlimited content, please log in or register below. A history of annual COPD-related hospitalizations was more frequent 2. However, COPD patients with polycythemia were more likely to report dyspnea compared to those without polycythemia. A lower FEV 1 level 0.

Our results indicated a higher proportion of COPD patients with polycythemia led high-altitude living than those without polycythemia However, COPD patients with polycythemia were more likely to report dyspnea compared with those without polycythemia. There was no difference in the initiation of anticoagulant therapy in both groups 1. Anticoagulant therapy was initiated when their situation permitted. The laboratory results demonstrated a higher proportion of arrhythmia on ECG ECG data showed that atrial arrhythmia was significantly more frequent in polycythemia group.

Significantly lower levels of PaO 2 9. Central PE i. In addition, higher velocity of TR 3. There were 16 Correspondingly, there were 56 There was no significant difference in initiation of anticoagulant therapy after admission between groups 1. COPD patients with polycythemia had a longer hospital stay The sensitivity, specificity, positive predictive value PPV , and negative predictive value NPV for mortality were Polycythemia was associated with mortality as determined on bivariate analysis OR 1.

However, some of those patients with COPD may still have an elevated risk of clinical deterioration and in-hospital death. Thus, a careful stratification of patients with acute PE seems to be particularly important for clinicians to guide the initial management and to protect patients against the hazard to be treated with an unacceptable level of risk, or to undergo unnecessary and potentially dangerous treatment.

Although data to support a key role for secondary polycythemia with increased the risk of PE is scant, we observed that PE with polycythemia was associated with increased all-cause in-hospital mortality rate in this multicenter, retrospective cohort study.

Our results are similar with Weber et al. It was remarkable to observe that no-specific symptoms of PE were described in most of the cases, thus supporting the concept that clinical suspicion of PE in acute exacerbation of COPD is particularly difficult, for clinical symptoms of COPD may mimic PE symptoms. In this study, we also observed that polycythemia in COPD patients was associated with more frequent re-hospitalization per year, more frequent rate of arrhythmia, a longer hospital stay and increased rate of mechanical ventilation including noninvasive , compared with COPD patients without polycythemia.

Overall, polycythemia could be an indicator of worse outcome in COPD patients with PE which warrants lower threshold for the clinical suspicion of PE in this group. Lippmann and Fein 28 suggested that the diagnosis of PE in patients with COPD should be suspected in patients with precipitous worsening of their dyspnea that is unresponsive to bronchodilator therapy.

The diagnosis is supported by a reduction in the PaCO 2 in a previously hypercapnic patient In our retrospective study, it was uncertain that patients were previously hyoxemia and hypercapnic or not.

There is good evidence to suggest that hypoxemia has a strong association with advanced COPD. Furthermore, it now seems clear that tissue hypoxia is a key player in many of the maladaptive processes and extra-pulmonary co-morbidities that characterize COPD 29 , On the other hand, COPD has long been recognized as an important cause of secondary polycythemia due to hypoxemia.

Several studies postulate hypercapnia as an independent predictor for survival and in-hospital deaths in the COPD patients 31 - It may reflect an inability to further increase minute ventilation in the face of a sudden increase in dead space ventilation imposed by the embolus Haemoglobin level and its clinical impact in a cohort of patients with COPD.

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Leuk Lymphoma. Download references. Investigator information and full acknowledgements for the COPDGene study are provided in supplemental material Additional file 2. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. The content of the manuscript is the sole responsibility of the authors and the above-mentioned funding bodies had no role in the design of the study; the collection, analysis, and interpretation of data; and in writing the manuscript.

Jingzhou Zhang, Dawn L. DeMeo, Edwin K. Silverman, Michael H. Dawn L. You can also search for this author in PubMed Google Scholar. All authors read and approved the final manuscript. Correspondence to Brian D. Institutional review board IRB approval was obtained at each of the participating study centers Additional file 2 prior to study initiation.

All participants provided written informed consent. JZ reports no conflict of interest. DLD reports grant support from Bayer and honoraria from Novartis. RCW reports no conflict of interest. BDH reports no conflict of interest.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Table S1. Multivariable logistic regression for polycythemia in COPD with further adjustment for education and income. Table S2.