MD Conference Express ATS 2013 - (Page 31)
Figure 2. Influence of CAD on IPF Mortality
Significant CAD (n=21)
Mild or no CAD (n=52)
100
p=0.003
50
25
0
Figure 3. Pulmonary Fibrois and VTE
0
250
500
750
1000
Days
1250
1500
1750
2000
Reproduced from Nathan SD et al. Prevalence and impact of coronary artery disease in
idiopathic pulmonary fibrosis. Respir Med 2010;104(7):1035-1041.
Mary Elizabeth Kreider, MD, Hospital of the University
of Pennsylvania, Philadelphia, Pennsylvania, USA,
discussed the concomitance of IPF and lung cancer, the
latter, of which appears elevated in IPF patients. The
frequency of lung cancer in patients with IPF and varies
widely by study type and country with prevalence rates
of 3% to 48% being reported compared with a non-IPF
population. Among more recent studies the lung cancer
prevalence rate is in the 5% to 10% range. Risk factors
may include male gender, increasing age, and smoking
history. Cancer cells are more likely to be peripheral
and in lower lobes but not all are near fibrotic areas. Dr.
Kreider suggested three possibilities for the link between
lung cancer and IPF: IPF causes lung cancer, lung cancer
causes IPF, or lung cancer and IPF occur independently
but share a common pathogenic mechanism. The impact
of the presence of cancer in IPF patients on survival is not
clear but survival from time of dual diagnosis is likely poor.
Therapy is complicated by high rates of acute exacerbation
and difficulty in tolerating interventions.
When a clot from a venous thromboembolism (VTE)
comes in contact with IPF, there is an increased risk of
worse outcome compared with either condition alone.
Amy L. Olson, MD, MSPH, University of Colorado, Denver,
Colorado, USA, addressed the question of whether the
coagulation pathway is activated by IPF or VTE triggers IPF.
Although not found in the normal lung, tissue factor
(TF) and fibrin have been found in the pneumocytes of
IPF patients [Imokawa S et al. Am J Respir Crit Care Med
1997]. In addition, TF levels are significantly higher in
advanced versus nonadvanced cases, indicating that
excessive procoagulant activity in the alveolar space
may play a relevant role in the pathogenesis of IPF [Fuji
Mean (SD) time to diagnosis
of PF after diagnosis of
VTE: –0.4 years (6.2 years)
30
20
Diagnosis of PF was
followed by a
diagnosis of CLOT
Percent
Survival (%)
75
M et al. Thromb Res 2000]. If this hypothesis is true, IPF
patients are at increased risk of vascular disease compared
with the general population. This effect is most marked
for acute coronary syndrome and deep-vein thrombosis
(DVT), which is diagnosed at a rate of 5.9/1000 person
years in patients with IPF versus 2.1/1000 person years in
the general population [Hubbard RB et al. Am J Respir Crit
Care Med 2008]. Time from a VTE event to a diagnosis of
IPF is -0.4 years. A diagnosis of IPF is just as likely to follow
a diagnosis of VTE as to precede it (Figure 3) [Sode BF et al.
Am J Respir Crit Care Med 2010].
Diagnosis CLOT was
followed by a
diagnosis of PF
10
0
-20
-10
0
10
20
Time From Diagnosis of Venous Thromboembolism (Years)
Reprinted with permission of the American Thoracic Society. Sode BF et al. Venous
Thromboembolism and Risk of Idiopathic Interstitial Pneumonia: A Nationwide Study. Am J
Respir Crit Care Med. 2010;181:1085-1092. Official journal of the American Thoracic Society.
The presence of VTE can result in a greater risk
of pulmonary fibrosis, COPD, and lung cancer, the
combination of which leads to earlier deaths in both men
(72.0 vs 74.4 years) and women (74.3 vs 77.4 years; p<0.0001
for both) [Sprunger DB et al. Eur Respir J 2012].
Pulmonary hypertension (PH) is hemodynamic
and pathophysiological condition characterized by the
pulmonary arterial pressure ≥25 mm Hg [Galie N et al.
Eur Respir J 2009]. Precapillary PH is common in patients
with severe IPF and is associated with increased mortality
and a worse clinical course. MJC Humbert, MD, PhD,
Hôpital Antoine Béclère, Université Paris-Sud, Clamart,
France, commented that PH usually is of mild-to-moderate
severity (mPAP 25 to 35 mm Hg), with slow progression
and preserved right ventricular function. Severe PH (mPAP
>35 mm Hg) may be found in a minority of patients, with
some similarities with idiopathic PAH (in this subgroup.
Therapies used in PH are generally discouraged (poor
efficacy, possible worsening of gas exchange); however,
long-term oxygen therapy is the most often therapy of
choice if one is used. More randomized controlled trials are
needed to test newer treatments.
Official Peer-Reviewed Highlights From the American Thoracic Society International Conference 2013
31
Table of Contents for the Digital Edition of MD Conference Express ATS 2013
MD Conference Express ATS 2013
Contents
Prevention and Early Treatment of Acute Lung Injury
Nocturnal Noninvasive Ventilation Improves Outcomes in Multiple Disorders
Hospital Readmissions: Challenges and Opportunities
EBUS-TBNA: Accurate and Safe for Detecting Sarcoidosis
Data Link Obstructive Sleep Apnea and Type 2 Diabetes
Statin Use Improves Respiratory-Related Mortality in Patients With COPD
Addition of Spironolactone to Ambrisentan May Be a Novel Treatment Strategy to Improve Outcome in Patients With PAH
Haloperidol Does Not Prevent Delirium in Ventilated ICU Patients
Beraprost Plus Sildenafil Effective in Pulmonary Arterial Hypertension
Dupilumab Is Safe and Effective for Controlling Asthma Attacks
Once-Daily QVA149 Improves Breathlessness in COPD Patients
CPAP in CVD and OSA Does Not Significantly Improve Cardiovascular Biomarkers
CPAP Reduces BP in Patients With Resistant Hypertension and Obstructive Sleep Apnea
Effects of Obesity on COPD
Pulmonary Embolism
Ventilator-Associated Pneumonia
Lung Cancer Screening
Idiopathic Pulmonary Fibrosis
Non-Small-Cell Lung Cancer
MD Conference Express ATS 2013
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