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Ann Thorac Surg 2009;88:930-936. doi:10.1016/j.athoracsur.2009.06.013
© 2009 The Society of Thoracic Surgeons
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Right arrow Lung - cancer

Original Articles: General Thoracic

Changes in Pulmonary Function Tests After Neoadjuvant Therapy Predict Postoperative Complications

Robert J. Cerfolio, MD, FACS, Amar Talati, BS, Ayesha S. Bryant, MSPH, MD*

Division of Cardiothoracic Surgery, Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama

Accepted for publication June 4, 2009.

* Address correspondence to Dr Bryant, Division of Cardiothoracic Surgery, Department of Surgery, University of Alabama at Birmingham, 703 19th St S, ZRB 739, Birmingham, AL 35294 (Email: abryant{at}uab.edu).

Presented at the Forty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, CA, Jan 26–28, 2009.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
Background: Neoadjuvant chemotherapy or chemoradiotherapy increases the risk of pulmonary resection. Changes in specific pulmonary function tests may be predictive.

Methods: A retrospective review of a prospective database of patients with non–small cell lung cancer who underwent neoadjuvant therapy, had pulmonary function tests performed both before and after therapy, and then underwent elective pulmonary resection was performed. Final values and change in the pulmonary function tests before and after treatment were entered as independent variables into a multivariate model in which the dependent variable was major or respiratory morbidity.

Results: There were 132 patients. The mean duration between pretherapy and posttherapy pulmonary function tests was 4.1 months. The mean change in the percent forced expiratory volume in 1 second, in the percent diffusion capacity of the lung for carbon monoxide, and in the percent diffusion capacity of the lung for carbon monoxide corrected for the alveolar volume was +1.0, –6.4%, and –6.6%, respectively. Fifty-five patients (42%) experienced a postoperative complication, and 39 of those patients experienced a major or respiratory complication. There were 7 (5.3%) operative mortalities (5 were respiratory related). On multivariate analysis the change in the percent diffusion capacity of the lung for carbon monoxide corrected for the alveolar volume was the only factor associated with major or respiratory morbidity (p = 0.028). When the posttherapy percent diffusion capacity of the lung for carbon monoxide corrected for the alveolar volume fell by 8% or more, there was an increased likelihood of major morbidity (p = 0.01).

Conclusions: A decrease in the percent diffusion capacity of the lung for carbon monoxide corrected for the alveolar volume after neoadjuvant chemotherapy or chemoradiotherapy may predict increased risk for pulmonary resection, especially if the decrease is 8% or greater. These results should be considered in the preoperative risk assessment of patients who are to undergo pulmonary resection after induction therapy.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Discussion
 References
 
The most common use of neoadjuvant therapy is for patients with stage IIIA non–small cell lung cancer from N2 disease. The optimal care of these patients is controversial. A select group of patients, such as those with single-station N2 disease, those with micrometastatic disease, or those with nonfixed or mobile N2 disease, may benefit from resection if they respond or are downstaged (rendered N2 negative) after neoadjuvant chemoradiotherapy [1]. Because the oncologic benefit is controversial, the risks of surgery in these patients need to be minimized. It is well known that the preoperative performance status of patients, their pulmonary function tests (PFTs), and their cardiac function are all important predictors of the risk for surgery [2–5]. It has also been shown that those who undergo chemotherapy or chemoradiotherapy have increased risk as well [6]. There are even data that show that the use of paclitaxel and carboplatin only, without concurrent radiotherapy, reduces pulmonary function [7]. In addition, Rivera and associates in 2009 [8], Leo and colleagues in 2004 [9], and others [10, 11] have shown that reduced PFTs after induction therapy are associated with postoperative morbidity. The objective of this study was to examine the changes in the PFTs in patients who have undergone neoadjuvant therapy and to assess which test(s) may serve as a predictor of increased operative risk to help guide the preoperative decision as to who is at increased risk of surgery.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Discussion
 References
 
Patients
This is a retrospective review of a prospective database of a single university-based general thoracic surgeon. Patients who were 19 years of age or older, had PFTs performed within 8 weeks of the start of neoadjuvant chemotherapy or chemoradiotherapy, had repeat PFTs after the completion of their medical therapy, and then underwent elective pulmonary resection were included in this study. The University of Alabama at Birmingham's institutional review board approved this study as well as the electronic prospective database used. Individual patient consent was obtained for use in the prospective database but was waived for inclusion in this particular study.

Pulmonary Function Testing
Pulmonary function testing was performed predominantly at our institution (University of Alabama at Birmingham). These measurements were obtained using the Viasys VMAX system (Cardinal Health, CA). Each patient had multiple PFT values reported, as we have previously described [12]. These include a reference value, a pretherapy (before albuterol is administered) value, and a percent reference reported. In this study the percent reference value was used consistently for all statistical analyses and calculations. The different types of PFT values recorded in our prospective database included the forced expiratory volume in 1 second (FEV1), the minute ventilation volume (MVV), the diffusion capacity of the lung for carbon monoxide (DLCO), the diffusion capacity of the lung adjusted (DL adjusted, which is the DLCO as described above but it is corrected for the patient's hemoglobin), and the DLCO divided by the mean alveolar volume (DLCO/VA) [13]. The DLCO was evaluated with the patient seated upright in a chair, with the nose pinched closed with a clip. The patient was asked to breathe normally and then exhale to residual volume. At residual volume, a gas mixture (a combination of carbon monoxide and helium) was forcefully inhaled to total lung capacity, held for 10 seconds, and then exhaled. The average value of two attempts within 10% of each other was recorded.

The DL adjusted is corrected for the patients' hemoglobin level [13]. The DLCO/VA adjusted is based on the alveolar volume, which is computed using the patient's spirometric values obtained during the PFT measurement. The calculations used to compute the PFTs have been previously reported [12], and some are shown below:



Formula 1

(1)
where VA is mean alveolar volume, t2 – t1 is the time interval during which carbon monoxide (CO) uptake occurred, ln (FACO(t1)/FACO(t2) is the exponential change in alveolar carbon monoxide concentration during the small time interval (t1 – t2), and k is the constant 1,000 x 60/(barometric pressure – 47).

The DLCO/VA adjusted is simply the DLCO (equation above) divided by the mean alveolar volume. Alveolar volume (VA) = TLC – VD [14], where TLC is the total lung capacity and the VD is the physiologic dead space and is computed by the following equation:



Formula 2

(2)
where VT is the tidal volume, PaCO 2 is the partial pressure of carbon dioxide in the arteries, PECO 2 is the partial pressure of carbon dioxide in exhaled air.

Definitions
Postoperative complications were defined as per The Society of Thoracic Surgeons' database. Complications were grouped as respiratory or nonrespiratory and major or minor. Table 1 lists the complications. Coronary artery disease was defined as any patient who had a history of myocardial infarction, any interventional procedure related to their coronary arteries, or a previous coronary artery bypass grafting. Major complications were defined as events that required transfer to the intensive care unit or prolonged hospital stay but excluded atrial fibrillation, air leaks, urinary retention, weakness, nausea, ileus, minor pneumothorax, tachycardia, and minor subcutaneous emphysema. Mortality was defined as death before discharge or within 30 days of the operation.


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  		Table 1 Types of Complications Graded as Major or Minor and Respiratory or Nonrespiratory
 
Statistical Analysis
Analysis was conducted using SAS software 9.01 (SAS Corp, Cary, NC). Continuous data are presented as median with one standard deviation (SD), and categorical data are presented as percentages. Fisher's exact test or Pearson's {chi}2 test was used to assess categorical data and the Wilcoxon test to evaluate continuous variables. Variables with a probability value of less than or equal to 0.1 on univariate analysis were entered into the multivariate model (dependent variable was major or respiratory morbidity). Variables were entered into a stepwise regression model to determine associations with morbidity. A two-sided probability value of less than 0.05 was considered statistically significant and unlikely caused by chance. Receiver operator characteristics curve was used to identify the optimal value at which there was an increased likelihood of morbidity.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Discussion
 References
 
There were 404 patients who underwent elective pulmonary resection after induction chemotherapy or chemoradiotherapy by one general thoracic surgeon between January 1999 and June 2008. However, only 132 of these patients met the entry criteria for this study. The most common reason for exclusion was the lack of both pretherapy and posttherapy PFTs. Patient characteristics are shown in Table 2. The most common indication for the use of neoadjuvant chemoradiotherapy was N2 disease; the most common neoadjuvant therapy given was carboplatin with paclitaxel. The most commonly delivered dose of chest irradiation was 6,600 cGy. There was no significant association observed between radiation therapy and PFT changes (recall PFTs were performed in this study within 4 to 8 weeks after the completion of the preoperative therapy). The mean change in the FEV1 was +1.0%, the mean change for the DLCO was –6.4%, and the mean change for the DLCO/VA was –6.6%.


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  		Table 2 Patient Characteristics (n = 132)
 
Table 3 compares variables of the 39 patients who experienced a respiratory or major morbidity with the rest of the patient population. On univariate analysis, age, change in the DLCO%, and change in the DLCO/VA% were significantly different among those who had a major or respiratory morbidity compared with those who did not. The type of pulmonary resection was not statistically significant. On multivariate analysis, only the change in the DLCO/VA% remained significantly associated with the dependent variable (major or respiratory morbidity). Figure 1 depicts the receiver operator characteristics curve for the changes in the DLCO/VA%. It identifies a decrease of 8% in the posttherapy DLCO/VA% as the optimal cutoff value, which suggests an increased likelihood of major morbidity (area under curve, 0.70; positive likelihood ratio, 2.0; p = 0.01; sensitivity, 89%; specificity, 48%).


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  		Table 3 Univariate Analysis of Patients With and Without Respiratory or Major Morbidity Postoperatively a
 

Figure 1
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  		Fig 1. Receiver operator characteristics curve for the change in diffusion capacity of the lung for carbon monoxide corrected for the alveolar volume, which shows a fall of 8% or more predicted postoperative major or respiratory morbidity (area under the curve, 0.70; positive likelihood ratio, 2.0; p = 0.013). Dashed lines indicate 95% confidence interval.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Discussion
 References
 
The decision to operate on a patient after he or she has received neoadjuvant chemotherapy or chemoradiotherapy is based on several factors that assess the risks compared with the benefits of surgery. The benefits of surgery are based on the oncologic advantage of undergoing pulmonary resection and removal of the mediastinal and hilar lymph nodes. The debates hinges on the patient's true pathologic stage before the induction of therapy. However, too often patients are only clinically staged, told "they have N2 disease," and then receive neoadjuvant therapy without ever having mediastinoscopy, esophageal ultrasound with fine-needle aspirate, or endobronchial ultrasound with fine needle aspirate to prove or disprove N2 or N3 disease. We have recently described our experience concerning the oncologic benefit of surgery in more than 402 patients with N2 disease who underwent neoadjuvant chemoradiotherapy. Once the true oncologic benefit of resection is established or estimated, the next factor that requires careful thought is assessment of the operative risk. This is based on the patient's physiologic profile. Preoperative neoadjuvant therapy clearly increases that risk. Chemotherapy alone and especially the combination of carboplatin and paclitaxel, a commonly used doublet by oncologists in North America and the one most commonly used in this series, is known to reduce the DLCO [7]. Rivera and colleagues [8] in 2009 showed gemcitabine-based chemotherapy led to a reduction in PFTs, specifically the DLCO% in about 15% of patients. However, this reduction was not predictive of increased operative risk. Our study's findings were different. We found on univariate analysis that a decrease in the DLCO% and in the DLCO/VA% were both predictive of increased risk. Similarly, Leo and coworkers in 2004 [9] also found that respiratory complications were directly linked to the loss of DLCO% and DLCO/VA%. Although the mechanism of action is unclear, it is believed that pneumonitis leads to a pulmonary infiltrate that is often seen within days after the delivery of chemotherapy [15]. There is a delayed type of hypersensitivity reaction that occurs that is thought to involve T lymphocytes [16, 17]. In addition, when these agents are combined with radiation, there is lymphocytopenia that may also lead to interstitial infiltrates from opportunistic pulmonary infections, and although the FEV1% may increase, the DLCO% is often reduced [7]. Similarly, in our study we found an increase in the FEV1% but a drop in the DLCO% and in the DLCO/VA%.

Another important factor in the risk-benefit assessment is the type of pulmonary resection that is required to remove all disease. Certain types of resections, such as right pneumonectomy, represent increased risk. Surprisingly, the statistically analysis of this study did not show the type of pulmonary resection to be a risk factor. However, Martin and colleagues in 2001 [18] reported an operative mortality of up to 24% for 46 patients who underwent right pneumonectomy after neoadjuvant chemoradiotherapy. In contrast, we and others have shown that selected patients can safely undergo right and left pneumonectomy after high-dose preoperative radiation with concurrent chemotherapy [19]. In this series, there were a large number of patients, 15, who underwent pneumonectomy. Twelve were left and 3 were right pneumonectomies, and 8 patients experienced a morbidity (4 of which were major morbidities). Two of these patients died (1 had a right and 1 had a left pneumonectomy). Thus, if pneumonectomy is known to be required before the induction of neoadjuvant therapy, this factor also has to be carefully weighed.

In this study we have attempted to further elucidate risk stratification of patients who have received neoadjuvant therapy. Some factors that may predict increased risk after neoadjuvant therapy include the patient's performance status, absolute values of their PFTs, age, underlying comorbidities, their desire and determination to have surgery and fight through it, and their cardiac function. However, there are little published data that have examined specific changes to the PFTs that may predict a greater risk of pulmonary resection after neoadjuvant therapy besides the few described above. In this study, we found that the fall in the DLCO% and the DLCO/VA% may be two factors to consider and not just the change in the FEV1%. This finding is explainable. It is known that radiation and chemotherapy worsen gas exchange, but the volume of the lung may be unchanged acutely. One important clinical strategy to be gleaned from this study is that if the repeat DLCO% or DLCO/VA% has significantly fallen, perhaps surgery should be postponed for a few weeks to allow the lung to recover. Repeat PFTs can be performed, and if improved perhaps surgery can then be performed at a reduced risk.

Importantly, in this study the change in PFTs was only measured 4 to 8 weeks after the completion of the neoadjuvant therapy. This is the most likely reason why radiation was not significantly associated with changes in the PFTs. This time frame may be too short to identify the well-described effects of radiation-induced pulmonary fibrosis. Most series report an onset of pulmonary symptoms and the effects of radiation therapy approximately 3 to 5 months after treatment [20, 21]. Some series have even reported an increase in FEV1% related to tumor regression after high-dose radiation therapy [20]. Thus, it makes sense that the DLCO% and other measurements of DLCO such as DL adjusted and the DLCO/VA% may be more important clinical variables that assess the risk of pulmonary resection after neoadjuvant therapy.

The limitations of this study include that fact that it was retrospective and performed in a single institution, and the DLCO/VA% was not obtained on all patients. Additionally, not all of the PFTs were obtained at the same facility. However, previous studies have shown that DLCO% measurements between laboratories are relatively (95%) accurate and reproducible providing that standard techniques are followed [22]. The strengths of this study include the tight inclusion criteria, the homogeneous patient population (all had non–small cell lung cancer), and the fact that 1 surgeon performed all the operations, thus eliminating other confounding variables.

In conclusion, the decrease in the DLCO/VA% is a predictor of increased operative risk after the delivery of neoadjuvant therapy, especially when it decreases by 8% or more. If this reduction is noted, a delay of surgery of 3 to 4 weeks may allow the pneumonitis to recover, at which time the DLCO/VA% and the DLCO% should improve. These results should be considered in the preoperative risk assessment of patients who are to undergo pulmonary resection after neoadjuvant chemoradiotherapy, as the benefit of surgery in these patients remains controversial.


   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
References
 
DR THOMAS J. WATSON (Rochester, NY): First of all, great job on a very nice, clear presentation. Thank you.

Cerf, I'm a little bit confused about the data. These patients represented a mixture of those receiving just chemotherapy and those receiving chemoradiation?

DR CERFOLIO: No. That entry slide was talking about the philosophy. These people had chemotherapy and radiation; some had just chemo.

DR WATSON: All of them did?

DR CERFOLIO: No but most, 39 did not have radiation.

DR WATSON: Did you look at radiation dose?

DR CERFOLIO: Yes, we did and the result is not what we expected. We didn't show a slide on that. I was surprised, but the data is the data. We looked at the effect of amount of radiation and really could not find a dose-dependent response. We added that bullet on the second to the last slide. That's probably because we're doing PFTs 4, 5, and 6 weeks after radiation and chemo is finished and perhaps that is not long enough to see the dose-related radiation fibrosis response. I think if we would have done the PFTs 3 months afterwards, we probably would have seen it. But our data didn't show it. I'm trying to come up with a reason as to why to explain that surprising finding.

DR MARK KRASNA (Towson, MD): First of all, again, congratulations to Dr Talati and congratulations, Cerf, for bringing another premed/med student to the STS here, getting all of our thoracic surgeons ready from your institution.

To follow up on Tom's comment, there were two recent studies from our group at Maryland, one that was using Velcade as one of the neoadjuvant chemotherapy regimens in conjunction with other chemotherapy and high-dose radiation. That was actually our first-ever negative study, which is, of course, why it's not yet published, but the results were presented at ASCO [American Society of Clinical Oncology]. It turned out that Velcade as a chemotherapy in addition to other chemoradiation had very significant negative pulmonary complications, and we shut that study down earlier. The second study that we did was a multiinstitutional study looking at a combination of drugs in the neoadjuvant setting for early stage lung cancers. I believe the paper was already published, with Frank Detterbeck as the lead surgical author. That paper, too, which had only chemotherapy and no radiation, also had some significant pulmonary toxicity. So to follow up with what you found, what would you postulate, then, are the mechanisms for pulmonary toxicity? I assume during such a wide range in time, you had different chemo regimens. Were there one or two drugs in particular that were perhaps associated with the pulmonary toxicity?

Again, excellent job, Dr Talati.

DR CERFOLIO: Mark, thank you for your comments.

I also want to thank Amar. I was remiss in not thanking him earlier. He actually started this as a college student and did it during his first year of medical school. He is now a second-year medical student. He's involved in three or four other projects as well. We look forward to seeing more presentations from Amar on a national level. I congratulate you, Amar.

Your questions are great questions. The truth is, I don't know why chemo alone reduces our patients' PFTs, but I can give you a few the theories. There are studies out there that show just carboplatin and Taxol by itself reduces the DLCO. The theories postulated are that patients get cytopenic from the chemo, they get leukopenia, and hence they develop pulmonary infiltrates and that is the cause for this. It is often self-limiting or improves with antibiotics. We have several references in our paper on these reports. But the truth is I do not know. But it's interesting to see that just chemotherapy alone significantly depresses the DLCO% and the DLCO/VA% but not your volumes, not your MVV% or FEV1%, and we are aware of your work in that area as well with other chemotherapeutic regimens. You know, we had 404 people in this study but only had 132 who had PFTs before and after at the same center that met the entry criteria, so not enough statistics to tell you that one regimen was really different than another. The majority got carboplatin/Taxol, first with 45 Gy, then, as you know, we go to 60, 66, and now we're using 72 Gy with carboplatin and Taxol routinely, and I was shocked that there wasn't a radiation effect, but there wasn't. So we didn't see a chemotherapeutic regimen effect nor did we see a radiation effect, and I think the reason why is that the numbers were too small for the chemo group and the PFT too soon for the radiation dose analysis.

DR PAUL SCHIPPER (Portland, OR): This might be asking the same question in a different way, but do you think that this is a transient response or permanent lung injury? Is there any benefit to waiting for it to get better or is it just going to get worse?

DR CERFOLIO: Again, thank you for your question.

That's the Holy Grail, isn't it? If you don't give them radiation, you might as well wait and see what happens, because the risk of waiting is low and the lung function may improve. I have seen it get better, but because most of my patients receive both radiation and chemo—because that is my preference, without data, is neoadjuvant chemo plus radiation for those with N2 and not chemo alone—I don't want to wait. I don't want to go in a chest that has gotten 72 cGy at 4 or 6 months. I want to be in there no more than 2 or 3 months because I know I can do the operation relatively safely. The truth is I still seem to have higher morbidity, higher mortality than many report, but it is still relatively safe. I think the risk escalates as you wait longer after radiation.

DR ERIC VALLIERES (Seattle, WA): Thank you. Dr Talati, this was a nice piece of work, and you don't have to listen to everything Dr Cerfolio says.

DR CERFOLIO: Nobody does. Don't worry. (Laughter.)

DR VALLIERES: Cerf, you've talked about the use of steroids during surgery a few years back. Do you have any data on how many of these patients actually got steroids preop and not? And then if you see someone today who has had a drop in their DLCO by 15%, what are you going to do? Are you going to turn them down? Are you going to treat them with steroids? Are you going to wait? What are you doing right now with such patients?

DR CERFOLIO: Great question. We don't have any good statistical analysis on that in the paper because the data just was not accurate enough to include it. About 40 patients had steroids given by the medical oncologist or radiation oncologist, but we do not have how long they were on it, what dose, etc. and so we threw that data out.

What we would do now if we see a patient that has really taken a hit in their PFTs is to no, not turn them down, especially if their repeat PET suggested that they responded or their repeat EBUS [endobronchial ultrasound] and their repeat EUS [esophageal ultrasound] showed they were N2 downstaged. I don't do repeat mediastinoscopies after high-dose radiation, but if they have had a previous mediastinoscopy, we do EBUS and EUS on them. So if they were oncologically favorable and their DLCO came down say over 20%, then we do give them steroids and we do wait, and, anecdotally, we have had several patients whose PFT dramatically improved after 3 to 4 weeks. But I put a time frame on that waiting. I've been in a couple of chests at 6 months, 8 months, and they have been very unfriendly. Maybe it's my technical inability, but those are lungs that I have had to do a pneumonectomy or nothing at all, and I think a pneumonectomy is high risk, especially on the right after radiation and chemo. We can do it, but it's higher risk. So I think you have to put a time limit on how long you wait.

DR PAUL DELEYN (Leuven, Belgium): Thank you very much for the very nice presentation. I do believe this is very important information. Did you look in the patients with reduced diffusion capacity whether there was any correlate on CT [computed tomography] or on PET/CT [positron emission tomography/computed tomography], because sometimes after induction we see lesions on PET/CT. Did you look at that?

DR CERFOLIO: Another terrific question, really very insightful. There is no statistically significant analysis in the paper on this, but we did look at that, and there were more infiltrates more commonly seen in the right lower lobe on the repeat integrated PET/CT with some inflammation more there than anywhere else. I don't know why, but that's where it seemed to be. Were these patients silently aspirating? I don't know. Again, there is not enough data to say, but that was our finding. Great question.

DR WALTER J. SCOTT (Philadelphia, PA): Very nice study.

As you know, hemoglobin affects the DLCO. I presume you looked at that.

DR CERFOLIO: Yes. That's DL adjusted. We presented a paper at the Southern Thoracic about the DLCO, the DL adjusted, which is adjusted for the hemoglobin, and then the DLCO/VA percents. So, yes, the DL adjusted is adjusted for the hemoglobin, and that didn't really pan out to show anything. It is affected for sure but no more so than the DLCO/VA% and the DLCO%.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 

  1. Cerfolio RJ, Maniscalco L, Bryant AS. The treatment of patients with stage IIIA non-small cell lung cancer from N2 disease: who returns to the surgical arena and who survives Ann Thorac Surg 2008;86:912-920.[Abstract/Free Full Text]
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  8. Rivera MP, Detterbeck FC, Socinski MA, et al. Impact of preoperative chemotherapy on pulmonary function tests in resectable early-stage non-small cell lung cancer Chest 2009;135:1588-1595.[Abstract/Free Full Text]
  9. Leo F, Solli P, Spaggiari L, et al. Respiratory function changes after chemotherapy: an additional risk for postoperative respiratory complications? Ann Thorac Surg 2004;77:260-265.[Abstract/Free Full Text]
  10. Takeda S, Funakoshi Y, Kadota Y, et al. Fall in diffusing capacity associated with induction therapy for lung cancer: a predictor of postoperative complication? Ann Thorac Surg 2006;82:232-236.[Abstract/Free Full Text]
  11. Abou-Jawde RM, Mekhail T, Adelstein DJ, et al. Impact of induction concurrent chemoradiotherapy on pulmonary function and postoperative acute respiratory complications in esophageal cancer Chest 2005;128:250-255.[Abstract/Free Full Text]
  12. Cerfolio RJ, Bryant AS. Different diffusing capacity of the lung for carbon monoxide as predictors of respiratory morbidity Ann Thorac Surg 2009;88:405-411.[Abstract/Free Full Text]
  13. Levitzky M. Pulmonary physiology5th ed.. New York: McGraw-Hill; 1999Chapters 1, 3, 6, 7.
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  17. Fujimori K, Yokomama A, Kurita Y, Uno K, Saijo N. Paclitaxel induced cell-mediated hypersensitivity pneumonitis. Diagnosis using leukocyte migration test, bronchoalveolar lavage and transbronchial lung biopsy. Oncology 1998;55:340-344.[Medline]
  18. Martin J, Ginsberg RJ, Abolhoda A, Bains MS, Downey RJ, Korst RJ. Morbidity and mortality after neoadjuvant therapy for lung cancer: the risks of right pneumonectomy Ann Thorac Surg 2001;72:1149-1154.[Abstract/Free Full Text]
  19. Cerfolio RJ, Bryant AS, Spencer SA, Bartolucci AA. Pulmonary resection after high dose and low dose chest irradiation Ann Thorac Surg 2005;80:1224-1230.[Abstract/Free Full Text]
  20. DeJaeger K, Seppenwoolde Y, Boersma LJ, et al. Pulmonary function following high-dose radiotherapy of non-small cell lung cancer Int J Radiat Oncol Biol Phys 2003;55:1331-1340.[Medline]
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Ann. Thorac. Surg., May 1, 2010; 89(5): 1707 - 1707.
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S. i. Takeda
Changes in Pulmonary Function Tests After Neoadjuvant Therapy Predict Postoperative Complications: DLCO/VA% is More Important Than Predicted Postoperative %DLCO?
Ann. Thorac. Surg., May 1, 2010; 89(5): 1706 - 1707.
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