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Metabolic Syndrome and Impaired Lung Function: Response
CHEST Metabolic Syndrome and Impaired Lung Function To the Editor: We read with great interest the recent article in CHEST (October 2009)1 by Watz and colleagues showing an independent association between metabolic syndrome and systemic inflammatory markers in chronic bronchitis and patients with COPD. The authors also demonstrate that the prevalence of metabolic syndrome does not increase for increasing COPD severity, as expressed by the Global Initiative for Chronic Obstructive Lung Disease stage. Interestingly, metabolic syndrome is also associated with a restrictive ventilatory pattern at spirometry, especially in patients with the highest waist circumference.2 In this population, visceral fat is known to produce prothrombotic and inflammatory mediators, including C-reactive protein, fibrinogen, interleukin-6, and tumor necrosis factor-a. Since lung restriction is frequently associated with systemic inflammation independent of obesity, the inflammatory burden due to restriction may add to that related to visceral obesity in patients having both diseases.3 For this reason we believe that the authors should have provided information on the prevalence of a mixed ventilatory pattern in their population instead of classifying patients only on the basis of the FEV1ⲐFVC ratio and FEV1%. This would have required the measurement of total lung capacity. Nonetheless, based on the available data, it would be of interest at least to know how prevalent was a spirometric pattern suggesting a restrictive component, which is known to be associated with systemic inflammation.4 Indeed, recent evidence is consistent with an FVC based on presumptive diagnosis of lung restriction being comparably accurate in people with and without obstruction.5 Finally, the authors provide the Charlson index of comorbidity, but they do not list individual comorbidities and their prevalences; selected conditions, such as renal failure, could per se promote systemic inflammation. Providing such information would allow the authors and the readers to verify whether the inflammatory pattern changes for different combinations of COPD, a restrictive component and visceral obesity. Otherwise, the authors might ascribe to COPD an inflammatory status, which in a relevant proportion of patients likely is multifactorial in origin. Simone Scarlata, MD Filippo Luca Fimognari, MD Leo Moro, MD Ruggiero Pastorelli, MD Rome, Italy Raffaele Antonelli-Incalzi, MD Taranto, Italy Affiliations: From the Health Center for Elderly (Centro per la Salute dell’Anziano) (Drs Scarlata, Moro, and Fimognari), Unit of Respiratory Pathophysiology, Università Campus Biomedico; the “Alberto Sordi” Foundation – Onlus (Drs Scarlata and Moro);
Correspondence
the Unit of Respiratory Diseases (Drs Fimognari and Pastorelli), Division of Internal Medicine, ASL Roma G Leopoldo ParodiDelfi no Hospital, Colleferro; and the S. Raffaele – Cittadella della Carità Foundation (Dr Antonelli-Incalzi). FinancialⲐnonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Simone Scarlata, MD, cⲐo Centro per la Salute dell’Anziano, Via Alvaro del Portillo, 21, 00128 Rome, Italy; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-1539
References 1. Watz H, Waschki B, Kirsten A, et al. The metabolic syndrome in patients with chronic bronchitis and COPD: frequency and associated consequences for systemic inflammation and physical inactivity. Chest. 2009;136(4):1039-1046. 2. Fimognari FL, Pasqualetti P, Moro L, et al. The association between metabolic syndrome and restrictive ventilatory dysfunction in older persons. J Gerontol A Biol Sci Med Sci. 2007;62(7):760-765. 3. Lin WY, Yao CA, Wang HC, Huang KC. Impaired lung function is associated with obesity and metabolic syndrome in adults. Obesity (Silver Spring). 2006;14(9):1654-1661. 4. Mannino DM, Ford ES, Redd SC. Obstructive and restrictive lung disease and markers of inflammation: data from the Third National Health and Nutrition Examination. Am J Med. 2003;114(9):758-762. 5. Vandevoorde J, Verbanck S, Schuermans D, et al. Forced vital capacity and forced expiratory volume in six seconds as predictors of reduced total lung capacity. Eur Respir J. 2008;31(2):391-395.
Response To the Editor: We thank Dr Scarlata and colleagues for their interest in our study results1 and the comments about possible mechanisms related to systemic inflammation. Dr Scarlata and colleagues argue that a restrictive component of lung function might contribute to the presence of systemic inflammation in our patients with a coexisting metabolic syndrome. We can exclude that such a restrictive component had that effect in our study population because no patient had a total lung capacity , 80%. We did not give the results of body plethysmography previously because they neither contribute to the severity of COPD according to the Global Initiative for Chronic Obstructive Pulmonary Disease nor are they part of the metabolic syndrome. We appreciate the comment regarding the Charlson index. The Charlson index can indeed only give the information that comorbidities exist at all and it does not discriminate between different entities. However, to date there are 45 studies available that applied the Charlson index in patients with COPD. Therefore, it allows some level of comparison among different study populations.
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Correspondence
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on February 9, 2010 © 2010 American College of Chest Physicians
We also appreciate the comment that the inflammatory status in COPD might be of multifactorial origin. It is our study that demonstrates the independent association of the metabolic syndrome, physical inactivity, and COPD with systemic inflammation.1 Therefore, we identified at least three conditions that might contribute to systemic inflammation in a population that was primarily classified according to severity of COPD. Henrik Watz, MD Benjamin Waschki, MD Anne Kirsten, MD Kai-Christian Müller, PhD Gunther Kretschmar, MD Grosshansdorf, Germany Thorsten Meyer, PhD Lübeck, Germany Olaf Holz, PhD Helgo Magnussen, MD Grosshansdorf, Germany Affiliations: From the Pulmonary Research Institute (Drs Watz, Waschki, Kirsten, Kretschmar, and Magnussen); Hospital Grosshansdorf (Drs Müller, Holz, and Magnussen); and University Lübeck (Dr Meyer). FinancialⲐnonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Henrik Watz, MD, Pulmonary Research Institute, Center for Pneumology and Thoracic Surgery, Hospital Grosshansdorf, Woehrendamm 80, D-22927 Grosshansdorf, Germany; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-2684
References 1. Watz H, Waschki B, Kirsten A, et al. The metabolic syndrome in patients with chronic bronchitis and COPD: frequency and associated consequences for systemic inflammation and physical inactivity. Chest. 2009;136(4):1039-1046.
Postobstructive Pulmonary Edema After Chronic Airway Obstruction Relief
to a T-piece as a weaning protocol. On the T-piece, he developed respiratory distress and went into pulmonary edema, requiring furosemide, nitroglycerin drip, and positive pressure ventilation with a positive end-expiratory pressure (PEEP) of 10. He was symptomatically relieved within a few hours. Repeat echocardiogram did not reveal any cardiac dysfunction, and ECG was also normal. He was gradually tapered off PEEP for the next 24 to 48 h; his intake and output were balanced to the negative side and weaned off by the end of 48 h. If we consider the hydrostatic mechanism described by Fremont et al1 as the only cause, then the edema should occur when there was an obstruction, but here edema occurred after the relief of obstruction. We hypothesize the following mechanism, in addition to the hydrostatic mechanism. In chronic obstruction of the upper airway, expiration occurs against a resistance, causing a PEEP effect in the bronchial tree. This PEEP is transmitted to alveoli, opposing the perialveolar hydrostatic pressure of heart physiology.1 While the obstruction is there, there is no influx of fluid into the alveoli and fluid remains in the interstitium and drains into the peribronchial lymphatics.2 Surgical relief of this obstruction causes a sudden release of the PEEP effect and as the hydrostatic forces do not come back to normal immediately,2 it causes alveolar flooding and pulmonary edema. The usual measures of decreasing preload and using positive pressure ventilation help in rapid recovery. This hypothesis may help the anesthetist to enable a slow and gradual weaning of patients with chronic upper airway obstruction postoperatively, with a gradual decreasing of the PEEP in the recovery room. Anand Joshi, Diplomate in NB Mahim, Mumbai, India Affiliations: From the Department of Critical Care Medicine, PD Hinduja National Hospital and Medical Research Center. FinancialⲐnonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Anand Joshi, Department of Critical Care Medicine (ICU), PD Hinduja National Hospital and MRC, Veer Savarkar Marg, Mahim, Mumbai 400016 India; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-1596
References
A Positive End-Expiratory Pressure Effect To the Editor: I refer to the article published in CHEST (June 2007) by Fremont et al1 describing the hydrostatic mechanism for postobstructive pulmonary edema. This theory only explains the situation in which acute obstruction occurs after extubation (eg, acute laryngospasm), but does not explain conditions with chronic upper airway obstruction. We came across a case of postextubation pulmonary edema that could not be explained solely by hydrostatic mechanism. We report on an elderly man with carcinoma of the larynx, with tumor growth over the vocal cords for 2 years. In preoperative evaluation his cardiovascular system was unremarkable with normal ejection fraction and no diastolic dysfunction. He underwent total laryngectomy with permanent tracheostomy in situ; the surgery was uneventful. Postoperatively he remained hemodynamically stable and was ventilated with positive pressure ventilation in the recovery room. Once he was conscious and obeying instructions, he was shifted www.chestjournal.org
1. Fremont RD, Kallet RH, Matthay MA, Ware LB. Postobstructive pulmonary edema: a case for hydrostatic mechanisms. Chest. 2007;131(6):1742-1746. 2. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005;353(26):2788-2796.
Vitamin D and Mortality From Pulmonary Fibrosis To the Editor: In a recent article in CHEST (July 2009) Olson and colleagues1 found that mortality rates from pulmonary fibrosis exhibited significant seasonal variation with the highest rates occurring in the winter; seasonal variation in pulmonary fibrosis mirrored COPD exacerbation and mortality. We suggest that some of the mechanisms involved in this detrimental association might also be due to seasonal variations in blood vitamin D levels. CHEST / 137 / 2 / FEBRUARY, 2010
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on February 9, 2010 © 2010 American College of Chest Physicians
495
Correspondence
the Unit of Respiratory Diseases (Drs Fimognari and Pastorelli), Division of Internal Medicine, ASL Roma G Leopoldo ParodiDelfi no Hospital, Colleferro; and the S. Raffaele – Cittadella della Carità Foundation (Dr Antonelli-Incalzi). FinancialⲐnonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Simone Scarlata, MD, cⲐo Centro per la Salute dell’Anziano, Via Alvaro del Portillo, 21, 00128 Rome, Italy; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-1539
References 1. Watz H, Waschki B, Kirsten A, et al. The metabolic syndrome in patients with chronic bronchitis and COPD: frequency and associated consequences for systemic inflammation and physical inactivity. Chest. 2009;136(4):1039-1046. 2. Fimognari FL, Pasqualetti P, Moro L, et al. The association between metabolic syndrome and restrictive ventilatory dysfunction in older persons. J Gerontol A Biol Sci Med Sci. 2007;62(7):760-765. 3. Lin WY, Yao CA, Wang HC, Huang KC. Impaired lung function is associated with obesity and metabolic syndrome in adults. Obesity (Silver Spring). 2006;14(9):1654-1661. 4. Mannino DM, Ford ES, Redd SC. Obstructive and restrictive lung disease and markers of inflammation: data from the Third National Health and Nutrition Examination. Am J Med. 2003;114(9):758-762. 5. Vandevoorde J, Verbanck S, Schuermans D, et al. Forced vital capacity and forced expiratory volume in six seconds as predictors of reduced total lung capacity. Eur Respir J. 2008;31(2):391-395.
Response To the Editor: We thank Dr Scarlata and colleagues for their interest in our study results1 and the comments about possible mechanisms related to systemic inflammation. Dr Scarlata and colleagues argue that a restrictive component of lung function might contribute to the presence of systemic inflammation in our patients with a coexisting metabolic syndrome. We can exclude that such a restrictive component had that effect in our study population because no patient had a total lung capacity , 80%. We did not give the results of body plethysmography previously because they neither contribute to the severity of COPD according to the Global Initiative for Chronic Obstructive Pulmonary Disease nor are they part of the metabolic syndrome. We appreciate the comment regarding the Charlson index. The Charlson index can indeed only give the information that comorbidities exist at all and it does not discriminate between different entities. However, to date there are 45 studies available that applied the Charlson index in patients with COPD. Therefore, it allows some level of comparison among different study populations.
494
Correspondence
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on February 9, 2010 © 2010 American College of Chest Physicians
We also appreciate the comment that the inflammatory status in COPD might be of multifactorial origin. It is our study that demonstrates the independent association of the metabolic syndrome, physical inactivity, and COPD with systemic inflammation.1 Therefore, we identified at least three conditions that might contribute to systemic inflammation in a population that was primarily classified according to severity of COPD. Henrik Watz, MD Benjamin Waschki, MD Anne Kirsten, MD Kai-Christian Müller, PhD Gunther Kretschmar, MD Grosshansdorf, Germany Thorsten Meyer, PhD Lübeck, Germany Olaf Holz, PhD Helgo Magnussen, MD Grosshansdorf, Germany Affiliations: From the Pulmonary Research Institute (Drs Watz, Waschki, Kirsten, Kretschmar, and Magnussen); Hospital Grosshansdorf (Drs Müller, Holz, and Magnussen); and University Lübeck (Dr Meyer). FinancialⲐnonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Henrik Watz, MD, Pulmonary Research Institute, Center for Pneumology and Thoracic Surgery, Hospital Grosshansdorf, Woehrendamm 80, D-22927 Grosshansdorf, Germany; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-2684
References 1. Watz H, Waschki B, Kirsten A, et al. The metabolic syndrome in patients with chronic bronchitis and COPD: frequency and associated consequences for systemic inflammation and physical inactivity. Chest. 2009;136(4):1039-1046.
Postobstructive Pulmonary Edema After Chronic Airway Obstruction Relief
to a T-piece as a weaning protocol. On the T-piece, he developed respiratory distress and went into pulmonary edema, requiring furosemide, nitroglycerin drip, and positive pressure ventilation with a positive end-expiratory pressure (PEEP) of 10. He was symptomatically relieved within a few hours. Repeat echocardiogram did not reveal any cardiac dysfunction, and ECG was also normal. He was gradually tapered off PEEP for the next 24 to 48 h; his intake and output were balanced to the negative side and weaned off by the end of 48 h. If we consider the hydrostatic mechanism described by Fremont et al1 as the only cause, then the edema should occur when there was an obstruction, but here edema occurred after the relief of obstruction. We hypothesize the following mechanism, in addition to the hydrostatic mechanism. In chronic obstruction of the upper airway, expiration occurs against a resistance, causing a PEEP effect in the bronchial tree. This PEEP is transmitted to alveoli, opposing the perialveolar hydrostatic pressure of heart physiology.1 While the obstruction is there, there is no influx of fluid into the alveoli and fluid remains in the interstitium and drains into the peribronchial lymphatics.2 Surgical relief of this obstruction causes a sudden release of the PEEP effect and as the hydrostatic forces do not come back to normal immediately,2 it causes alveolar flooding and pulmonary edema. The usual measures of decreasing preload and using positive pressure ventilation help in rapid recovery. This hypothesis may help the anesthetist to enable a slow and gradual weaning of patients with chronic upper airway obstruction postoperatively, with a gradual decreasing of the PEEP in the recovery room. Anand Joshi, Diplomate in NB Mahim, Mumbai, India Affiliations: From the Department of Critical Care Medicine, PD Hinduja National Hospital and Medical Research Center. FinancialⲐnonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companiesⲐorganizations whose products or services may be discussed in this article. Correspondence to: Anand Joshi, Department of Critical Care Medicine (ICU), PD Hinduja National Hospital and MRC, Veer Savarkar Marg, Mahim, Mumbai 400016 India; e-mail: [email protected] © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.orgⲐ siteⲐmiscⲐreprints.xhtml). DOI: 10.1378Ⲑchest.09-1596
References
A Positive End-Expiratory Pressure Effect To the Editor: I refer to the article published in CHEST (June 2007) by Fremont et al1 describing the hydrostatic mechanism for postobstructive pulmonary edema. This theory only explains the situation in which acute obstruction occurs after extubation (eg, acute laryngospasm), but does not explain conditions with chronic upper airway obstruction. We came across a case of postextubation pulmonary edema that could not be explained solely by hydrostatic mechanism. We report on an elderly man with carcinoma of the larynx, with tumor growth over the vocal cords for 2 years. In preoperative evaluation his cardiovascular system was unremarkable with normal ejection fraction and no diastolic dysfunction. He underwent total laryngectomy with permanent tracheostomy in situ; the surgery was uneventful. Postoperatively he remained hemodynamically stable and was ventilated with positive pressure ventilation in the recovery room. Once he was conscious and obeying instructions, he was shifted www.chestjournal.org
1. Fremont RD, Kallet RH, Matthay MA, Ware LB. Postobstructive pulmonary edema: a case for hydrostatic mechanisms. Chest. 2007;131(6):1742-1746. 2. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005;353(26):2788-2796.
Vitamin D and Mortality From Pulmonary Fibrosis To the Editor: In a recent article in CHEST (July 2009) Olson and colleagues1 found that mortality rates from pulmonary fibrosis exhibited significant seasonal variation with the highest rates occurring in the winter; seasonal variation in pulmonary fibrosis mirrored COPD exacerbation and mortality. We suggest that some of the mechanisms involved in this detrimental association might also be due to seasonal variations in blood vitamin D levels. CHEST / 137 / 2 / FEBRUARY, 2010
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on February 9, 2010 © 2010 American College of Chest Physicians
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