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Original Research: ANOREXIA NERVOSA |

Respiratory Function in Patients With Stable Anorexia Nervosa FREE TO VIEW

Giovanni Gardini Gardenghi, MD; Enrico Boni, MD; Patrizia Todisco, MD; Fausto Manara, MD; Andrea Borghesi, MD; Claudio Tantucci, MD
Author and Funding Information

Affiliations: From the Department of Medical and Surgical Sciences (Drs. Gardini Gardenghi, and Tantucci), and the Eating Disorders Center (Dr. Manara), University of Brescia, Brescia, Italy; and First Medicina (Dr. Boni), the Eating Disorders Center (Dr. Todisco), and Second Radiology (Dr. Borghesi), Spedali Civili, Brescia, Italy.

Correspondence to: Claudio Tantucci, MD, University of Brescia, Scienze Mediche e Chirurgiche, 1a Medicina Piazzale, Spedali Civili 1, Brescia 25123, Italy; e-mail: tantucci@med.unibs.it


The work was performed at the First Medicina, Spedali Civili, Brescia, Italy.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(5):1356-1363. doi:10.1378/chest.08-3020
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Background:  The impact of undernutrition on lung physiology and respiratory muscle performance is still incompletely investigated. The purpose of this study was to assess the functional consequences of malnutrition on the respiratory system in stable patients with anorexia nervosa (AN).

Methods:  Pulmonary function tests, maximal inspiratory pressure (Pimax), maximal expiratory pressure (Pemax), and the parameters of control of breathing were obtained in 27 patients with AN (mean [± SD] age, 24 ± 7 years; BMI, 16 ± 1 kg/m2; duration of disease, 6 ± 6 years) and in a group of matched healthy subjects.

Results:  Compared with control subjects, significant reductions in the diffusing capacity of the lung for carbon monoxide (Dlco) and lung diffusion capacity corrected for alveolar ventilation (p < 0.001), which progressively worsened with the duration of disease, were found in the AN group. Only the membrane diffusing capacity was reduced in patients with AN (p < 0.05), while pulmonary capillary blood volume was similar to that of control subjects. Lung density measurements based on CT scan analysis were normal in a subgroup of eight patients with AN with low Dlco. Both Pimax and Pemax were decreased in patients with AN (p < 0.001), but the mild-to-moderate impairment to generate force of the respiratory muscles did not progress with time. In these patients with AN, the parameters of control of breathing were in the normal range and were comparable to those of control subjects.

Conclusions:  The functional alterations found in patients with AN indicate the presence of the progressive enlargement of peripheral lung units without relevant alveolar septa destruction. In the first 3 years of disease, appreciable weakness of respiratory muscles develops in patients with stable AN without further impairment over time.

Figures in this Article

Anorexia nervosa (AN) is an eating disorder that is characterized by malnutrition due to psychological factors, the diagnostic criteria of which are described in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition.1 This disorder affects young people, mainly women, who generally have no other diseases. For this reason, AN is a sort of peculiar natural model in which it is useful to study the effects of malnutrition on the respiratory system, since it excludes the consequences that some chronic diseases can have on the lung and chest wall. A number of experimental studies in animals showed that caloric restriction is associated with alveolar enlargement and loss26 with prompt recovery following refeeding.7,8 If undernourishment provokes an obligatory rearrangement of the lung architecture inducing these “emphysema-like” abnormalities or if these alterations are an evolutionary adaptation to reduced oxygen consumption during food scarcity is a matter of debate.9 Recently, an association has been suggested between AN and emphysema, based on radiographic10 studies, but pulmonary function testing failed to demonstrate unequivocally functional changes compatible with pulmonary emphysema in patients with AN.11 The recruitment of subjects with different severity and/or duration of AN could has been a confounding factor in the interpretation of the previously reported data. The aim of this study was to examine stable patients with moderate-to-severe AN who had different durations of disease, before they were admitted to a recovery treatment plan, in order to better define the short-term and long-term effects of AN on baseline respiratory function.

Subjects

Twenty-seven subjects who had the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, criteria for the diagnosis of AN were consecutively evaluated before they were admitted to the Eating Disorders Centre of University Hospital of Brescia (Italy). Anthropometric data, including sex, age, BMI, length of disease, and smoking history, were collected. Eighteen healthy volunteers, age and sex matched, were assessed as control subjects. Patients with AN were also divided into the following two subgroups according to the duration of the disease: 16 patients with a ≤ 3-year history of disease; and 11 patients with a > 3-year history of disease.

Measurements

Arterial blood was collected at rest when subjects were breathing room air in a seated position by puncture of the radial artery, and immediately analyzed. Spirometry was performed through a flanged mouthpiece when subjects were in a sitting position wearing a nose clip for measuring slow vital capacity (VC), inspiratory capacity, and maximal flow-volume curves, using a bell spirometer (Biomedin; Padova, Italy). Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV) were obtained by using the multibreath helium dilution technique in a closed circuit (DIMO module; Biomedin). The diffusing capacity of the lung for carbon monoxide (Dlco) was measured twice by the single-breath method (DIMO module; Biomedin) breathing a gas mixture either with 18% or 68% of oxygen to compute the membrane diffusing capacity (DM) and pulmonary capillary blood volume (PCBV), according to the method of Roughton and Foster.12 The predicted values of the lung function parameters were those obtained from European Community for Coal and Steel (or ECCS) equations.13

Maximum voluntary maximal inspiratory pressure (Pimax) and maximal expiratory pressure (Pemax) were measured (CadNet System 2001; Medical Graphics; St. Paul, MN). Pimax was measured at FRC and RV, and Pemax was measured at FRC and TLC. The best value of three acceptable measurements in each maneuver was used for analysis. The predicted values were those obtained from Cook et al.14

Mouth occlusion pressure at 0.1 second after the onset of inspiratory effort (P0.1), minute ventilation (V̇e), and the ventilatory pattern were determined in the baseline condition and during progressive hyperoxic, hypercapnic rebreathing into a closed circuit through a 7-L Douglas bag filled with an initial mixture of 7% CO2 and the rest O2, according to the method of Read.15 The baseline P0.1 value was obtained as a mean of at least three measurements after excluding the lowest and the highest values.16 The P0.1/end-expiratory CO2 pressure (PETCO2) ratio and the V̇e/PETCO2 slopes were then obtained by fitting the respective points according to the least squares method.

Each patient with AN who had a reduced Dlco agreed to undergo a thoracic CT scan was examined with a 16 multidetector-row CT scanner (Somatom Sensation 16; Siemens Medical Solution; Forchheim, Germany). CT scans were systematically obtained at the end of full inspiration from the apex of the lung to the diaphragm. The scanning parameters were as follows: 0.75-mm collimation; 120 kilovolt peak; and 150 mA. Thin sections (with 1-mm slice thickness) were reconstructed with an increment of 0.75 mm by using a high-resolution reconstruction algorithm with standardized window level and width settings for the lung parenchyma (window width, 1,500 Hounsfield units [HU]; window level, −500 HU). In each subject, there were also acquired thin-section images during full expiration; in this case, images (26 contiguous 1-mm transverse CT scans) were obtained at the following three lung levels: aortic arch; tracheal carina; and the posterior aspect of the eighth rib. The inspiratory and expiratory images were also used to create a minimum intensity projection slab (MinIP).17 MinIP consists of projecting the voxel with the lowest attenuation value on every view throughout the volume onto a two-dimensional image. MinIP images have demonstrated better detection of mild forms of emphysema.18 In addition, expiratory MinIP images were superior to thin-section scans for depicting focal airtrapping.18

The images analysis was performed by one thoracic radiologist (A.B.) who used the visual scoring method19 to evaluate the presence and extension of areas of low and patchy attenuation during inspiration and of airtrapping during expiration. The study protocol was approved by the local ethics committee, and informed consent was obtained from each subject.

Statistical Analysis

The data are shown as the mean ± SD. The comparison between patients and control subjects was performed using the Mann-Whitney test for unpaired data. The comparisons among different groups were performed according to the Friedman test, followed by multiple comparisons, when allowed, by the significance of the p value. Linear regressions were performed between different variables, and the result of each correlation was expressed as the Pearson correlation coefficient. A p value < 0.05 was considered as significant. Calculations were made using a data analysis system (Statistica; StatSoft, Inc; Tulsa, OK).

The anthropometric and functional pulmonary parameters are displayed in Table 1 for control subjects, all patients with AN, and for two subgroups of patients with AN divided according to the duration of disease (≤ 3 years or > 3 years). In both subgroups, the mean erythrocyte sedimentation rate was normal and the WBC count was in normal limits, amounting to 5.6 ± 1.6 × 103 cells/μL in patients with AN and 5.9 ± 1.6 × 103 cells/μL, respectively (normal limits of WBC count, 4 to 10.8 × 103 cells/μL), showing the absence of low-grade systemic inflammation, which is typical of more severe starvation. In addition, our subjects with AN had normal values of albuminemia, equal to 4.4 ± 0.6 g/dL and 4.1 ± 0.4 g/dL, respectively, for patients with shorter and longer duration of disease, revealing a stable situation of uncomplicated malnutrition.

Table Graphic Jump Location
Table 1 Anthropometric Data and Respiratory Function Parameters

Data are presented as the mean 3 ± SD. PEF = peak expiratory flow.

*p < 0.05 (vs patients with AN duration ≤ 3 years).

†p < 0.001 (vs control subjects).

‡p < 0.001 (vs patients with AN duration ≤ 3 years).

§p < 0.01 (vs patients with AN duration ≤ 3 years).

‖p < 0.05 (vs control subjects).

The Dlco and lung diffusion capacity corrected for alveolar ventilation (KCO) values were significantly reduced in the AN group compared with the control group, and were markedly lower in patients with AN with longer duration of disease. Dlco and KCO are inversely related to the duration of AN (Fig 1). In the subgroup of patients with a history of AN of ≤ 3 years, the PCBV was similar to that measured in the control group, while DM was significantly decreased (Fig 2).

Figure Jump LinkFigure 1 The relationship between the duration of AN and Dlco (A) and KCO (B) percent predicted values in patients with AN. There is a progressive impairment of Dlco and KCO with duration of the disease.Grahic Jump Location
Figure Jump LinkFigure 2 PCBV and DM in patients with AN of ≤ 3 years duration and control subjects. Only the DM was significantly reduced in patients with AN.Grahic Jump Location

In Table 2 arterial blood gases and the parameters related to the control of breathing at rest and during the rebreathing test are shown together with the indexes of the respiratory muscle strength. Percent predicted values of Pimax and Pemax were moderately reduced in patients with AN and significantly lower than those in control subjects (p < 0.01). On the other hand, the duration of AN did not further impair the early weakness of the respiratory muscles, with Pimax and Pemax being similar in patients with AN with different durations of disease. The parameters of control of breathing and arterial blood gas levels were in the normal range in patients with AN and were similar to those found in control subjects (Table 2). In eight patients with AN with reduced Dlco (68 ± 8% predicted) and KCO (58 ± 9% predicted), a CT scan analysis of the lungs was performed. In all inspiratory and expiratory CT scan images, which were subjectively assessed by a chest radiologist (A.B.), no signs of emphysema or airtrapping were found. No other abnormal findings were recognized. In all cases, the lung density measurements revealed a mean density that was higher than the mean threshold value of −950 HU, amounting, on average, to −863 ± 11 HU for right lungs, −859 ± 14 HU for the left lungs, and −861 ± 12 HU for both lungs (Fig 3, left and right). No significant correlations were found between functional pulmonary parameters as well as indexes of respiratory muscle strength and degree of BMI in our patients with AN.

Table Graphic Jump Location
Table 2 Indices of Ventilatory Pattern, Control of Breathing, Gas Exchange, and Respiratory Muscle Strength

Data presented as mean ± SD. RR = respiratory rate.

*p < 0.001 (vs control subjects).

†p < 0.01 (vs control subjects).

‡p < 0.05 (vs control subjects).

Figure Jump LinkFigure 3 Left: density CT scan analysis performed in the upper, middle, and lower sections of the lung from a representative patient with AN (age, 22 years; BMI, 18 kg/m2) with Dlco (75% predicted) and KCO (65% predicted). The density distribution values, displayed at the bottom of the single CT scan images, show no clue of pulmonary emphysema, suggesting that the low Dlco measured in this patient is not related to alveolar septa destruction. Right: thin-section CT scan and MinIP images of the lower lung section of the same patient. Left: thin section CT images (1-mm collimation) obtained during deep inspiration and expiration, respectively. Right: MinIP images (1-mm collimation) obtained during deep inspiration and expiration, respectively. Neither emphysema nor airtrapping were detected even with the more sensitive MinIP reconstruction technique, corroborating the thin-section CT scan results.Grahic Jump Location

The main results of this study, which was performed in stable patients with AN with moderate-to-severe illness but different durations of disease, are the significant reduction of Dlco and the mild-to-moderate decrease of maximal isometric strength of both inspiratory and expiratory muscles. The Dlco impairment worsens with the duration of the disease, while the degree of respiratory muscle weakness remains unchanged with time.

A series of articles28 using rats, hamsters, and mice has demonstrated that caloric restriction causes gas-exchange unit enlargement and alveolar loss, which is usually defined as nutritional emphysema. In the rats, however, after moderate starvation airspace enlargement with minimal loss of alveolar septa was found to be associated with an increase of mean linear intercept and volume fraction of air spaces and with a decrease in corrected internal surface area and surface fraction of airspace.4 A concomitant decrease in pulmonary static elastic recoil pressure over the entire volume-pressure loop was observed. Refeeding was able to reverse, at least partially, these morphologic and functional alterations. Studies of long-term caloric restriction in animals whose lungs have been appropriately fixed to detect destructive emphysema are not available.

A first description of lung morphology in starving humans was reported by Stein and Fenigstein20 in the Warsaw ghetto during the Second World War. In 370 autopsies, they observed 50 cases (13.5%) of emphysema. They believed that the pathologic features were similar to those seen in senile emphysema as the result of involutional processes.10 Lamy et al21 reported autopsy findings in 13 chronically starved humans, but the detail of the nontuberculous cavitary lesions found in five cases were not available. Therefore, pathologic studies in humans appear inconclusive and cannot give a definite picture of the lung parenchyma in severely undernourished individuals.

Although these findings observed in the setting of severe starvation would not apply to the majority of subjects with AN in which only marked caloric restriction is generally present; recently, Coxon et al10 were able to detect emphysema-like changes in a group of patients with AN based on CT scan measurements of lung density. The authors, however, reported normal values of Dlco in their patients, which were similar to those of matched healthy control subjects.10

In addition, by examining 24 patients with AN (mean age, 21 ± 7 years; mean BMI, 14 ± 1 kg/m2; and median duration of disease, 24.5 months), Pieters et al11 found the Dlco values to be within normal limits. In some contrast with previous lung function studies and radiographic findings, our patients with AN showed abnormal baseline respiratory function indexes, namely, the Dlco and the respiratory muscle strength, in the absence of any significant emphysematous lesions seen in the thin-section CT scan of the lung.

Concerning the alteration in Dlco, since the alveolar volume was always preserved, its diminution must be ascribed to the impairment of KCO that actually was abnormally reduced. Interestingly, the Dlco decrease cannot be attributable to the PCBV reduction, as could be expected from the low stroke volume and bradycardia described in anorexic subjects.2224 In fact, the measured PCBV in our patients with AN with short duration of disease was not different from that found in matched control subjects. Conversely, DM was significantly impaired, likely causing the reduced KCO and Dlco found in this group of patients with AN. It is highly improbable, however, that the DM reduction can be ascribed to the development of pulmonary emphysema, which, by definition, implies the presence of large airspaces due to alveolar septa destruction, at least according to the CT scan score of the lung that showed a normal percentage of pixels with attenuation higher than −950 HU. Moreover, the normal PCBV that we found in these patients with AN argues against the destruction of alveolar septa and does not support pulmonary emphysema as a cause of DM reduction.

Therefore, the most reasonable explanation for the DM impairment is a pulmonary tissue reduction for lung volume unit with mild enlargement of alveolar spaces, as seen, for instance, in the lungs of senile individuals, that cannot be detected by CT scan analysis. This alteration could well induce an abnormal DM because of a decrease of alveolar surface area for lung volume unit and an increase in diffusing distance for alveolar carbon monoxide. The thinning of the blood-gas alveolar barrier following the malnutrition-related lung tissue catabolism could also be possible in patients with AN, with opposite effect on DM. The clear decrease in Dlco and KCO coupled with an abnormal DM component, however, argues against the relevance of this effect.

The patients with AN with longer duration of disease exhibited greater deterioration of Dlco and KCO compared with those patients with a shorter history of AN, suggesting a progressive structural derangement of the pulmonary gas exchange units. In addition, both Dlco and KCO were inversely related with the duration of disease (Fig 1). Unfortunately, we had no opportunity to measure DM and PCBV in this subgroup of patients with chronic AN, and we cannot say whether PCBV is still normal after longer duration of disease.

As previously reported,25,26 our patients also exhibited reduced levels of Pimax and Pemax, which were significantly lower than those of control subjects. It should be stressed that Pimax takes into account the maximal isometric force produced by all inspiratory muscles, including the diaphragm. These data confirm the presence of a mild-to-moderate weakness of the respiratory muscles in patients with AN that develops rather quickly, that is present in patients with a short duration of disease (≤ 3 years). Nevertheless, the reduction of Pimax and Pemax was similar in patients with longer duration of AN, suggesting that the loss of force of the respiratory muscles does not further increase. In this respect, we have to note that patients with AN showed a lower TLC and greater RV, although the decrease was not significant compared with control subjects. This observation has been made previously by other authors12 and was reasonably ascribed to the decrease in Pimax and Pemax.

In the past, a severe impairment of diaphragmatic function was also described25 in malnourished patients with AN who were free from other diseases with a marked reduction of transdiaphragmatic pressure, as assessed by both maximal sniff maneuver and electrical phrenic nerve stimulation. Under nutritional depletion such as that occurring in our patients with AN, the weakness of diaphragm and respiratory muscles is due to a skeletal muscle impairment mainly with atrophy of type-2X, type-2A, and type-1 fibers, which is caused by enhanced protein breakdown and diminished synthesis of muscle proteins, abnormal accumulation of glycogen within muscle fibers, and reduced enzymatic activity, which seems reversible during refeeding.2729

Finally, in our hands the parameters of the control of breathing were normal in patients with AN with both short and long duration of disease, either in the baseline condition or during progressive hypercapnic-hyperoxic stimulation. These findings are in contrast with those reported by Gonzales-Moro et al,26 who found low basal neuromuscular drive and reduced ventilatory and neuromuscular response to CO2 in patients with AN. We have no clear explanation for these controversial results, and further investigation is needed in this field.

No functional data were related to BMI in our series of patients with AN. This was not unexpected because we chose to study patients with similar severity of disease, and, consequently, the range of BMI was too narrow to allow any significant correlation.

In conclusion, stable patients with moderate-to-severe AN have a significant reduction of Dlco and KCO, due to the DM component impairment, that worsens progressively with the duration of disease. These functional alterations indicate the presence of a progressive enlargement of the peripheral lung units without relevant alveolar septa destruction, as observed in the lung of senile individuals and not in patients with classic pulmonary emphysema. Moreover, a few years of disease induce appreciable weakness of respiratory muscles without further impairment of their force with time.

AN

anorexia nervosa

Dlco

diffusing capacity of the lung for carbon monoxide

DM

membrane diffusing capacity

FRC

functional residual capacity

HU

Hounsfield units

KCO

lung diffusion capacity corrected for alveolar ventilation

MinIP

minimum intensity projection slab

P0.1

mouth occlusion pressure at 0.1 second after the onset of inspiratory effort

PCBV

pulmonary capillary blood volume

Pemax

maximal expiratory pressure

PETCO2

end-expiratory CO2 pressure

Pimax

maximal inspiratory pressure

RV

residual volume

TLC

total lung capacity

VC

vital capacity

e

minute ventilation

Author contributions: Drs. Gardenghi and Boni planned the study design and collected functional data. Dr. Todisco collected metabolic data of AN patients and performed statistical analysis. Dr. Manara evaluated and recruited the AN patients. Dr. Borghesi performed CT scans and assessed the CT score of the lung density. Dr. Tantucci coordinated the study and wrote the article.

Financial/nonfinancial disclosures: The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: We acknowledge Mr. Michele Guerini for his invaluable technical assistance.

American Psychiatric Association Diagnostic and statistical manual of mental disorders. 1994;4th ed Washington, DC American Psychiatric Association
 
Harkema JR, Maulderly JL, Gregory RE, et al. A comparison of starvation and elastase models of emphysema in the rat. Am Rev Respir Dis. 1984;129:584-591. [PubMed]
 
Kerr JS, Riley DJ, Lanza-Jacoby S, et al. Nutritional emphysema in the rat: influence of protein depletion and impaired lung growth. Am Rev Respir Dis. 1985;131:644-650. [PubMed]
 
Sahebjami H, Vassallo C. Effects of starvation and refeeding on lung mechanics and morphometry. Am Rev Respir Dis. 1979;119:443-451. [PubMed]
 
Sahebjami H, Wirman JA. Emphysema-like changes in lung of starved rats. Am Rev Respir Dis. 1981;124:619-624. [PubMed]
 
Sahebjami H. Effects of nutritional depletion on lung parenchyma. Eur Respir Mon. 2003;24:113-122
 
Massaro GD, Radaeva S, Clerch LB, et al. Lung alveoli: endogenous programmed destruction and regeneration. Am J Physiol. 2002;283:L305-L309
 
Massaro D, DeCarlo Massaro G, Barras A, et al. Calorie-related rapid onset of alveolar loss, regeneration, and changes in mouse lung gene expression. Am J Physiol Cell Mol Physiol. 2004;286:896-906. [CrossRef]
 
Massaro D, DeCarlo Massaro G. Hunger disease and pulmonary alveoli. Am J Respir Crit Care Med. 2004;170:723-724. [PubMed]
 
Coxon H, Chan IHT, Mayo JR, et al. Early emphysema in patients with anorexia nervosa. Am J Respir Crit Care Med. 2004;170:748-752. [PubMed]
 
Pieters T, Boland B, Beguin C, et al. Lung diffusion study and diffusion capacity in anorexia nervosa. J Intern Med. 2000;248:137-142. [PubMed]
 
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Figures

Figure Jump LinkFigure 1 The relationship between the duration of AN and Dlco (A) and KCO (B) percent predicted values in patients with AN. There is a progressive impairment of Dlco and KCO with duration of the disease.Grahic Jump Location
Figure Jump LinkFigure 2 PCBV and DM in patients with AN of ≤ 3 years duration and control subjects. Only the DM was significantly reduced in patients with AN.Grahic Jump Location
Figure Jump LinkFigure 3 Left: density CT scan analysis performed in the upper, middle, and lower sections of the lung from a representative patient with AN (age, 22 years; BMI, 18 kg/m2) with Dlco (75% predicted) and KCO (65% predicted). The density distribution values, displayed at the bottom of the single CT scan images, show no clue of pulmonary emphysema, suggesting that the low Dlco measured in this patient is not related to alveolar septa destruction. Right: thin-section CT scan and MinIP images of the lower lung section of the same patient. Left: thin section CT images (1-mm collimation) obtained during deep inspiration and expiration, respectively. Right: MinIP images (1-mm collimation) obtained during deep inspiration and expiration, respectively. Neither emphysema nor airtrapping were detected even with the more sensitive MinIP reconstruction technique, corroborating the thin-section CT scan results.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Anthropometric Data and Respiratory Function Parameters

Data are presented as the mean 3 ± SD. PEF = peak expiratory flow.

*p < 0.05 (vs patients with AN duration ≤ 3 years).

†p < 0.001 (vs control subjects).

‡p < 0.001 (vs patients with AN duration ≤ 3 years).

§p < 0.01 (vs patients with AN duration ≤ 3 years).

‖p < 0.05 (vs control subjects).

Table Graphic Jump Location
Table 2 Indices of Ventilatory Pattern, Control of Breathing, Gas Exchange, and Respiratory Muscle Strength

Data presented as mean ± SD. RR = respiratory rate.

*p < 0.001 (vs control subjects).

†p < 0.01 (vs control subjects).

‡p < 0.05 (vs control subjects).

References

American Psychiatric Association Diagnostic and statistical manual of mental disorders. 1994;4th ed Washington, DC American Psychiatric Association
 
Harkema JR, Maulderly JL, Gregory RE, et al. A comparison of starvation and elastase models of emphysema in the rat. Am Rev Respir Dis. 1984;129:584-591. [PubMed]
 
Kerr JS, Riley DJ, Lanza-Jacoby S, et al. Nutritional emphysema in the rat: influence of protein depletion and impaired lung growth. Am Rev Respir Dis. 1985;131:644-650. [PubMed]
 
Sahebjami H, Vassallo C. Effects of starvation and refeeding on lung mechanics and morphometry. Am Rev Respir Dis. 1979;119:443-451. [PubMed]
 
Sahebjami H, Wirman JA. Emphysema-like changes in lung of starved rats. Am Rev Respir Dis. 1981;124:619-624. [PubMed]
 
Sahebjami H. Effects of nutritional depletion on lung parenchyma. Eur Respir Mon. 2003;24:113-122
 
Massaro GD, Radaeva S, Clerch LB, et al. Lung alveoli: endogenous programmed destruction and regeneration. Am J Physiol. 2002;283:L305-L309
 
Massaro D, DeCarlo Massaro G, Barras A, et al. Calorie-related rapid onset of alveolar loss, regeneration, and changes in mouse lung gene expression. Am J Physiol Cell Mol Physiol. 2004;286:896-906. [CrossRef]
 
Massaro D, DeCarlo Massaro G. Hunger disease and pulmonary alveoli. Am J Respir Crit Care Med. 2004;170:723-724. [PubMed]
 
Coxon H, Chan IHT, Mayo JR, et al. Early emphysema in patients with anorexia nervosa. Am J Respir Crit Care Med. 2004;170:748-752. [PubMed]
 
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