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Year : 2001  |  Volume : 47  |  Issue : 2  |  Page : 89-94

Use of static lung mechanics to identify early pulmonary involvement in patients with ankylosing spondylitis.

Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, India., India

Correspondence Address:
A N Aggarwal
Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, India.
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Source of Support: None, Conflict of Interest: None

PMID: 11832596

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 :: Abstract 

AIM: To assess if a detailed analysis of lung mechanics could help in early recognition of pulmonary abnormalities in patients with ankylosing spondylitis. METHODS: Static pulmonary mechanics were studied in 17 patients (16 men and one woman) of ankylosing spondylitis with no obvious clinical or radiological evidence of pulmonary involvement. Lung pressure-volume relationship was generated using a whole body plethysmograph, and a monoexponential equation fitted to this data. RESULTS: Total lung capacity (TLC) was reduced in one (5.9%) and static lung compliance (Cst) in nine (52.9%) patients. Four (23.5%) patients had normal TLC, yet Cst and shape constant (K) were reduced. Five (29.4%) patients had reduced TLC and Cst; four of them had low K. One (5.9%) patient had normal TLC but elevated Cst and K. CONCLUSIONS: Pulmonary involvement in patients with ankylosing spondylitis is probably diffuse and begins much earlier than generally presumed. Evaluation of static lung mechanics can identify pulmonary involvement early in the course of disease in several of these patients.

Keywords: Adolescent, Adult, Female, Human, Lung Diseases, Interstitial, diagnosis,etiology,physiopathology,Male, Middle Age, Plethysmography, Respiratory Function Tests, Respiratory Mechanics, physiology,Spondylitis, Ankylosing, complications,

How to cite this article:
Aggarwal A N, Gupta D, Wanchu A, Jindal S K. Use of static lung mechanics to identify early pulmonary involvement in patients with ankylosing spondylitis. J Postgrad Med 2001;47:89-94

How to cite this URL:
Aggarwal A N, Gupta D, Wanchu A, Jindal S K. Use of static lung mechanics to identify early pulmonary involvement in patients with ankylosing spondylitis. J Postgrad Med [serial online] 2001 [cited 2023 Sep 24];47:89-94. Available from:

Ankylosing spondylitis (AS) is a chronic inflammatory disorder of unknown aetiology, affecting primarily the joints of axial skeleton. It is a systemic disorder with several extra-articular manifestations that include ocular, cardiovascular and neurological complications.[1] Pulmonary involvement is usually recognized in patients with a long history of joint disease, and manifests either as chest wall restriction due to involvement of thoracic cage, or as upper lobe fibrobullous disease.[2] Pulmonary parenchymal disease, unless extensive, is typically clinically silent. Radiographic abnormalities are generally seen only in the presence of advanced disease. In view of the systemic and progressive nature of AS, it is likely that onset of pulmonary involvement is much earlier than its clinical or radiological recognition. Pulmonary function tests may help to identify lung involvement. Although restrictive ventilatory defects have been described in these patients, these abnormalities have been largely ascribed to diminished chest wall mobility.[3] It is not possible to differentiate chest wall from pulmonary interstitial involvement using routine studies. Study of static pulmonary mechanics can better characterize the contribution of lung fibrosis to these changes.

A few studies have previously documented normal or reduced lung compliance in patients with AS.[3],[4],[5],[6],[7] However, most reports included patients with varying stages of established AS, and information on lung mechanics is rather scanty. We performed a detailed analysis of static pulmonary mechanics in patients with AS who had no obvious clinical or radiological evidence of pulmonary disease.

  ::   Patients and methods Top

The study was conducted on previously diagnosed patients with AS, attending the Rheumatology Clinic of this Institute during a six-month period. Diagnosis in these patients had been established on the basis of modified New York criteria.[8] Patients with respiratory symptoms (dyspnoea and/or cough) or abnormal plain chest radiographs were not included. Current or former smokers, as well as patients with concomitant cardiopulmonary disorders, were also excluded. The nature and purpose of the study were explained to each eligible subject and informed consent was obtained prior to pulmonary function testing. The study protocol had been approved by our Hospital Ethics Committee.

Spirometry was performed on a dry rolling seal spirometer (Spiroflow, P K Morgan Ltd., UK). Vital capacity (VC), forced expiratory volume in first second (FEV1) and peak expiratory flow were measured and compared to norms for healthy north Indian adults previously derived by us.[9] Static expiratory pressure-volume relationship was generated using a computerized whole body plethysmograph system (Autolink; P K Morgan Ltd., UK). Oesophageal pressure was measured through a thin latex balloon positioned in the oesophagus at approximately 40 cm from the nares and inflated with 0.4 ml air.[10] After a period of tidal breathing, during which the position of functional residual capacity (FRC) was identified, each subject took a series of three full inspirations to total lung capacity (TLC) to ensure a constant volume history. Static transpulmonary pressure at TLC (PTLC) was recorded at the end of third inspiration as the difference between mouth and oesophageal pressures. Patients were subsequently asked to exhale slowly in a stepwise fashion while the airway was intermittently occluded by a shutter placed close to the mouthpiece. During each occlusion, patients kept their glottis open to measure static transpulmonary pressure and lung volume. This procedure was repeated until 10 or more readings were obtained. Static lung compliance (Cst) was computed as the slope of the composite pressure-volume curve thus plotted in its relatively straight portion above the FRC. The observed TLC was compared to previously described norms for healthy north Indian adults.[11],[12] Pressure-volume data were also subjected to monoexponential analysis, using the equation

V = Vmax - Ae-KP

where V is the lung volume, Vmax is the extrapolated lung volume at infinite distending pressure, K is a constant describing the shape of the curve, P is the static transpulmonary pressure and A = Vmax - V0 (where V0 is the volume extrapolated to zero transpulmonary pressure).[13],[14] The observed values for compliance, shape constant (K), and PTLC were compared to predicted norms previously described for healthy subjects.[15] Limits of normality for all pulmonary function variables were defined as the predicted value ± 1.645 times the residual standard deviation of the relevant regression equation.[16]

  ::   Results Top

Seventeen patients (16 men and one woman) with mean age of 28.2 ± 11.9 years (range 16-63 years) were studied. They were symptomatic with low backache of one to 20 years’ duration. Seven patients had peripheral arthritis involving knee and/or hip joints, and another had an episode of uveitis six months prior to pulmonary function evaluation [Table - 1].

Vital capacity was reduced in five (29.4%) patients [Table - 2]. A restrictive ventilatory defect, defined as a diminished TLC, was present in six (35.3%) patients; TLC ranged from 85-105% of predicted in the remaining patients. No patient had any obstructed defect, as seen by normal FEV1/VC values in all subjects [Table - 2]. PTLC was reduced in one (5.9%) and increased in seven (41.2%) patients. Cst was reduced in nine (52.9%) patients; only five of them had reduced TLC [Table - 2]. In another patient, Cst was increased but TLC was within normal limits. All patients with normal Cst, except one, had normal lung volumes. Detailed analysis of pressure-volume data showed that K was reduced in all except one patient with low Cst. This pattern suggested reduced lung distensibility.

Abnormalities in static lung mechanics were detected both in patients with and without peripheral arthritis and/or extra-articular manifestations [Table - 2]. There was also no correlation between the duration of articular symptoms and impairment of pulmonary mechanics. Overall, three broad types of abnormalities were identified [Figure - 1]: (a) four (23.5%) patients had normal TLC, yet Cst and K were found reduced; (b) five (29.4%) patients had a restrictive ventilatory defect (reduced TLC) as well as reduced Cst, and four of them had a low K; (c) one (5.9%) patient had normal TLC but elevated Cst and K.

  ::   Discussion Top

We have studied patients of AS with no obvious clinical or radiological evidence of pulmonary complications of the disease. To assess the true contribution of the underlying disease, we had excluded all current and former smokers, as well as patients with concomitant cardiopulmonary disorders. A restrictive ventilatory defect in patients with AS has traditionally been attributed to limited chest wall expansion.[3] The methodology used in measuring lung compliance in this study eliminates the contribution from thoracic cage abnormalities, as our pressure measurements were the difference between alveolar pressure (represented by mouth pressure under static conditions) and pleural pressure (represented by oesophageal pressure). Hence the abnormalities detected, in all probability, reflected pulmonary complications of AS in these patients. It has earlier been suggested that of all respiratory function parameters, those derived from a static pressure-volume curve are the best predictors of the degree of pulmonary fibrosis.[17]

Compliance was reduced in nine of 17 subjects included in this study. Comparison of our results with those obtained by previous investigators is, however, difficult because of several reasons. Earlier studies, for example, had not employed limits of normality as is now recommended for interpretation of pulmonary function tests.[16] Thus values below the predicted normal were reported as reduced or normal using arbitrary cut-off points, which had often not been clearly defined. Secondly, different techniques had been used to measure Cst in various studies. Finally, the composition of our study population was different from several previous reports. For example, 60% patients with low or borderline compliance in one study had associated pulmonary disorders that could have partly explained this abnormality.[5] In another study, four of 11 patients found to have compliance values below the predicted normal had complicating pulmonary diseases.[3] However, in a study on patients with no pulmonary symptoms and normal chest radiographs, lung compliance values were no different from those in the reference study population.[6] In another study carried out on 21 patients with no clinical evidence of lung disease, there was close agreement between observed and predicted values in all but three patients.[4] Further analysis was, however, not provided in either study.

Alterations in lung parenchyma start much earlier than when radiologically recognised. In fact, cases have been documented where pulmonary manifestations have appeared quite early in the course of disease or have even antedated joint symptoms.[18],[19] It also appears that interstitial changes could be diffuse and not merely confined to the upper lobes.[20] Whether these changes are related to an ongoing inflammatory process is not clear. The observation that decreased lung volumes were related to inflammatory intensity of disease may suggest an inflammatory involvement of the lung parenchyma.[6] Although characteristic features suggestive of alveolitis have not been identified on analysis of bronchoalveolar lavage fluid in these patients, a non-specific inflammatory response has been seen.[21],[22] This early pulmonary involvement can explain loss of compliance seen in half of our patients.

The static lung pressure volume relationship is non-linear over a substantial portion of lung volumes. Cst, which represents the slope of this curve in its relatively linear portion, is only a gross approximation of static pulmonary mechanics. Exponential analysis of pressure-volume data better describes static lung mechanics over a wide range of lung volumes.[13],[14] The shape constant of this curve (K), the single most important variable describing this curve, is an index of lung compliance. Unlike compliance, it is largely independent of sex, ethnicity, patient effort and lung size.[14],[23] Among patients with restrictive ventilatory defects, exponential analysis also helps to differentiate restriction due to reduced elastic properties (low value for K) from that due to loss of lung volume (normal K).[24] Cst was reduced in nine of 17 of our patients. Interstitial fibrosis can induce restriction either by reducing distensibility or by obliterating existing alveoli. Detailed analysis of pressure volume data helped in identifying reduced distensibility as the dominant pathophysiology in these patients. The severe reduction in compliance and K values seen in some patients suggests that lung involvement is diffuse rather than focal; similar findings have earlier been described on HRCT scans carried out in patients with AS.[19]

One of our patients had increased Cst and an increased value for K. This combination is seen in conditions characterized by distension of airspaces, such as emphysema.[23] This patient, however, had a normal TLC. The precise reason for such abnormality in a non-smoking patient is not clear. Although bullous lesions are described in patients with long standing disease, this patient had been symptomatic for only three years. Recently, panacinar and paraseptal emphysematous changes have been described on HRCT in these patients.[20] Whether this patient had similar changes is a matter of conjecture.

Only one patient in our study had reduced PTLC. Majority of patients had normal values and 6 (35.3%) showed high PTLC. Previous studies had shown a reduction in mean PTLC values in patients with AS.[3],[6],[7] The reason for such a change is not clear. It is known that although rib mobility decreases in patients with AS, a supranormal diaphragmatic excursion helps to maintain normal ventilation.[26],[27] The normal or increased diaphragmatic strength may, however, be overwhelmed by a reduced strength or atrophy of intercostal or accessory muscles, or both.[28] It has been speculated that immobilization of these muscles due to thoracic rigidity and decreased inspiratory muscle activation are important factors, especially in long standing cases. Since most of our patients were evaluated relatively early in the course of disease, it is possible that the strength of inspiratory muscles was well preserved and the increase in PTLC was a reflection of increased diaphragmatic excursion.

In conclusion, the evaluation of static lung mechanics can identify pulmonary interstitial fibrosis early in the course of disease in several patients with AS, even when they do not have significant clinical and radiological findings. This suggests that pulmonary involvement in these patients possibly begins much earlier than what has been generally presumed, and is probably diffuse rather than confined to the apical portions of the lung.

 :: References Top

1. Luthra HS. Extra-articular manifestations of ankylosing spondylitis. Mayo Clin Proc 1977; 52:655-656.  Back to cited text no. 1    
2.Lee-Chiong T Jr . Pulmonary manifestations of ankylosing spondylitis and relapsing polychondritis. Clin Chest Med 1998; 19:747-757.  Back to cited text no. 2    
3.Travis DM, Cook CD, Julian DG, Crump CH, Heliesen P, Robin ED, et al. The lungs in rheumatoid spondylitis. Gas exchange and lung mechanics in a form of restrictive pulmonary disease. Am J Med 1960; 29:623-632.  Back to cited text no. 3    
4.Hart DF, Emerson PA, Gregg I. Thorax in ankylosing spondylitis. Ann Rheum Dis 1963; 22:11-18.   Back to cited text no. 4    
5.Sharp JT, Sweany SK, Henry JP, Pietras RJ, Meadows WR, Amaral E, et al. Lung and thoracic compliance in ankylosing spondylitis. J Lab Clin Med 1964; 63:254-263.  Back to cited text no. 5    
6.Feltelius N, Hedenstrom H, Hilledral G, Hallgren R. Pulmonary involvement in ankylosing spondylitis. Ann Rheum Dis 1986; 45:736-740.  Back to cited text no. 6    
7.van Noord JA, Cauberghs M, Van de Woestijne KP , Demedts M. Total respiratory resistance and reactance in ankylosing spondylitis and kyphoscoliosis. Eur Respir J 1991; 4:945-951.  Back to cited text no. 7    
8.van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. Arthritis Rheum 1984; 27:361-368.  Back to cited text no. 8    
9.Jindal SK, Wahi PL. Pulmonary function laboratory in the tropics: needs, problems and solutions. In: Sharma OP, editor. Lung disease in the tropics. New York; Marcel Dekker: 1991. pp 523-542.  Back to cited text no. 9    
10.Milic-Emili J, Mead J, Turner JM, Glauser EM. Improved technique for estimating pleural pressure from esophageal balloons. J Appl Physiol 1964; 19:207-211.  Back to cited text no. 10    
11.Jain SK, Ramiah TJ. Influence of age, height and body surface area on lung functions in healthy women 15-40 years old. Indian J Chest Dis 1967; 9:13-19.  Back to cited text no. 11    
12.Jain SK, Ramiah TJ. Normal standards of pulmonary function tests for healthy men 15-40 years old: comparison of different prediction equations (prediction formulae). Indian J Med Res 1969; 57:1453-1466.  Back to cited text no. 12    
13.Colebatch HJ, Ng CKY, Nikov N. Use of an exponential function for elastic recoil. J Appl Physiol 1979; 46: 387-393.  Back to cited text no. 13    
14.Knudson RJ, Kaltenborn WT. Evaluation of lung elastic recoil by exponential curve analysis. Respir Physiol 1981; 46:29-42.  Back to cited text no. 14    
15.Colebatch HJ, Greaves IA, Ng CK. Exponential analysis of elastic recoil and aging in healthy males and females. J Appl Physiol 1979; 47:683-691.  Back to cited text no. 15    
16.American Thoracic Society. Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis 1991; 144:1202-1218.  Back to cited text no. 16    
17.Fulmer JD, Roberts WC, von Gal ER, Crystal RG . Morphologic-physiologic correlates of the severity of fibrosis and degree of cellularity in idiopathic pulmonary fibrosis. J Clin Invest 1979; 63:665-676.  Back to cited text no. 17    
18.Crompton GK, Cameron SJ, Langlands AO, Robertson GG. Pulmonary fibrosis, mimicking tuberculosis, presenting before joint symptoms in a female with ankylosing spondylitis. Tubercle 1973; 54:317-320.   Back to cited text no. 18    
19.Ferdoutsis M, Bouros D, Meletis G, Patsourakis G, Siafakas NM. Diffuse interstitial lung disease as an early manifestation of ankylosing spondylitis. Respiration 1995; 62:286-289.  Back to cited text no. 19    
20.Fenlon HM, Casserly I, Sant SM, Breatnach E. Plain radiographs and thoracic high-resolution CT in patients with ankylosing spondylitis. AJR Am J Roentgenol 1997; 168:1067-1072.  Back to cited text no. 20    
21.Wendling D, Dalphin JC, Toson B, Depierre A, Guidet M. Bronchoalveolar lavage in ankylosing alveolitis. Ann Rheum Dis 1990; 49:325-326.  Back to cited text no. 21    
22.Scherak O, Kolarz G, Popp W, Wottawa A, Ritschka L, Braun O. Lung involvement in rheumatoid factor-negative arthritis. Scand J Rheumatol 1993; 22:225-228.  Back to cited text no. 22    
23.Chan CC, Cheong TH, Poh SC, Wang YT. Lung elastic recoil in normal young adult Chinese compared with Caucasians. Eur Respir J 1995; 8:446-449.  Back to cited text no. 23    
24.Gibson GJ, Pride NB, Davis J, Schroter RC. Exponential description of static pressure-volume curve of normal and diseased lungs. Am Rev Respir Dis 1979; 120:799-811.  Back to cited text no. 24    
25.Greaves IA, Colebatch HJ. Elastic behavior and structure of normal and emphysematous lungs postmortem. Am Rev Respir Dis 1980; 121:127-136.  Back to cited text no. 25    
26.Josenhans WT, Wang CS, Josenhans G, Woodbury JF. Diaphragmatic contribution to ventilation in patients with ankylosing spondylitis. Respiration 1971; 28:331-346.  Back to cited text no. 26    
27.Grimby G, Fugl-Meyer AR, Blomstrand A. Partitioning of the contributions of rib cage and abdomen to ventilation in ankylosing spondylitis. Thorax 1974; 29:179-184.  Back to cited text no. 27    
28.Vanderschueren D, Decramer M, Van den Daele P, Dequeker J. Pulmonary function and maximal transrespiratory pressures in ankylosing spondylitis. Ann Rheum Dis 1989; 48:632-635.   Back to cited text no. 28    


[Figure - 1]


[Table - 1], [Table - 2]

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© 2004 - Journal of Postgraduate Medicine
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