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Year : 2004  |  Volume : 21  |  Issue : 4  |  Page : 41-45 Table of Contents   

A follow up study on interstitial alveolitis

Former Professor of Respiratory Medicine., India

Correspondence Address:
S R Kamat
B-2, Dattaguru Co.op. Housing Society Deonar, Mumbai 400 088.
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Source of Support: None, Conflict of Interest: None

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Objective : To study the benefits of steroid therapy in interstitial alveolitis.
Method and Materials : One hundred five adult clinic patients were studied with clinical evaluation, chest radiography, CT scan, bronchoscopic lavage, pulmonary function studies and a regular follow up. They were put on daily prednisolone (in 19 on intravenous methyl prednisolone), for several months.
Results: Only a few had no cough or dypnoea; 91 cases had atleast gr. III exertional breathlessness; 61(58%) had been given steroids earlier and 32(31%) were on a prior antitubercular treatment. Only 16% had GERD symptoms. On radiography, interstitial deposits were seen in 102 cases. While 53 cases belonged to idiopathic variety, 41 were sarcoidosis. A majority had poor lung function with a restrictive disability; but 50% showed a significant response (10%+) to bronchodilators. On follow up in 92 cases, 14 died, 8 went in remission; 32 had a fluctuating course. At some stage 66 had showed improvement.
Conclusion : A large majority of our interstitial alveolitis cases are very disabled. They show clinical, functional, and radiographic improvement to long term oral prednisolone. In nonresponsive cases, intravenous steroids show an objective response.

Keywords: Interstitial Lung Fibrosis, Lung Function, Idiopathic Alveolitis

How to cite this article:
Kamat S R. A follow up study on interstitial alveolitis. Lung India 2004;21:41-5

How to cite this URL:
Kamat S R. A follow up study on interstitial alveolitis. Lung India [serial online] 2004 [cited 2021 Jan 22];21:41-5. Available from: https://www.lungindia.com/text.asp?2004/21/4/41/44467

   Introduction Top

From our Institute a large series on this syndrome has been reported [1] . Later we reported on the value of bronchoalveolar lavage in this disease [2] and a series of 100 patients with a beneficial effect of parenteral methyl prednisolone [3] . While we had earlier preferred to obtain a proof of pathology by open lung biopsy, we had found this difficult to implement, and preferred doing bronchoalveolar lavage and transbronchial biopsy. It was seen that irrespective of causation, many patients presented at an advanced stage and those in acute exacerbation and non responsive to oral steroids responded to parenteral drug priming [3] . We are herewith reporting a follow up on a series of 105 cases.

   Material and Methods Top

A consecutive series of 105 cases seen between 1996 and 2003 in a personal practice were studied with clinical assessment, chest radiographs, lung functions and regular follow up. Wherever possible, newly diagnosed without a prior administration of steroids, bronchoalveolar lavage and biopsy were done (24 patients). The patients who were critically ill or did not agree to bronchoscopy or were given steroids earlier were put on oral prednisolone in appropriate dosages if other specific pathology was excluded. In 43 cases, HRCT chest was also done. Chest radiographs were classified as normal, hilar nodes, interstitial deposits (in upto 1-6 zones). Other abnormalities like ground glass opacities, pleural reaction, reticular changes, enlarged heart and pulmonary hypertension were noted. This was also confirmed by echocardiography and ECG. Serial radiographic changes were categorised as nil (+/­10%), 1+(upto 25%), 2+(26-50%), 3+(above 50%). Lung functions were categorised as FVC/FEV 1 , below 1.0 lit, between 1-2 lit and above 2.0 lit. MVV was categorised as below 50.0 lit, 51-75 lit and above 75 lit. Diffusion parameters were categorised as low (below 80%) or normal. Arterial PO 2 was labelled low if below 80mm (S a 0 2 90%): Airway obstruction was assessed as FEV 1 /FVC%, below 75% and above. Bronchodilator testing by salbutamol/ ipratropium nebulisation through electric nebuliser was done in all and an improvement above 10% was taken as significant.

   Results Top

There was slight preponderance of females and older persons [Table 1]. There were no smokers among females but 76% of males gave a smoking history. Of 105 patients, 2 had no cough, 7 did not complain of breathlessness [Table 2]. Among 103 with cough, 33(31%) had no sputum; a significant quantity of sputum was present in 25(24%) cases. When seen initially in clinic, 54(51%) had cough and 50(48%) had dyspnoea on exertion, for atleast 2 years. When the latter was graded by British Medical Research Council grading, it was gr.I in 8(8%), gr.II in 6(6%) (as tiredness), gr.III (on climbing) in 43(41%), gr. IV (on level walking upto 100 yards) in 20(19%) and gr. V (severe on short exertion viz-bathing) in 28(26%).

Thus many in our series had a prolonged history and were quite disabled.

Many had general symptoms of bodyache (25%), and joint pains (31%); clubbing was present in 33(31%), GERD/Indigestion was complained by 17(16%), Enlarged lymph nodes in neck, axilla or mediastinum were seen in 40(38%), while clinically enlarged liver was seen in 26(25%). Clinical or radiographically enlarged heart was seen in 37(35%). Only in a few, cutaneous rashes or eye changes were observed.

Changes of pulmonary hypertension(e.g. large proximal arteries with peripheral narrowing) were seen in 45(43%), [Table 3]. The changes of interstitial deposits or ground glass effect or honeycomb changes were seen within 1-2 zones in 13(12%); 3-4 zones 33(31%) and 5-6 zones (57%). In 3 cases on radiography, lungs showed no deposits. HRCT scan was done in 43 cases - which basically corroborated the pattern seen on plain radiography. In 32 (31%) cases, previous history of anti TB treatment was found while in 61 cases (58%) oral steroids had been taken earlier. In those who were not given steroids, after usual investigations to detect other changes, we advised bronchoscopic lavage and CT scan. The former were done in 24 cases (adequate lung biopsy in 18 was obtained).

[Table 4] details the probable aetiology as judged by clinical history, radiography, BAL, lung histology and evidence of other diseases. Thus 50% had idiopathic lung fibrosis while 39% had sarcoidosis. A few other causes observed were exposure to industrial chemicals (6), rheumatoid arthritis(1) pneumoconiosis(2) and systemic sclerosis(1). In those with other causes, response to steroids appeared to be poor. As many of patients were old, it was expected that prevalence of hypertension, ischemia and diabetes would be significant.

As several patients had a variable follow up, we have analysed the initial lung function [Table 5].

Diffusion values were low in most, so was resting PaO 2 . MVV values were variable and in half (50%) cases more than 10% improvement in FEV 1 , after bronchodilator nebulisation was seen.

We could not obtain follow up in 13 cases [Table 6], while in 25 patients, it was 2 years. In our series 14(13%) died and 8(8%) went into full remission.There was improvement in 66(64%), though in 32, it was a fluctuating course (mainly due to infective or anoxic exacerbations). Overall general deterioration was seen in 26(25%). In 19 cases, we administered intravenous methyl prednisolone; in 17 there was significant improvement in lung function and radiography. One case died of acute ischemia soon after and in another cases tuberculosis got activated. This patient died later of cerebrovascular complications.

   Discussion Top

Our data on follow up in this study can not compare with other series. In some cases, we found it difficult to differentiate sarcoidosis from idiopathic alveolitis. In the former, there was more prominent lymph node involvement, while in latter, there was greater progression of disability. In those with associated cancers, we noticed poor improvement after steroids. Presence of hypothyroidism, hypertension, diabetes or ischemia did not affect the response to oral prednisolone. Those with pneumoconiosis, or collagen diseases showed no real response. In contrast to other workers [4],[5],[6],[7] we have not found any relationship to occupational dust [8] or diabetes, tobacco smoking [9] hypertension, or gastroesophageal symptoms [10] . Ward et al [11] have reported on the value of BAL in sarcoidosis. We do not think that either high total cell count or predominence of PMN or lymphocytes can definitively differentiate idiopathic fibrosis from sarcoidosis or indicate response to prednisolone. Shorr et al [12] have recently reported that patients with low PO 2 and high PA pressure were prone to fare worse. Only in few cases, we have obtained evidence of pulmonary hypertension on ECHO studies. It is our impression that this does indicate greater disability and rapid progress. But poor lung function or low PO 2 may not indicate poor prognosis. If response to oral prednisolone is seen in 2-4 weeks, its dosage has to be adjusted slowly over several months; this need to be titrated to clinical and radiologic improvement along with improvement in lung function. We have found it difficult to compare changes on CT scan or PO 2 /PCO 2 . The latter seem to depend on acute infection or cardiac failure. We also do not think that azathioprine or methotrexate have much role. Our data indicate that in majority of patients, oral/parenteral steroids give an objective improvement on radiography and lung function testing. This in some respects differs from the consensus ATS statement [13] . We have found that clinical improvement for dyspnoea along with above two parameters, allow us to do a good therapeutic adjustment. While HRCT may be useful in early or doubtful cases, the changes such as ground glass effect, honeycombing, reticular or cystic changes do not add to the picture seen on plain radiographs. In conclusion, our interstitial spectrum is that of more advanced disease; in most cases, steroid treatment is required, after excluding primary causes and tuberculosis. Each case needs individual attention and a long term follow up with serial chest radiograph and lung function studies.

   References Top

1.Mahashur AA, Dave KM, Kinare SG, Kamat SR, Shetye VM, Kolhatkar VP. Diffuse fibrosing alveolitis - an Indian experi­ence. Lung India 1983 ; 1 : 173-79.  Back to cited text no. 1    
2.Potdar PV, Jain PK, Prabhakaran Laxmi, Kamat SR, Value of bronchoalveolar lavage in interstitial lung diseases. J Assoc physicians India 1989 ; 37 : 449-53.  Back to cited text no. 2    
3.Kamat SR. Spectrum of Interstitial Lung disease in Mumbai over 1990-95. La Internista 1998 ; 6 : 29-34.  Back to cited text no. 3    
4.Kucera GP, Rybicki BA, Kirkey KL et al. Occupational risk factors for sarcoidosis in African - American siblings. Chest 2003 ; 123 : 1527-35.  Back to cited text no. 4    
5.Enomoto T, Usuki J, Azuma A, Nakagawa T, Kudoh S. Diabe­tes mellitus may increase risk for idiopathic pulmonary fibro­sis. Chest 2003 ; 123 : 2007-11.  Back to cited text no. 5    
6.Baumgartner KB, Samet JM, Stiddey CA et al. Cigarette smoking - a risk factor for idiopathic pulmonary fibrosis. Am J Resp Crit Care Med 1997 ; 155 : 242-48.  Back to cited text no. 6    
7.Hubbard R, Venu A, Smith C,et al. Exposure to commonly prescribed drugs and the aetiology of cryptogenic fibrosing alveolitis. Am J Resp Crit Care Med 1997 ; 158 : 743-47.  Back to cited text no. 7    
8.Baumgartner KB, Samet JM, Coultas DB, et al. Occupational and environmental risk factors for idiopathic pulmonary fibrosis - a Multi Centre Study. Am J Epidemiol, 2000 ; 152 : 307-15.  Back to cited text no. 8    
9.Vassalo R. Jensen EA, Colby TV et al. The overlap between respiratory bronchiolitis and desquamative interstitial pneumonia in pulmonary Langerhans Cell Histiocytosis: High resolution CT, Histologic and functional Correlation. Chest 2003 ; 124 : 1199-1205.  Back to cited text no. 9    
10.Tobin RW, Pope CE, Pelegrini CA et al. Increased preva­lence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis. Am J Resp Crit Care Med 1998 ; 158 : 1804 - 1808.  Back to cited text no. 10    
11.Ward K, O' Connor C, Odlum C.et al. Prognostic value of bronchoalveolar lavage in Sarcoidosis : the critical influence of disease presentation. Thorax 1989 ; 44 : 6-12.  Back to cited text no. 11    
12.Shorr AF, Davies DB, Nathan SD,Predicting Mortality in patients with Sarcoidosis awaiting lung transplantation. Chest 2003 ; 124 : 922-28.  Back to cited text no. 12    
13.American Thoracic Society, Idiopathic pulmonary fibrosis­diagnosis and treatment, International Consensus Statement ATS & The European Respiratory Society (ERS) Am J Respir Crit Care Med 2000 ; 161 : 646-64.  Back to cited text no. 13    


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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