Changes in respiratory function impairment following the treatment of severe pulmonary tuberculosis - limitations for the underlying COPD detection.

BACKGROUND: During the treatment phase of active pulmonary tuberculosis (PTB), respiratory function impairment is usually restrictive. This may become obstructive, as a PTB-associated airflow obstruction (AFO) or as a later manifestation of underlying COPD. PURPOSE: The aim of the study was to examine the potential causes and risks for AFO development in PTB by exploring the aspects of spirometry limitations and clinical implications for the underlying COPD detection, taking into account various confounding factors. PATIENTS AND METHODS: Prospective, nest case-control study on 40 new cases of PTB with initial restrictive respiratory function impairment, diagnosed and treated according to the directly observed treatment short course (DOTS) strategy. RESULTS: From all observed patients, 37.5% of them developed AFO upon the completion of PTB treatment, with significantly increased average of forced vital capacity (%) (P<0.01). Their changes in forced expiratory volume in the first second (%) during the PTB treatment were strongly associated with the air pollution exposure in living (0.474%-20.971% for 95% confidence interval [CI]; P=0.041) and working environments (3.928%-20.379% for 95% CI; P=0.005), initial radiological extent of PTB lesions (0.018%-0.700% for 95% CI; P=0.047), leukocyte count (0.020%-1.328% for 95% CI; P=0.043), and C-reactive protein serum level (0.046%-0.205% for 95% CI; P=0.003) compared to the other patients. The multivariate logistic regression analysis model shows initial radiological extent of pulmonary tuberculosis lesions (OR 1.01-1.05 for 95% CI; P=0.02) and sputum conversion rate on culture (OR 1.02-1.68 for 95% CI; P=0.04) as the most significant predictors for the risk of AFO development. CONCLUSION: AFO upon PTB treatment is a common manifestation of underlying COPD, which mostly occurs later, during the reparative processes in active PTB, even in the absence of major risk factors, such as cigarette smoking and biomass fuel dust exposure. Initial spirometry testing in patients with active PTB is not a sufficient and accurate approach in the detection of underlying COPD, which may lead to their further potential health deterioration.

Role of D-dimer in predicting mortality in patients with community-acquired pneumonia.

AIM: To determine whether D-dimer in patients with communityacquired pneumonia (CAP) can predict mortality risk better than standard biomarkers. METHODS: White blood cell (WBC), C-reactive protein (CRP) and D-dimer in 129 patients with CAP were analyzed. The recommended Pneumonia Severity Index (PSI) score was used to classify CAP patients into five groups according to the severity of disease (Group PSI I-V), and for predicting mortality. Additionally, the patients were divided in surviving and non-surviving group. RESULTS: White blood cell and CRP were not in correlation with the severity of CAP and the risk of mortality. The correlation between plasma D-dimer and severity of CAP was found (r=0.4993; p less than 0.001). The level of D-dimer was significantly higher in nonsurviving (2498.38 ± 1248.83 ng/mL) than in surviving patients (966.44 ± 968.73 ng/mL) (p less than 0.001). In predicting mortality risk, D-dimer showed sensitivity of 0.84 (cut of >1538 mg/mL), specificity 0.86 and AUC 0.859 (95%CI; 0.787-0.914). Pneumonia Severity Index in predicting of mortality risk for cut of > PSI III showed sensitivity of 0.92, specificity 0.62 and AUC 0.868 (95%CI; 0.797-0.921). There was no statistical difference between AUC of PSI and D-dimer (delta AUC= 0.00895) (p=0.9005). CONCLUSION: Coagulation abnormalities were presented in older patients with severe infections and comorbidity. Plasma D-dimer correlated better than standard inflammatory markers with severity of disease and risk of mortality in patients with CAP. In predicting mortality risk, D-dimer did not show difference among the PSI score.

Peroxisome proliferator-activated receptor gamma as modulator of inflammation in pulmonary sarcoidosis.

Peroxisome proliferator-activated receptor (PPAR) includes the family of ligand-activated transcription factors which belong to the group of nuclear hormone receptors and are connected to retinoid, glucocorticoid and thyroid hormone receptors. There are three subtypes of PPARs: PPARalpha (also known as NR1C3), PPARgamma (known as NR1C1) and PPARdelta (known as PPARbeta or NR1C2). All of them take part in the metabolism, cell proliferation and immune response. PPARgamma and PPARalpha are identified as important immunomodulators and potentially represent an anti-inflammatory target for respiratory diseases. PPARgamma deficiency in the lungs has been observed in the inflammatory diseases such as asthma, pulmonary alveolar proteinosis, fibrosis and sarcoidosis, as well as in the animal models of the lung inflammation. A small number of papers concerned with PPARgamma in sarcoidosis pointto the lowered activity of this factor in the alveolar macrophages and a lowered gene expression for the PPARgamma, while the activity is preserved in healthy individuals. At the same time, an increased activity of the nuclear factor kappa B (NF-kappaB) in the bronchoalveolar lavage has been recorded in patients with sarcoidosis. The reason for the decrease in the production of PPARgamma in sarcoidosis remains unknown. Several possible mechanisms are mentioned: genetic defect with lowered production, down-regulation due to the increased values of IFN-gamma or an increased decomposition of PPARgamma. Further investigation will explain the mechanisms regarding the decreased production of PPARgamma in sarcoidosis.

Nutrition disorder and systemic inflammation in patients with chronic obstructive pulmonary disease.

AIM: To detect nutrition disorders (underweight and obesity) in patients with chronic obstructive disease (COPD) and presence of systemic inflammation by determination of inflammatory mediators serum values C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α) and leptin. METHODS: The examination involved 85 patients with COPD. Nutrition categories were defined by body mass index (BMI). Fat free mass (FFM) was evaluated by mid upper-arm circumference (MUAC) and fat mass (FM) by tricipital skin-fold thickness (TFS). Values of TNF-α and leptin were measured by standardized ELISA kits and, CRP by latex turbidimetry. RESULTS: There were 14 (16.5%) underweight patients, 28 (32.9%) normal, 28 (32.9%) pre-obese and 15 (17.6%) obese. Values of MUAC and TSF were significantly different among the nutrition categories (p=0.000). The lowest MUAC and TSF values were in the underweight, and the highest in the obese. There was no significant difference of CRP and TNF-α among nutrition categories. Leptin of the underweight and normal nutrition was significantly different from leptin of the pre-obese and obese (p=0.000). The highest CRP and the lowest TNF-α and leptin were in the underweight patients. The obese had the lowest CRP (although increased as compared to normal values) and the highest leptin, while the pre-obese had the highest TNF-α. CONCLUSION: Two basic nutrition disorders (underweight and obesity) were manifested in COPD patients. The inflammatory profile differs between underweight COPD patients and obese. Probably that happens due to systemic inflammation, and in part due to dysfunction of adipose tissue.

Tumor necrosis factor alpha gene polymorphism in serbian patients with sarcoidosis.

INTRODUCTION: Sarcoidosis is a multisystemic disease of unknown etiology. Genetic factors play a considerable role in the onset of the disease. Tumor necrosis factor alpha (TNF-a) is a proinflammatory cytokine which plays an important role in the pathogenesis of the disease and the formation of granuloma by regulating cellular proliferation and apoptosis. OBJECTIVE: The aim of this study was to investigate the role of TNF-alpha-308 G/A polymorphism in the development of sarcoidosis and to evaluate the association between the aforementioned type of polymorphism and the clinical course of the disease. METHODS: Seventy patients with sarcoidosis and 50 healthy volunteers were genotyped for the TNF-alpha-308G/A polymorphism. Polymorphism variants were examined by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism) on the DNA isolated from blood leukocytes. RESULTS: There were no significant differences in TNF-alpha-308A allele frequency distribution between sarcoidosis patients and the control group, but the TNF-alpha-308A allele was observed significantly more frequently in the sarcoidosis patients with Löfgren's syndrome when compared with non-Löfgren's patients. CONCLUSION: We have found that the TNF-alpha-308A variant is associated with Löfgren's syndrome in Serbian patients with sarcoidosis.

Osteoporosis in patients with chronic obstructive pulmonary disease.

UNLABELLED: One of the extrapulmonary effects of chronic obstructive pulmonary disease (COPD) is osteoporosis. Osteoporosis is characterized by a low bone mineral density (BMD). THE AIM: The aim of this study was to determine relationship between bone mineral density and severity of COPD and body mass index (BMI). PATIENTS AND METHODS: in this study 85 COPD patients were recruited. Diagnosis and severity of COPD was made according to the GOLD guidelines. Height and weight were measured, and BMI was calculated. BMD (at the lumbar spine and at the femoral neck) were performed using Dual energy X-ray absorptiometry (DXA). BMD was expressed in g/cm2 and standardized T-score. RESULTS: The increase of COPD severity leads to the decrease of average values of BMD (femoral neck p = 0.005; lumbar spine p = 0.026), as well as T score (femoral neck p = 0.026; lumbar spine = 0.156). Also, the decrease of BMI leads to the decrease of average values of BMD (femoral neck p = 0.034; lumbar spine p = 0.269) and T score (femoral neck p = 0.001; lumbar spine p = 0.105), as well as to the increase of total osteoporosis (p = 0.009). CONCLUSION: patients with severe COPD and lowe BMI have lower BMD and T score and more frequently have osteoporosis.

Chronic airflow obstruction syndrome due to pulmonary tuberculosis treated with directly observed therapy--a serious changes in lung function.

UNLABELLED: The origin of Chronic airflow obstruction (CAO) syndrome in active Tuberculosis (TB), despite significant similarities with chronic obstructive pulmonary disease (COPD), still remains unknown. The aim of the study was to examine the potential causes and risks for the development of CAO syndrome in new cases of pulmonary TB. DESIGN: Prospective, nest case-control study. PATIENTS: 40 patients with newly detected cavitary pulmonary TB and initial normal respiratory function, diagnosed and treated according to DOTS strategy. MEASUREMENTS AND RESULTS: The average values of Snider's radiological score during TB treatment were significantly reduced (p < 0.001), as well as average values of non-specific systemic serum markers of inflammation. The average values of FEV1 (%), both before, during and at the end of completion of TB treatment were significantly decreased (p < 0.05;). Linear regression analysis confirmed a statistically significant association between changes in the values of FEV1 (%), resulting in TB treatment completion, and the value of Snider's radiological score and the sputum culture conversion rate. From the initial findings of normal pulmonary ventilation tests, upon the completion of TB treatment 35.0% of observed patients developed the CAO syndrome. Logistic regression analysis confirmed a positive familiar burden for COPD, Snider's radiological score at the beginning of TB treatment and sputum conversion rate on culture, as statistically significant predictors, while multivariate logistic regression analysis confirmed Snider's radiological score at the beginning of TB treatment and sputum conversion rate on culture as most significant risk factors for CAO syndrome occurrence and development. CONCLUSION: The CAO syndrome is often a consequence and significant functional impairment of the respiratory system, during the reparative processes in active TB, even in the absence of risk factors for COPD. Only microbiological cure of TB patients with underlying risks for disorders of lung function, is not sufficient and effective approach for prevention of their further potential health deterioration.

[The impact of inhaled corticosteroids on cough and bronchial hyperreactivity in cough variant asthma].

INTRODUCTION: Classic asthma is characterized by cough, wheezing and dyspnea. Cough, however, may be the sole presenting symptom of asthma and this type of asthma is known as cough-variant asthma. The therapeutic approach to cough variant asthma is similar to that of the typical form of asthma. A diagnosis of cough-variant asthma is made when a chronic cough is associated with airway hyperresponsiveness and a favorable response to asthma therapy in the absence of other discernible cause. The aims of this study were to analyse the influence of inhaled corticosteroids on cough and bronchial hyperresponsiveness. MATERIAL AND METHODS: The study included 55 patients with cough as the sole presenting symptom. 40 patients (Group A) were treated with inhaled corticosteroids and beta2 agonists for eight weeks while 15 patients (Group B) were treated only with oral beta2 agonists. The nonspecific bronchoprovocative test with histamine was performed on all the patients before the treatment and after the examination and there was established the provocative dose of histamine causing the 20% fall in FEVI (PD20). RESULTS: At the end of the study in Group A we found a statistically significant decrease of PD20 0.98 +/- 0.86 vs. 1.58 +/- 1.06 (p < 0.005), while in Group B there were no significant changes. In 90% of the patients treated with inhaled corticosteroids the cough was completely relieved while in 80% of the patients treated with only beta2 agonists the cough has remained unchanged. CONCLUSION: Inhaled corticosteroids are choice drugs for the treatment of cough-variant asthma because they relieve cough and decrease bronchial hyperresponsiveness, thus ultimately reducing the risk of classic asthma.

[Prognostic factors of mortality in elderly with community acquired pneumonia].

BACKGROUND/AIM: Community acquired pneumonia in elderly has specific clinical aspect and higher mortality in relation to younger patients. According to specific pneumonia severity assessment on admission and its importance in proper prediction of clinical course and outcome, the aim of this study was defining prognostic factors of mortality. METHODS: This study included 240 patients aged > or = 65 years with community acquired pneumonia. On admission, demographic characteristics, underlying diseases, physical symptoms and findings, laboratory values, chest radiography and oxygen blood saturation (SaO2) were analyzed. Multivariate analysis was used to identify characteristic prognostic factors which showed a statistical significance in relation to mortality. RESULTS: Altered mental status, respiratory frequency > or = 23/min and the presence of bilateral pneumonic infiltrates were defined as the most important prognostic factors of mortality (p < 0.001). These factors displayed 57.89% sensitivity, 100% specificity and 93.33% accuracy. CONCLUSION: The presence of identified characteristic prognostic factors on admission pointed out an adverse clinical course and outcome of community acquired pneumonia in elderly. Age and sex were not significantly associated with mortality.

[Pulmonary embolism in patients with chronic hypoxemia].

INTRODUCTION: The aim of this prospective, originally designed, clinical--diagnostic study including 200 chronic hypoxemic patients was to assess the possibility of implementation of noninvasive diagnostic strategy and to investigate the incidence of pulmonary embolism and parameters of diagnostic accuracy of radiological findings according to Shintz criteria, echocardiography, lung perfusion scanning according to PIOPED criteria. MATERIAL AND METHODS: The study included 200 chronic hypoxemic patients divided into 2 groups, the group I consisting of 42 women and 58 men and the group II consisting of 48 women and 52 men. RESULTS AND CONCLUSION: Out of 200 hypoxemic patients, 49 patients (24.5%) were found to have pulmonary embolism. In the group I of 100 patients (42 women and 58 men) with chronic hypoxemia and secondary erythrocytosis the diagnosis of pulmonary embolism was confirmed in 39%, that being statistically significantly different (p < 0.001) from 100 patients (48 women and 52 men) in the group II with chronic hypoxemia without secondary erythrocytosis, where pulmonary embolism was found in 10% of the patients. The predictive value was positive for direct radiological signs in 92.3% of patients in the group I for PTE, for indirect ones in 74.35%, and in the group II it was positive for direct radiological signs in 60% and for indirect ones in 90%. The predictive value of perfusion scan was positive in 59% of the group I and in only 22% of the group II. The predictive value for high pressure in the pulmonary artery was positive in 93.7% of the group I and in 66.6% of the group II. The following were found to be a variable predictor: hypoxemia, enlargement of the pulmonary artery, peripheral oligemia and elevation of diaphragm. Logistic regression according to backward--conditional method showed that the chronic hypoxemic patients with secondly erythrocytosis, who had radiological sign of peripheral oligemia--Westermark sign, had 2.286 times higher probability of having pulmonary embolism than similar patients without this sign.

Difficulties in establishing a timely diagnosis of pulmonary artery sarcoma misdiagnosed as chronic thrombo-embolic pulmonary disease: a case report.

INTRODUCTION: Pulmonary artery sarcomas are rare neoplasms that are often confused with chronic thrombo-embolic disease, as both can have similar clinical and imaging presentation. CASE PRESENTATION: In this report, we present a case of a 50-year-old man initially diagnosed with chronic thrombo-embolic pulmonary disease, but who was later found to have pulmonary artery sarcoma with poor survival prognosis. We review the clinical and imaging characteristics of the two diseases and discuss the difficulties in establishing a timely diagnosis. CONCLUSION: Similar clinical features and imaging presentation of pulmonary artery sarcoma and chronic thrombo-embolic pulmonary disease make definitive diagnosis difficult. This case report also illustrates and emphasizes that in any case with no predisposition factors for embolism, no evidence of deep venous thrombosis and pulmonary emboli, and inadequate relief of symptoms with anticoagulation, an alternative diagnosis of pulmonary artery sarcoma should be considered. If pulmonary artery sarcoma is diagnosed late in the course of the disease, there is usually a poor survival outcome.

Diagnostic value of CEA in pleural fluid for differential diagnosis of benign and malign pleural effusion.

UNLABELLED: The diagnostic value of tumor markers in pleural fluid is still the subject of debate. The aim of this work was to evaluate diagnostic value of carcinoembryonic antigen (CEA) in pleural fluid for differentiating malignant from non malign pleural effusion, and their additive value to cytological examination. DESIGN: Prospective, case control study. SETTING: Tertiary University hospital, Clinic for Lung Disease, Knez Selo. PATIENTS: Eighty two patients with pleural effusion, forty one with malignant, and forty one with non malignant pleural effusion. MEASUREMENTS AND RESULTS: Levels of CEA in pleural fluid was measured by IRMA CEA methods, INEP Belgrade. Patients with lung cancer were found to have significantly higher CEA levels than patients with non malign pleural effusion. Using cut off values of 2.4 ng/ml, the sensitivity of marker was 78%, and specificity 95.1% (CI 95%). The addition of CEA to cytology increase diagnostic rate from 68 to 85.3%. CONCLUSION: CEA may represent a helpful adjunct to cytology in order to include malignancy as probable diagnosis, thus guiding the selection of patients for more invasive procedures.

[Pulmonary rehabilitation in patients with chronic obstructive pulmonary disease].

BACKGROUND/AIM: Chronic obstructive pulmonary disease (COPD) irreversibly damages pulmonary function leading to disorder of arterial bloodgases, arterialpartial prescure of oxygen (PaO2) and arterial partial pressure of carbon dioxide (PaCO2), appearance of dyspnea, and decrease of physical condition. The aim of this study was to establish if medical treatment and respiratory rehabilitation in COPD used simultaneously lead to the greater improvement of PaO2, PaCO2 and physical condition and decreaseing dyspnea than medical treatment alone. METHODS: A total of 60 patients divided into three groups according to the severity of obstruction (mild--I, severe--II, very severe--III) weretested. Each group had the two subgroups of patients--first one with those treated both with medical treatment and respiratory rehabilitation (A) and the second one with the patients treated only with medical treatment (B). The treatment took 21 days. The measurements of PaO2 and PaCO2) intensity of dyspnea at rest and exercise (10--point Borg Category Scale), and physical capacity (Six-Minute Walk Test--6MWT) were done on the first and on the last day of testing. RESULTS: The results showed that all of the patients who were treated with the combination of medical treatment and respiratory rehabilitation had significantly higher increase in the values of PaO2 (I--p < 0.01; II--p < 0.05; III--p < 0.01), score of Borg's scale (I--p < 0.05, p < 0.001; II--p < 0.05, p < 0.001; III--p < 0.001, p < 0.001) and 6MWT (I--p < 0.001; II--p < 0.001; III--p < 0.001), and that statistically significant increase of the values of PaCO2 (p < 0.05) had only the patients with very severe COPD treated with the combination of drugs and respiratory rehabilitation. CONCLUSION: Based on the obtained results we conclude that using respiratory rehabilitation in combination with pharmacological treatment of COPD gives statistically higher improvement of values of PaO2 and PaCO2, and physical condition, and also leads to decrease of intensity of dyspnea than using just drug therapy.

Is there any point in a corticosteroid treatment of intermittent asthma?

International guidelines advocate the early introduction of inhaled corticosteroids (ICS) in all types of persistent asthma. Our study was undertaken to assess the effects of ICS on bronchial hyperresponsiveness (BHR) as a hallmark of inflammation, and to assess the symptoms, the use of rescue medications, and the parameters of lung function in patients with mild intermittent asthma. The patients with intermittent asthma (n = 85) were randomly allocated to a treatment with ICS, beclomethasone dipropionate 250 microg/day and short-acting beta2 agonists salbutamol as needed (Group A, n = 45) or to a treatment with only short-acting beta2 agonists as needed (Group B, n = 40) during the 6-month treatment period. At the end of the study, in Group A, we found a statistically significant decrease of BHR (PD20 0.98 vs. 2.07) (p < 0.001), diurnal peak expiratory flow (PEF) variability (17.9 vs. 13.8) (p < 0.001), symptom scores (0.63 vs. 0.30) (p < 0.001), and used rescue medication (p < 0.001), while the parameters of lung function remained unchanged except for forced expiratory volume in 1 sec (FEV1), which had a statistically significant increase (3.58 vs. 3.66) (p < 0.001). In Group B, there was a statistically significant decrease of lung function parameters FEV1 (3.80 vs. 3.71) (p < 0.001), forced vital capacity (FVC) (4.43 vs. 4.37) (p < 0.001), FEV1/FVC (88.2 vs. 85.3) (p < 0.05), PEF (8.05 vs. 7.51) (p < 0.01), PEF variability (17.85 vs. 18.33) (p < 0.001), increased BHR (PD20 1.04 vs. 0.62) (p < 0.05), and symptom scores (0.46 vs. 0.62) (p < 0.01), as well as the use of rescue medication during the day (p < 0.001). Early introduction of low doses of ICS may be more beneficial than beta2 agonists alone in patients with intermittent asthma.

[Bronchoalveolar lavage and pulmonary sarcoidosis].

INTRODUCTION: Bronchoalveolar lavage is a procedure of washing out of the lungs and the lavage fluid may contain different immunophenotypisation cells. Accordingly, the analysis of bronchoalveolar lavage fluid is an important part in diagnosis of interstitial lung diseases. The aim of this study was the examination of cellular composition of the lavage fluid in patients with lung sarcoidosis. MATERIAL AND METHODS This prospective study included 58 patients (30 women, 28 men), average age 42+ 10.32 years, who underwent standard biochemical analysis, lung radiography, lung function, analysis as well as analysis of cellular composition and immunophenotypisation of lavage fluid cells. RESULTS: 43/58 patients had the first radiological stage of sarcoidosis; 8/58 had second and 7/58 had third radiological stage of sarcoidosis. The majority of patients had preserved lung ventilation (71%), changes in small airways and obstructive ventilation disorder was established in 22% patients, and 7% of' patients presented with restrictive ventilation disorder. The pulmonary transfer factor for CO and transfer coefficient were reduced in 40/58 patients (69%), even in those with normal ventilation. The majority of patients 53/58 had hypercellular lavage fluid, 96.55% of patients had lymphocytic alveolitis (x 34%) in regard to relative reduction of alveolar macrophage (x 63%). The immunophenotypisation of lavage fluid done in 25 patients showed the domination of CD4+ lymphocyte (x 54%) and raised ratio CD4+/CD8+. CONCLUSION: Our results show that lymphocytic alveolitis is one of the best criteria in the diagnosis of pulmonary sarcoidosis.

[Correlation between bronchoalveolar lavage and lung function in patients with systemic sclerosis and rheumatoid arthritis].

Fibrous alveolitis (FA), or diffuse interstitial fibrosis, is used as a term for diseases in patients suffering from some kind of systemic connective tissue (SCT) disorder and lung fibrosis. FA is not unusual in clinical practice in patients with SS and rheumatoid arthritis (RA) and can be found in the definitive fibrosis phase of the disease; the early detection of FA is of great importance. The aim of this study was to determine whether there was a correlation between certain lung function parameters and cellular components of BAL in patients with SS and RA. Lung function (LF) and BAL examination was carried out in all 20 SS patients and 38 RA patients. LF was evaluated via spirometry, flow volume curves, the lung transfer factor for carbon monoxide (DLco), and the coefficient of transfer factor (K/DLco), as well as body plethysmography and blood gas analysis. A differential number of cells were taken in all BAL samples. Normal cellular components of lavage were found in 19 patients (50%). Ly-alveolitis was found in 10 patients (4 with SS and 6 with RA) (26%), and N-alveolitis in 9 patients (8 with SS and 1 with RA) (23.7%). An increased percentage of CD8+T lymphocytes in relation to CD4+T lymphocytes, and a decreased level of CD4+/CD8+ was found through BAL. Restrictive ventilation disorder was discovered in 6 patients (15.7%), TLC values were reduced in 6 patients (15.7%), and K/DLco was decreased in 5 patients. DLco was normal in 20 patients (53%) and reduced in 18 patients (47%). We discovered a significant correlation between DLco and cellular components (neutrophile or lymphocyte) present in BAL, but there was no significant correlation between other lung function parameters. Analysis of BAL and DLco examination can be considered to be suitable parameters of interstitial lung changes in SS and RA patients.