DLCO In Patients Research Articles

Deterioration of lung function is associated with presence of IgM rheumatoid factor and smoking in patients with systemic sclerosis

Smoking is a known risk factor for the development of several lung diseases, autoimmune diseases, and IgM rheumatoid factor (RF) in nonrheumatic persons. In patients with rheumatoid arthritis and IgM RF the diffusion capacity is decreased in smokers but not in nonsmokers. In the present study of patients with systemic sclerosis (SSc) the influence of smoking and IgM RF on the lung function was calculated. One hundred fifty-five persons with SSc had vital capacity (VC) and diffusing capacity (DLco) measured at least twice with at least 1-year interval as percents of predicted values according to gender, age, height, and weight. The yearly changes in VC and DLco were calculated, Delta VC and Delta DLco, respectively. IgM RF was measured at the beginning of the study. Smoking was defined as having ever smoked. Statistically significant deterioration of VC and DLco in patients with circulating IgM RF was found only in smokers or previous smokers, P = 0.007 and P = 0.01, respectively. These findings were confirmed by means of multiple regression analyses. The presence of IgM RF in smoking SSc patients is associated with deteriorating lung function. Whether this is a causal association and whether the presence of IgM RF in smoking patients with SSc actually confers an increased risk of pulmonary damage remains to be determined.

Interdialytic weight gain and pulmonary membrane diffusing capacity in patients on hemodialysis

Measurement of pulmonary diffusion capacity for carbon monoxide (DLCO) may be useful for assessing disease affecting the alveolar-capillary bed or the pulmonary vasculature. It was reported that hemodialysis (HD) therapy causes DLCO reduction via decrease of pulmonary capillary blood volume components. The aim of the study was to evaluate the effect of interdialytic weight gain on pulmonary function and especially DLCO. We further determined whether intravascular volume status, assessed by inferior vena cava diameter (IVCD) contributes to DLCO in patients on HD. Routine pulmonary function testing including forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1/FVC, forced mid-expiratory flow rate (FEF25-75), DLCO IVCD index and other echocardiographic parameters were evaluated in 20 patients (mean age 48.6+/-18.3 years, mean dialysis duration 17.4+/-19.2 months) on chronic HD, 1 hour after HD and after an interdialytic period (1 hour before HD therapy). Single-breath DLCO measurements were corrected for hemoglobin concentration (cDLCO). Routine pulmonary function tests (spirometry) showed no significant changes in FEV1, FVC and FEF25-75 whereas a statistically significant fall in FEV/FVC was found. At the end of the interdialytic period a statistically significant increase in weight, IVCD index, left ventriculer diastolic diameter (LVDD), and diastolic blood pressure (DBP) were observed (P < 0.05). Using the single-breath DLCO, we found unchanged cDLCO at the end of the interdialytic period. There was no correlation of cDLCO with increases in weight, DBP, IVCD index, LVDD (P > 0.05). The accumulation of body water between dialyses has no significant influence on DLCO.

Membrane and Capillary Blood Components of Diffusion Capacity of the Lung for Carbon Monoxide in Pulmonary Sarcoidosis: Relation to Exercise Gas Exchange

Resting pulmonary diffusing capacity of the lung for carbon monoxide (DLCO) is known to be the best predictor of arterial desaturation during exercise in patients with sarcoidosis. However, the relative contribution of each of the two components of DLCO-alveolar membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc)-remains unclear. To evaluate which component is responsible for the decrease of resting DLCO in patients with sarcoidosis, and to determine which resting pulmonary function test, including Dm and Vc, is the best predictor of gas exchange abnormalities during submaximal exercise. Prospective analysis of patients referred to our department of respiratory medicine. Twenty four patients with pulmonary sarcoidosis were separated into two groups according to chest radiographic findings: group 1, stages 2 and 3 (n = 15); group 2, stage 4 (n = 9). All the patients completed pulmonary function tests (flows, volumes, single-breath DLCO, transfer coefficient [Ka], Dm, Vc) and submaximal exercise (two steady-state levels of mild and moderate exercise corresponding respectively to a target oxygen consumption of approximately 10 to 15 mL/min/kg). DLCO was reduced in the two groups (group 1, 63 +/- 16% of predicted; group 2, 64 +/- 16% of predicted). Dm was severely decreased (group 1, 58 +/- 24% of predicted; group 2, 51 +/- 15% of predicted), whereas Vc was unchanged or only mildly decreased (group 1, 81 +/- 18% of predicted; group 2, 85 +/- 28% of predicted). Whatever the group of patients and the exercise level, Dm and DLCO were the strongest predictors (p < 0.001) of gas exchange abnormalities. Ka or volumes were weak predictors, and Vc or flows were not related with exercise gas exchange. This study demonstrates that a decrease in Dm mostly accounts for resting DLCO reduction, and that Dm as well as DLCO are highly predictive of gas exchange abnormalities at exercise in patients with sarcoidosis.

Visualization and Functional Consequence of Pulmonary Vascular Impairment in Patients With Rheumatic Diseases

Systemic rheumatic diseases impair the vasculature in lungs. The aim of this study was to visualize vascular impairment and determine its consequence on lung function. Seventy-two patients with rheumatic diseases were evaluated by pulmonary function tests, ventilation-perfusion scintigraphy, and thermography of the hands. The ventilation-perfusion mismatch of the lungs was visualized and quantified by calculating the ventilation-perfusion ratio (/) at each pixel. The microvascular impairment in fingers was assessed by the temperature difference between the nail fold and the dorsal hand. Patients with rheumatic diseases exhibited an increased / that distributed at the periphery of the lungs. The diffusing capacity of the lung for carbon monoxide (DLCO) decreased (mean [+/- SD], 76.4 +/- 27.4% of predicted) relative to the vital capacity (VC) [mean, 88.4 +/- 21.8% of predicted; p < 0.01] regardless of the presence or absence of interstitial lung disease (ILD). The distal-dorsal temperature difference showed colder fingers in patients with Raynaud phenomenon (mean temperature, - 0.6 +/- 2.1 degrees C) than in those without it (mean temperature, 0.3 +/- 1.5 degrees C) and significantly correlated with the ventilation-perfusion mismatch of the lungs both in patients with ILD (p = 0.04) and in those without ILD (p = 0.02). The ventilation-perfusion mismatch of the lungs significantly correlated with the relative reduction in DLCO evaluated by the percent DLCO/percent VC ratio both in patients with ILD (p < 0.01) and in those without ILD (p = 0.02). These results suggest that the periphery-distributed microvascular impairment in the lungs leads to ventilation-perfusion mismatch that functionally causes a relative reduction in DLCO in patients with rheumatic diseases. The reduction in DLCO relative to VC represents the vascular impairment in the lungs both in patients with ILD and in those without.

Static Lung Compliance as an Index of Early Pulmonary Disease in Systemic Sclerosis

Pulmonary function abnormalities constitute the most important cause of morbidity and mortality in patients with systemic sclerosis (SSc). A restrictive ventilatory defect with a reduction in pulmonary carbon monoxide diffusion capacity (DLCO) is the commonest finding. Static lung compliance (Cst) is perhaps the most sensitive parameter for the detection of abnormal pulmonary mechanics. We compared the results of Cst and DLCO in patients with SSc and normal spirometry to identify early pulmonary disease. Sixteen of 50 patients had normal spirometry, eight of whom had abnormal Cst. Four of them also had a reduced DLCO. Two patients had abnormal DLCO but their Cst was normal. One of them had pulmonary hypertension on echocardiography. We conclude that Cst was helpful in diagnosing early pulmonary abnormality in 50% of patients with normal spirometry. Among these patients Cst was a better index of abnormality than DLCO.

Low-Attenuation Areas of the Lungs on High-Resolution Computed Tomography in Asthma

To investigate the low-attenuation areas of the lungs (LAA) in asthma, we compared the mean lung density (MLD) and the LAA in 22 asthmatics (12 ex-smokers and 10 nonsmokers) and 13 patients with chronic obstructive pulmonary disease (COPD) by high-resolution computed tomography. The MLD and the relative area of the lung with attenuation values lower than −950 Hounsfield Units at full inspiration (inspiratory RA950) were significantly different in nonsmoking asthmatics compared to patients with COPD and asthmatics with a smoking history. The MLD and the RA950 correlated significantly with the FEV1 in all groups and with the DLCO in patients with COPD and asthmatics with a smoking history but not in nonsmoking asthmatics. We concluded that the LAA in asthmatics with a smoking history indicates the presence of emphysema, but in nonsmoking asthmatics it reflects hyperinflation and nonemphysematous expiratory airflow limitation rather than emphysematous lesions.

Lung membrane diffusing capacity, heart failure, and heart transplantation

The pulmonary diffusing capacity for carbon monoxide (DLCO) is reduced in chronic heart failure and remains decreased after heart transplantation. This decrease in DLCO may depend on a permanent alteration after transplantation of one or the other of its components: diffusion of the alveolar capillary membrane or the pulmonary capillary blood volume (Vc). Therefore, we measured DLCO, the membrane conductance, and Vc before and after heart transplantation. At the time of hemodynamic measurements, the Roughton and Forster method of measuring DLCO at varying alveolar oxygen concentrations was used to determine the membrane conductance, Vc, DLCO/alveolar volume (VA), the membrane conductance/VA and θVc/VA (θ = carbon monoxide conductance of blood, VA = alveolar volume) in 21 patients with class III to IV heart failure before and after transplantation, and in 21 healthy controls. Transplantation normalized pulmonary capillary pressure and increased cardiac index. DLCO was decreased before transplantation (7.11 vs 10.0 mmol/min/kPa in controls), but DLCO/VA was normal (1.67 ± 0.44 vs 1.71 ± 0.26 mmol/min/kPa/L in controls). DLCO/VA remained unchanged after transplantation, because the decrease in Vc (82 ± 30 vs 65 ±18 ml before and after transplantation) and θVc/VA was not compensated by the changes in membrane conductance (11 ± 4 vs 12 ± 5 mmol/min/kPa before and after transplantation, respectively) and membrane conductance/VA. We conclude that the decrease in DLCO in patients with chronic heart failure is due to a restrictive ventilatory pattern because their DLCO/VA remains normal; the decrease in the membrane conductance is compensated by the increase in Vc. After transplantation, the decrease in Vc due to normalization of pulmonary hemodynamics is not completely compensated for by an increase in membrane conductance. Because the membrane conductances, measured before and after transplantation, are negatively correlated with duration of heart failure, its abnormal pulmonary hemodynamics may have irreversibly altered the alveolar capillary membrane.

Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLCO). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLCO. Angiotensin-converting enzyme inhibition improves DLCO in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLCO is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 h and 1 and 2 months after starting enalapril treatment (10 mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLCO despite a decrease in VC. In group 2 patients, nitrates failed to improve DLCO and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.

Determinants of progression in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive form of lung disease with a median survival of less than 5 yr. To address the progressive nature of this disease process, we investigated the determinants of decrements in lung function in patients with IPF. We prospectively evaluated 39 subjects with IPF. Our study subjects were followed for an average of 2 yr (range, 49 to 1,883 days) and lung function was measured on at least two separate occasions (mean = 9.1 separate tests) during the follow-up period. Since IPF is characterized by reduced lung volume and abnormal gas exchange, our analysis focused on the determinants of total lung capacity (TLC) and diffusing capacity of carbon monoxide (DLCO) during the period of observation. Although, on average, there was a 5.3% increase in the TLC and a 9.8% increase in DLCO between the first and last measure of lung function, 25% of the study population experienced a decline in the TLC and 28% of the study population experienced a decline in the DLCO. Decrements in TLC were independently associated with severe dyspnea (p = 0.01) and treatment with cyclophosphamide (p = 0.03). Decrements in DLCO were significantly and independently associated with more pack-years of cigarette smoking (p = 0.02), moderate (p = 0.03) or severe (p = 0.02) dyspnea, and treatment with cyclophosphamide (p = 0.0002). These findings indicate that several clinical characteristics are independently associated with subsequent declines in TLC and DLCO in patients with IPF.(ABSTRACT TRUNCATED AT 250 WORDS)

A study on CO diffusing capacity with reference to pulmonary hemodynamics and ventilatory functions in patients with cardiac or chronic pulmonary disease

The pulmonary diffusing capacity (DL) is a value relating to the flow rate of gas across the alveolo-capillary membrane to the pressure gradient. In patients with cardio-pulmonary diseases, an impediment of DL is caused by many factors. The relationship between DL and plumonary hemodynamics or ventilatory functions was studied in order to clarify these f actors. Material and Methods In 14 normal subjects, 20 patients with cardiac valvular disease (mitral valvular disease 13 and aortic valvular disease 7), 15 patients with essential hypertension and 30 patients with chronic pulmonary disease (emphysema 9, asthma 16 and others), the pulmonary diffusing capacity for carbon monoxide (DLco) was measured by FILLEY'S steady state method. Right heart catheterization was performed simultaneously. Ventilatory functions were measured by 13.5 L Benedict-Roth respirometer. Results The average value of DLCO for 14 normal subjects was 15cc per minute per mmHg. These DLco values were divided by body surface area (DLco/M2), because DLco Was cor-related with BSA. Normal values for DLco/M2 were in a range from 9 to 11cc per minutes per mmHg per squaremeter BSA. A. DLco in patients with various cardiopulmonary diseases 1) Cardiac valvular diseases a) mitral stenosis and mitral insufficiency DLco was slightly decreased in all patients with mitral stenosis and mitral insufficiency (7∼9cc/min/mmHg/M2). b) mitral steno-insufficiency DLco Was markedly decreased in all patients except for one patient (4.3∼5.9cc/min/mm Hg/M2). c) aortic steno-insufficiency DLco was within normal limits in 3 patients and slightly decreased in 4 patients (6.5∼8.5 cc/min/mmHg/M2). 2) Essential hypertension DLco was within normal limits in 6 patients, slightly decreased in 8 patients (6.8∼8.9cc/ min/mmHg/M2) and moderately decreased in one patient (5.7 cc/min/mmHg/M2).