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Pulmonary function in healthy young adult Indians in Madras.

Forced vital capacity, forced expiratory volume in one second, functional residual capacity, residual volume, total lung capacity, and single breath diffusing capacity measurements (effective alveolar volume, carbon monoxide transfer factor, and transfer coefficient) were measured in 247 young healthy adults (130 male, 117 female) aged 15-40 years living in Madras. Subjects were of Dravidian stock, living at sea level with rice as their staple diet. Regression equations were derived for men and women for predicting normal pulmonary function for young adults in South India. The values were similar to those reported for subjects from Western India and lower than those reported for North Indians and caucasians.

Adolescent↗

Pulmonary function is diminished in older asymptomatic smokers and ex-smokers with low attenuation areas on high-resolution computed tomography.

OBJECTIVES: The relation between pulmonary function and low attenuation areas (LAAs) on high-resolution computed tomography (HRCT) is not clear in subclinical pulmonary emphysema. Accordingly we examined pulmonary function and HRCT in asymptomatic community-based volunteers. DESIGN: The existence of LAAs on CT was evaluated independently by three respiratory physicians who were blind to the pulmonary function test data and smoking histories of the subjects. The LAA grade was assessed by a visual scoring method from 0 to 5, and the individual LAA score and the values of pulmonary function tests were compared. PARTICIPANTS: 57 subjects aged from 32 to 82 years [mean 62 +/- (SD) 11] years were enrolled in the study. RESULTS: LAAs were found in 20 of the 49 subjects who were current or ex-smokers but in none of the 8 who never smoked. LAAs observed were mostly less than 25% of the total areas of the lungs. Although all mean values were within normal limits, the forced expiratory volume in 1 s (%pred), maximal expiratory flow at 50% of forced vital capacity (%pred), diffusing capacity of the lungs for carbon monoxide (DLCO; %pred) and diffusing capacity for carbon monoxide per unit alveolar volume (DLCO/VA; %pred) were all significantly less in those with LAAs than in those without LAAs. There was also a significant tendency for DLCO %pred and DLCO/VA %pred to decrease as the LAA scores increased. CONCLUSION: Those who have LAAs on CT have a small but significant deterioration in pulmonary function tests even if the LAAs observed are minimal or mild in degree. Longitudinal studies will be necessary to determine whether LAAs on CT identify the subjects who will develop airflow obstruction over time.

Adult↗

Characteristics of pulmonary function in patients with diabetes mellitus.

The incidence of pulmonary diseases among diabetics in Japan has been found to be more than 50% at death. This suggests the existence of some pulmonary risk factors. We analyzed pulmonary functions in 50 diabetics (31 males and 19 females) without overt lung disease, compared to 21 healthy male subjects of the same age (around 50 years old). Forced vital capacity and timed vital capacity were lower in diabetics (P less than 0.005). Diffusing capacity was also decreased in male diabetics (P less than 0.05). Among diabetics, a decrease in the diffusing capacity was dominant in patients with diabetic retinopathy, which correlated with an increasing duration of their diabetes. Analysis by the partial correlation method which accounts for the smoking index showed that standardized indices for peripheral airflow in male diabetics decreased significantly as the patient's age increased (P less than 0.005); the rate of decrement was greater than that of the control subjects. Diabetic patients showed abnormal lung function in the peripheral airways which increased with age and gas transfer was also affected by diabetic microangiopathy as well as the duration of diabetes. These changes seemed to deteriorate progressively, possibly combining and contributing to respiratory insufficiency in critical pathological conditions.

Adult↗

Pulmonary function in sickle cell disease with or without acute chest syndrome.

Recurrent acute chest syndrome (ACS) has been suggested as a risk factor for chronic lung dysfunction in sickle cell disease. To investigate this hypothesis, lung function tests were performed in 49 sickle cell disease outpatients whose condition was stable, including 23 patients with a history of two to four episodes of ACS (ACS+) and 26 with no history of ACS (ACS-). The two groups were comparable regarding the sex ratio, body mass index, smoking history, physical characteristics, clinical history and usual lung function tests. Respiratory resistance (Rrs), measured using the forced oscillation technique, increased with the number of ACS episodes (r=0.55, p<0.0001) and a significant relationship was observed between Rrs as an independent variable and the expiratory flow rates at 25, 50 and 25-75% of the forced vital capacity as explanatory variables (r= 0.36, p<0.02; r=0.35, p<0.02; and r=0.4, p<0.006, respectively), with higher Rrs being associated with lower expiratory flow rates. The transfer factor (TL,CO) and transfer coefficient (KCO) for CO were significantly higher in the ACS+ group than in the ACS-group (TL,CO=84+/-4 versus 71+/-3%, p<0.004 and KCO=102+/-5 versus 90+/-3%, p<0.05, respectively). The data demonstrate that obstructive lung dysfunction is fairly common in sickle cell disease and suggest that recurrent acute chest syndrome may contribute specific obstructive defects. The increase in respiratory resistance associated with acute chest syndrome was accompanied by an increase in diffusion capacity, suggesting that it may have been related to an increase in lung blood volume.

Acute Disease↗

Evolving strategies in lung transplantation for emphysema.

Evolving strategies of pulmonary preservation, bronchial revascularization, immunosuppression, and infectious disease management were used in 15 initial consecutive patients undergoing lung transplantation for emphysema. There were 10 women and 5 men with a mean age of 49 years (range, 36 to 60 years). All patients required supplemental oxygen therapy. One bilateral, 9 left, and 5 right transplantations were performed. Mean preoperative forced expiratory volume in 1 second and total lung capacity were 16% and 146%, respectively, of predicted. Quadruple drug immunosuppression was used. Actuarial 1-year survival in this initial series is 93.3% +/- 6.4% (Kaplan-Meier) with one early cardiac death at day 71. Mean forced expiratory volume in 1 second and diffusing capacity for carbon monoxide at discharge were 43% and 62%, respectively, of predicted. Rehabilitation has been excellent, and all survivors are active and free of supplemental oxygen. During the study, the following treatment strategies have evolved: (1) University of Wisconsin solution has replaced Euro-Collins' solution for pulmonary preservation; (2) direct bronchial revascularization with the internal thoracic artery now is used; (3) an algorithm-based variable dose OKT3 induction regimen has resulted in a major reduction in dosage; and (4) infectious disease management focuses on the prophylaxis of cytomegalovirus and fungal infection using prolonged ganciclovir and early itraconazole therapy as well as the avoidance of Epstein-Barr virus mismatches. Single-lung transplantation for emphysema has excellent early results with continuing evolving management strategies.

Adenosine↗

Pi-Z phenotypes in a pulmonary clinic. Their prevalence and physiologic state.

A series of 1,458 consecutive patients referred to the Cleveland Veterans Administration Pulmonary Clinic for pulmonary function studies was evaluated for alpha 1-antitrypsin deficiency by determination of serum trypsin inhibitory capacity (STIC). Protease inhibitor (Pi) phenotyping was performed on all sera with STIC values less than 1.6 mg/ml. The following non-MM phenotypes were found: 1FZ, 32MZ, 2ZZ, 3SZ, 5SS, 33MS, 21M. The prevalence of Pi Z heterozygosity is 2.74%. This figure is not significantly greater than that observed in a healthy population. A group ( n = 12) with heterozygous Z phenotype (MZ + SZ) was compared with a control (MM) group (n = 13) matched for age, race and smoking history from this same population. Our findings indicate similar deviations from predicted normal values in both control (MM) and Z-heterozygotic groups for physiologic tests of airway resistance, lung volumes, diffusing capacity, and static and dynamic compliance. There was no significant difference between MM controls and MZ heterozygotes in the physiologic variables measured.

Adult↗

Exhaled nitric oxide in chronic obstructive pulmonary disease: relationship to pulmonary function.

The following study was undertaken in order to determine how exhaled nitric oxide (eNO) levels in former smokers with chronic obstructive pulmonary disease (COPD) compared to eNO levels in patients with asthma and in healthy nonsmoking volunteers. The study also aimed to determine any relationship between eNO levels in COPD and: 1) conventional measures of lung function; and 2) inhaled corticosteroid (ICS) use. In former smokers with COPD, nonsmokers with asthma and volunteers, eNO levels, spirometry, lung volumes, carbon monoxide diffusion capacity of the lung (DL,CO) and resting oxygen saturation (Sa,O2) were measured. Median eNO was significantly higher among patients with COPD than among healthy volunteers (p = 0.003) but lower than among patients with asthma (p < 0.01). There was no significant difference in eNO levels between COPD patients using ICS and those not using ICS. By contrast, eNO was lower among asthma patients who used ICS (median 32 parts per billion (ppb); 25-75% range 16-54) than among asthma patients who did not (51 ppb; 32-87) (p = 0.034). Among patients with COPD, eNO was inversely correlated with forced expiratory volume in one second, DL,CO and Sa,O2, and was positively correlated with the residual lung volume/total lung capacity ratio. Among patients with asthma, no significant correlations were found. Exhaled nitric oxide is increased in patients with chronic obstructive pulmonary disease, an increase that is influenced by structural abnormalities of tobacco-induced lung damage.

Administration, Inhalation↗

Pulmonary diffusion abnormalities in heart transplant recipients. Relationship to cytomegalovirus infection.

Lung function of patients with heart failure is characterized by a variety of changes proposed as being due to passive congestion, secondary pulmonary fibrosis, and/or recurrent pulmonary emboli. A diffusion impairment thought to be due to cyclosporine has also been noted in patients following heart transplantation. Similar changes of unclear origin have been observed in renal transplant recipients. The objective of this study was to determine the extent to which lung function changes are reversible by cardiac transplantation and relate changes to the status of the recipients lung in the presence of possible vascular, iatrogenic, immune, or infectious injury. We analyzed the data of 22 patients who underwent lung function testing before and after heart transplantation and correlated changes to hemodynamic change, episodes of rejection, concentration of cyclosporine, and cytomegalovirus infection. Despite excellent graft function, the carbon monoxide transfer factor deteriorated to a mean of 57 percent of predicted postoperatively. The fall in diffusion factor did not correlate with episodes of cardiac rejection, cyclosporine levels, or hemodynamic status. In those patients who had serologic evidence of cytomegalovirus infection, the reduction in transfer factor was greater compared to those without infection despite a normal chest radiograph. The effects of cardiopulmonary bypass were unlikely to have been responsible for the abnormalities as lung function was assessed at a mean of 14 months after surgery. In heart transplant recipients, a change in diffusion capacity may represent an additional marker for cytomegalovirus infection and reflect infectious/immune injury late following surgery.

Cyclosporine↗

Use of pulmonary function tests in the management of sarcoidosis.

The literature on pulmonary function testing in sarcoidosis is critically reviewed. The results indicate that pulmonary function tests are not a reliable means for detecting the presence of parenchymal sarcoidosis, nor do they provide an accurate estimate of the extent of parenchymal disease. There are at present no known pulmonary function criteria that allow the clinician to predict the natural cause of pulmonary sarcoidosis or the response to therapy. The major value of pulmonary function testing is to assess changes in the disease course of the individual patient through sequential measurements. Currently there is no conclusive evidence that measurements of arterial blood gas tensions or pulmonary compliance add significantly to the sensitivity and specificity of the vital capacity and diffusing capacity in the management of sarcoidosis.

Adrenal Cortex Hormones↗

Bronchiolitis obliterans with organizing pneumonia.

In 1955, Epler and Colby first described idiopathic bronchiolitis obliterans with organizing pneumonia. Davison and colleagues termed the entity cryptogenic organizing pneumonia. Clinically, the disease resembles a flu-like syndrome of acute or subacute onset. Other features include crackles, patchy infiltrates on chest radiograph, restrictive function, and decrease in diffusing capacity. Most cases of idiopathic bronchiolitis obliterans with organizing pneumonia (BOOP) respond dramatically to corticosteroids. However, some patients deteriorate rapidly. Differences between idiopathic or secondary BOOP and other interstitial lung diseases are vast. CT findings and bronchoalveolar lavage fluid lymphocytosis are helpful in differentiating BOOP from idiopathic pulmonary fibrosis.

Adrenal Cortex Hormones↗

The effect of transfusion on pulmonary function in patients with thalassemia major.

Pulmonary involvement has been documented in thalassemia major (TM). We studied 12 patients with TM before and 24 hr after transfusion to evaluate the effect of transfusion on baseline lung function. Personal and family histories of respiratory illnesses were obtained by a questionnaire. Spirometry and carbon monoxide diffusion capacity (KCO) measurements were made. Blood gases (PO2 and SO2) were determined on arterialized samples. Baseline expiratory volumes and flows were within normal range in all patients. Transfusion resulted in a significant reduction of forced expiratory volume in 1 sec (FEV1) and forced expiratory flow between 25 and 75% vital capacity (FEF25-75%). In two subgroups of patients identified by the questionnaire, those with no history of airway disease had normal baseline flows and no posttransfusion changes; those with history of airway obstruction had lower pretransfusion flows and significantly decreased posttransfusion FEV1 and FEF25-75%. The mean pretransfusion KCO value of 80% predicted for the whole group, significantly increased after transfusion (P < 0.05). Blood gases also significantly increased after transfusion (P < 0.05). When tested for the spirometric response to albuterol, patients with a history of asthma had a slightly greater increase in FEV1 and FEF25-75% than those who had never had asthma. We conclude that in our small study group, transfusion resulted in improved gas exchange and lung perfusion. The effect on flow limitation evident in some patients could, in part, be related to a preexisting bronchial hyperreactivity. Accurate evaluation of pulmonary function and of bronchial reactivity is advisable for patients with TM.

Adolescent↗

Reducing lung strain after pneumonectomy impairs oxygen diffusing capacity but not ventilation-perfusion matching.

After pneumonectomy (Pnx), mechanical strain on the remaining lung is an important signal for adaptation. To examine how mechanical lung strain alters gas exchange adaptation after Pnx, we replaced the right lung of adult dogs with a custom-shaped inflatable silicone prosthesis. The prosthesis was kept 1) inflated (Inf) to reduce mechanical strain of the remaining lung and maintain the mediastinum in the midline, or 2) deflated (Def) to allow lung strain and mediastinal shift. Gas exchange was studied 4-7 mo later at rest and during treadmill exercise by the multiple inert gas elimination technique while animals breathed 21 and 14% O2 in balanced order. In the Inf group compared with Def group during hypoxic exercise, arterial O2 saturation was lower and alveolar-arterial O2 tension difference higher, whereas O2 diffusing capacity was lower at any given cardiac output. Dispersion of the perfusion distribution was similar between groups at rest and during exercise. Dispersion of the ventilation distribution was lower in the Inf group at rest, associated with a much higher respiratory rate, but rose to similar levels in both groups during hypoxic exercise. Mean pulmonary arterial pressure at a given cardiac output was higher in the Inf group, whereas peak cardiac output was similar between groups. Thus creating lung strain by post-Pnx mediastinal shift primarily enhances diffusive gas exchange with only minor effects on ventilation-perfusion matching, consistent with the generation of additional alveolar-capillary surfaces but not conducting airways and blood vessels.

Animals↗

Pulmonary function in chronic heart failure. Changes after heart transplantation.

To investigate the impact of chronic heart failure on pulmonary function in heart transplant recipients, pulmonary function was evaluated in 41 consecutive patients (mean age 43 years, range 15-57 years) before and 6 months after successful heart transplantation. The pulmonary function tests included measurements of forced vital capacity [FVC], forced expiratory volume in 1.s [FEV1], FEV1/FVC ratio, total lung capacity [TLC], and diffusion capacity for carbon monoxide [TLCO] and KCO [TLCO per l alveolar volume]. Compared to pretransplant values, spirometry after transplantation revealed modest improvements in FVC (from 77 +/- 16 to 88 +/- 21% of predicted [%pred]; p < 0.001) and FEV1 (from 75 +/- 16 to 85 +/- 22%pred; p < 0.001), whereas the FEV1/FVC ratio was unchanged (81% +/- 11 and 80% +/- 10; p = NS). A slight but statistically significant increase in TLC (from 78 +/- 15 to 86 +/- 18%pred, p < 0.001) was also observed. Prior to transplantation the mean TLCO was 76 +/- 17%pred; 7 of the patients had a TLCO below 60%pred (mean 51% pred). In 33 of the 41 patients a reduction in TLCO was observed after transplantation; for all 41 patients the mean fall in TLCO was 14% of the predicted value (SD 12%pred) (p < 0.0001). Likewise, a significant reduction in KCO was noted (p < 0.0001). Multiple regression analysis revealed that high pretransplant TLCO %pred (p = 0.02) and FVC %pred (p = 0.04) were associated with a less favorable outcome concerning posttransplant TLCO %pred. Although normalization of FEV1, FVC and TLC can be anticipated after correction of severe chronic left ventricular failure by heart transplantation, the pronounced concomitant decline in diffusion capacity observed in this study may be explained by underlying pulmonary disease caused by factors other than long-standing heart failure. Our findings support the notion that pulmonary function abnormalities attributable to chronic heart failure should not preclude consideration for heart transplantation.

Adolescent↗

Subacute and chronic bird breeder hypersensitivity pneumonitis: sequential evaluation with CT and correlation with lung function tests and bronchoalveolar lavage.

PURPOSE: To evaluate lung involvement in the subacute (group 1) and chronic (group 2) stages of bird breeder hypersensitivity pneumonitis. MATERIALS AND METHODS: Computed tomographic (CT) findings in 45 patients were correlated with pulmonary function testing and bronchoalveolar lavage. Twenty-seven patients underwent sequential CT examination 0.3-4 years apart, with functional evaluation in 20 of them. RESULTS: In group 1, CT showed diffuse micronodules, ground-glass attenuation, focal air trapping or emphysema, and mild fibrotic changes, with normal lung volumes but impaired diffusing capacity and a predominant lymphocyte alveolitis. In group 2, two categories of chronic forms were identified at CT on the basis of presence or absence of honeycombing. After cessation of exposure, CT showed a return to normal or dramatic improvement in group 1 and considerable reduction in ground-glass attenuation and micronodules in group 2. CT depicted no fibrotic or emphysematous changes during follow-up. CONCLUSION: Subacute bird breeder hypersensitivity pneumonitis may share CT features with other types of hypersensitivity pneumonitis. CT may help in identification of emphysematous and fibrotic forms of chronic disease.

Acute Disease↗

Lung CT density correlates with measurements of airflow limitation and the diffusing capacity.

We studied 80 subjects (63 M, 17 F; 23-82 yrs) and related lung computerized tomography (CT) density with age, height, spirometry, lung volumes, diffusing capacity and arterial blood gas tensions. These subjects demonstrated a wide range of physiological impairment (forced expiratory volume in one second (FEV1) 8-116% predicted; diffusing capacity (Kco) 15-139% predicted; arterial oxygen tension (Pao2) 38-91 mmHg). They ranged from normal subjects to patients with chronic respiratory failure. Lung density was derived from CT density histograms measured as both mean Emergency Medical Information (EMI) number (EMI scale: 0 = water, -500 = air, EMI number of normal lung tissue range approximately -200 to -450) and the lowest 5th percentile EMI number, the latter value being more likely to represent the density of lung parenchyma. Lung CT density correlated most strongly with airflow obstruction (EMI 5th percentile versus FEV1/forced vital capacity (FVC) % predicted, r = 0.73, p less than 0.001) and diffusing capacity (EMI 5th percentile versus Kco, r = 0.77, p less than 0.001). This suggests that reduction in lung density, which reflects loss of the surface area of the distal airspaces, is a major index of respiratory function in patients with smoking related chronic obstructive pulmonary disease (COPD). These data provide no indication of other factors such as small and large airways disease, and loss of elastic recoil, which may contribute to airflow limitation, or disruption of the pulmonary vascular bed which may also affect CT lung density.

Adult↗