To investigate the role of airflow limitation on the increase of end-expiratory lung volume (EELV) during bronchoconstriction, nine stable asthmatic subjects and seven healthy subjects were challenged with inhaled methacholine (MCh). Changes in airway caliber were assessed by using forced expiratory volume in 1 s, partial forced expiratory flow at 50% of control forced vital capacity, and specific airway conductance. To detect airflow limitation, tidal flow-volume curves were superimposed on partial forced flow-volume curves at absolute lung volume. The electromyogram of the diaphragm was recorded by surface electrodes in four asthmatic and four healthy subjects, and the electrical diaphragmatic activity (DIA) during expiration was expressed as a percentage of the duration of expiratory time. In 10 subjects (9 asthmatic and 1 healthy) the partial forced expiratory flow recorded after some MCh dose impinged on tidal expiratory flow recorded before MCh. When this occurred it was associated with an increase in EELV by 0.54 +/- 0.07 (SE) liter (P < 0.001), which was larger than that occurring when lower MCh doses (0.11 +/- 0.04 liter, P < 0.05) were used, and with a moderate increase in DIA of 15 +/- 2.5% (P < 0.01). Six healthy subjects did not increase EELV after MCh despite a significant degree of bronchoconstriction; in these subjects tidal expiratory flow never impinged on forced expiratory flow, and DIA never increased. These results suggest that hyperinflation during MCh-induced bronchoconstriction is triggered by dynamic compression of the airways and is associated with moderate increase of DIA during expiration.
Two groups of subjects were studied: one with (group 1: 5 healthy and 4 mildly asthmatic subjects) and another without (group 2:9 moderately and severely asthmatic subjects) a plateau of response to methacholine (MCh). We determined the effect of deep inhalation by comparing expiratory flows at 40% of forced vital capacity from maximal and partial flow-volume curves (MEF40M/P) and the quasi-static transpulmonary pressure-volume (Ptp-V) area. In group 1, MEF40M/P increased from 1.58 +/- 0.23 (SE) at baseline up to a maximum of 3.91 +/- 0.69 after MCh when forced expiratory volume in 1 s (FEV1) was decreased on plateau by 24 +/- 2%. The plateau of FEV1 was always paralleled by a plateau of MEF40M/P. In group 2, MEF40 M/P increased from 1.58 +/- 0.10 at baseline up to a maximum of 3.48 +/- 0.26 after MCh when FEV1 was decreased by 31 +/- 3% and then decreased to 2.42 +/- 0.24 when FEV1 was decreased by 46 +/- 2%. Ptp-V area was similar in the two groups at baseline yet was increased by 122 +/- 9% in group 2 and unchanged in group 1 at MCh end point. These findings suggest that the increased maximal response to MCh in asthmatic subjects is associated with an involvement of the lung periphery.
We hypothesized that maximal bronchoconstriction can be predicted from the bronchomoter effect of deep inhalation (DI) and the degree of airway sensitivity to methacholine (MCh). We studied 26 healthy or mildly asthmatic subjects with limited response to MCh (maximal FEV1 decrease, 23 +/- 9 SD%; Group 1) and 26 subjects with moderate to severe asthma with exaggerated response (maximal FEV1 decrease > 40%, Group 2). The effect of DI was quantified as the linear regression coefficient of the percent decrements of maximal (Vm50) versus partial (Vp50) forced expiratory flow at 50% of FVC over the initial steps of challenge (MP slope). Airway sensitivity was inferred from the MCh doses (PDs) causing Vm50 or Vp50 to decrease by 40% or FEV1 by 15%. The absence of limit to bronchonstriction was predicted by either MP slope or any PD with accuracies between 71 and 81%, but with an accuracy of 87% by a discriminant function including MP slope and PD40Vp50. Within Group 1, the maximal FEV1 decrease correlated linearly with MP slope (r2 = 0.41); but it was better predicted by a multiple regression including MP slope and PD40Vp50 (In mg) (r2 = 0.54). We conclude that the magnitude of the bronchodilator effect of DI during induced bronchoconstriction and airway sensitivity predict the level of maximal bronchoconstriction in vivo. We speculate that these parameters reflect some of the mechanisms modulating the response to bronchoconstrictor stimuli such as airway wall structure, airway-to-parenchymal interdependence, and contractile properties of airway smooth muscle.
One hundred six patients with histologically proven bronchogenic carcinoma were tested for carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), and carbohydrate antigenic determinant 19-9 (CA19-9). A total of 349 CEAs, 350 TPAs, and 317 CA19-9s were measured. In addition, sera were assayed from 57 patients with pulmonary benign diseases and their CEA, TPA, and CA19-9 levels were used as negative controls for specificity and accuracy. One hundred twenty healthy subjects provided our normal CA19-9 reference value. Sensitivity, specificity, and accuracy were obtained for CEA, TPA, and CA19-9, respectively. Significant intermarker correlations were found both at diagnosis and during follow-up, CEA and CA19-9 being the most closely related substances. The percentage of patients with elevated levels of TPA increased significantly according to tumor load. Individual values of TPA related significantly to the stage of disease. Concentrations of CEA, TPA, and CA19-9 varied significantly during the course of the illness in relation to treatment response; however, TPA showed the closest relationship to the clinical status assessments of the follow-up period. Abnormal pretreatment levels of TPA were significantly associated with a poor outcome. Biomarker combinations were clinically evaluated by calculating the mean of the percentage of the reference value for each combined marker. Using this method, any association of TPA with CEA and/or CA19-9 revealed neither a greater diagnostic accuracy nor a more reliable predictive capacity for the above clinical variables than TPA evaluated on its own. The authors believe that a single TPA assay should be added to the initial and subsequent clinical assessments of patients with bronchogenic carcinoma.
In 98 newly diagnosed patients with histologically proven bronchogenic carcinoma seen at Cuneo Hospital of Chest Diseases from July 1983 to December 1984, multiple biomarker assays were performed. Fiftynine cases had more than one carcinoembryonic antigen (CEA) and/or tissue polypeptide antigen (TPA) assay during the course of the disease, at 3- to 12-week intervals. A total of 209 CEA (91 pretreatment), 170 TPA (80 pretreatment), 62 human chorionic gonadotropin (HCG)-beta subunits and 60 lactate dehydrogenase (LDH) was assayed. In addition, serum samples were taken from 141 blood donors and their TPA values were used as a control. The percentages of elevated values were, respectively, 37%, 52%, 18%, and 25%. In 85% of the patients at least one biomarker was found to be higher than normal. Neither significant differences between mean biomarker levels in tumors of various histologic types nor positive intermarker correlations were found. The number of patients with elevated CEA, TPA, and LDH serum levels and their mean values increased significantly according to the disease extent. Among evaluated markers TPA showed the highest accordance to tumor burden. The raising of two markers was never associated with Stage I-II disease, except in one patient. Both CEA and TPA concentrations changed significantly during the course of the illness in relation to the clinical status assessment. Abnormal pretreatment levels of CEA, LDH, and particularly, TPA were independently and significantly associated with a poor outcome. Patients with abnormal levels of TPA and LDH and, to a lesser degree, TPA and beta-HCG had shorter survival as compared with patients with high TPA values, irrespective of the LDH and beta-HCG levels, although not significantly so.
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