Measured Diffusion Capacity versus Prediction Equation Estimates in Blacks without Lung Disease.

摘要

Background: Lung volumes in African-Americans are on average 10-15% less than in Caucasians for the same height and are race corrected accordingly. Despite this fact, prediction equation estimates (PEE) of diffusion capacity of CO (DL(CO)) developed in Caucasians are not adjusted for lung volume in the black population. This could result in healthy blacks being labeled as abnormal. Objective: To test the hypothesis that healthy black subjects might be labeled as abnormal using three commonly used PEE of DL(CO) which are currently used in the United States. Methods: Forty-two nonsmoking black subjects with no history of any disease underwent DL(CO) testing. Controls consisted of 12 healthy Caucasian volunteers and the prediction equations themselves. The single breath diffusion capacity was used with a Collins system. The measured diffusing capacity was compared with the Miller, Knudson, and Crapo PEE by entering age, gender, height and weight for each subject into the appropriate equation. Abnormal wasdefined as a DL(CO) <80% predicted. Methane gas dilution and body plethysmography were used to determine alveolar volume. Values in parentheses in the results section are DLCO adjusted for alveolar volume proportions. Results: The average measured DL(CO) in blacks was 25.85 +/- 6.37 ml/min/mm Hg. This value was significantly different (p < 0.01) compared to the predicted DL(CO) of 29.80 +/- 4.77, 36.45 +/- 6.64, and 35.33 +/- 5.27 for the Miller, Knudson, and Crapo equations, respectively. This resulted in 14/42 (0/42), 33/42 (3/42), and 33/42 (9/42) DL(CO) (DL(CO)/VA) measurements being defined as abnormal using the Miller, Knudson, and Crapo prediction equations, respectively. In Caucasians, the average measured DL(CO) was not different from the Miller PEE. However, the measured DL(CO) was significantly lower than the Knudson and Crapo PEE, although less so than in blacks. This resulted in no Caucasian DL(CO) measurements defined as abnormal with the Miller PEE and some with the Knudson and Crapo PEE, but less so than in blacks. The measured alveolar volumes by methane dilution were slightly but not significantly decreased compared to those determined by plethysmography. Both measured values were significantly different (p < 0.01) compared to the predicted alveolar volumes of 6.19 +/- 0.91, 6.38 +/- 1.07, and 6.05 +/- 0.96 liters for the Miller, Knudson, and Crapo PEE in blacks, with no difference in predicted and measured lung volumes in Caucasians. The difference in predicted versus measured DL(CO) measurements in blacks was 13.2, 29.1, and 26.8%, respectively, for the Miller, Knudson, and Crapo prediction equations. These differences were similar to the reduction in predicted values of 22.5, 24.7, and 20.7% for the above-mentioned prediction equations, respectively, versus the measured alveolar volume by methane (in blacks). A race correction (reduction) of the Miller PEE for diffusion of 12% resulted in only 2/42 DL(CO) measurements being labeled as abnormal. Conclusions: Current PEE for DLCO when used in healthy blacks can result in an abnormal reading in up to 50% or more of the time. This failure of the PEE is related to a reduction in lung volume in African-Americans that is not accounted for. One approach to overcome this problem, until separate PEE are developed in blacks, is to race correct the Miller PEE for diffusion by 12%. This reduces the DL(CO) error to less than 5% for this population. Copyright (c) 2004 S. Karger AG, Basel.