Ellen L Burnham1, Raghuveer Halkar, Marsha Burks, Marc Moss. 1. Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Denver and Health Sciences Center, Denver, CO, USA. ellen.burnham@uchsc.edu
Abstract
AIMS: Alcohol abuse is associated with the development of the acute respiratory distress syndrome, a disorder characterized by abnormal alveolar-capillary permeability. We hypothesized that individuals with a history of alcohol abuse would have clinical evidence of abnormal alveolar-capillary permeability even in the absence of symptoms. This could contribute to their propensity for the development of this disorder. METHODS: Thirty-three subjects with a history of alcohol abuse, but no other medical problems, and 13 age- and smoking-matched controls inhaled (99m)Tc-DTPA (technetium-labeled diethylenetriamine penta-acetate; an isotope used to measure lung permeability) for a 3-min period, and washout of this isotope was measured for a 90-min period. The rate at which it was cleared from the lungs was assessed and compared between subjects and controls. RESULTS: The half-life of (99m)Tc-DTPA in the lungs of subjects with alcohol abuse was significantly shorter than that observed in matched controls, even when correcting for the effects of concomitant tobacco use. When the half-life of the isotope for smoking alcohol-abusing subjects and smoking controls were compared separately, there was a trend for the alcohol-abusing subjects to have a shorter half-life of the isotope present in the lungs. This was also true when non-smokers were compared. CONCLUSIONS: These observations provide further evidence that alcohol abuse affects the normal permeability of the alveolar-capillary barrier and thereby may contribute to the development of the acute respiratory distress syndrome in individuals with alcohol abuse.
AIMS: Alcohol abuse is associated with the development of the acute respiratory distress syndrome, a disorder characterized by abnormal alveolar-capillary permeability. We hypothesized that individuals with a history of alcohol abuse would have clinical evidence of abnormal alveolar-capillary permeability even in the absence of symptoms. This could contribute to their propensity for the development of this disorder. METHODS: Thirty-three subjects with a history of alcohol abuse, but no other medical problems, and 13 age- and smoking-matched controls inhaled (99m)Tc-DTPA (technetium-labeled diethylenetriamine penta-acetate; an isotope used to measure lung permeability) for a 3-min period, and washout of this isotope was measured for a 90-min period. The rate at which it was cleared from the lungs was assessed and compared between subjects and controls. RESULTS: The half-life of (99m)Tc-DTPA in the lungs of subjects with alcohol abuse was significantly shorter than that observed in matched controls, even when correcting for the effects of concomitant tobacco use. When the half-life of the isotope for smoking alcohol-abusing subjects and smoking controls were compared separately, there was a trend for the alcohol-abusing subjects to have a shorter half-life of the isotope present in the lungs. This was also true when non-smokers were compared. CONCLUSIONS: These observations provide further evidence that alcohol abuse affects the normal permeability of the alveolar-capillary barrier and thereby may contribute to the development of the acute respiratory distress syndrome in individuals with alcohol abuse.
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