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Tokyo University Hospital, Tokyo, Japan
Correspondence to: Shinji Teramoto, MD, FCCP, Department of Geriatric Medicine, Tokyo University Hospital, 7-3-1 Hongo Bunkyo-ku, Tokyo, Japan 113-8655; e-mail: shinjit@umin.ac.jp
To the Editor:
The American Thoracic Society guidelines for community-acquired pneumonia have been widely introduced, however, the outcomes and the costs associated with adherence to these guidelines were very different in younger patients and older adults.1 Although the outcomes were better and the costs were lower among younger patients receiving guideline-recommended treatment than with those receiving other treatments, guideline-recommended treatment in elderly patients was less effective and costs were greater than with other treatments. Because the respiratory system and immune function are considerably affected by age, the recent review in CHEST by Chan and Welsh (December 1998)2 of the new field of "geriatric respiratory medicine" had very important information for all the physicians. Although the functional and structural alterations of the respiratory system with aging were concisely described in the article, the important issue of the aging lung was not discussed.
Because airspace enlargement, including ductectasia and loss of elastic recoil of the lung, is commonly investigated in aged humans without noxious insults,3 4 Verbeken and coworkers5 6 proposed that the changes in structural and functional characteristics caused by isolated airspace enlargement that are seen in the elderly, such as "senile lung" or aging lung, be differentiated from emphysema by the absence of alveolar wall destruction. Ductectasia and airspace enlargement without alveolar wall destruction were quantitatively assessed by the morphometric indices mean linear intercept and destructive index, while the loss of lung elastic recoil was assessed by the left-sided shifts of pressure-volume curves of lungs and by the exponential equivalent K. It is, therefore, important to understand the normal progression of the changes in respiratory function and the implications of the loss in pulmonary reserve for the elderly person with lung disease.7
However, it is difficult in human lungs to separate the true age effect (ie, physiologic aging) from the cumulative environmental effects (ie, the combination of physiologic and pathologic aging) since the human respiratory system is directly open to the environment, continuously exposing the lung to air and a variety of pollutants. Appropriate animal models are needed to study the senile lung/aging lung in relation to pathologic changes that occur with aging. Recently, the senescence-accelerated mouse (SAM) has been proposed as a good model to investigate the differences between the aging lung and cigarette smoke-related airspace enlargement.8 9 10 11 The airspace enlargement seen in senescence-prone strains of SAM with aging is not accompanied by alveolar wall destruction, so that senescence-prone strains of SAM are appropriate animal models for senile lung. The airspace enlargement induced by chronic exposure to cigarette smoke has been investigated in SAM-P strains in association with imbalances of oxidant-antioxidant and elastase-antielastase. The exploration of the differences in pathogenesis between progressive pulmonary emphysema and senile lung/aging lung may help to further our understanding of the significance and pathogenesis of airspace enlargement in elderly patients with respiratory diseases.
References
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