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: email@example.com
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
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.8–11 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.
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