Document 364143

the individual hosts response to the MAC after
After
exposure? all, these are not called atypical mycobacteria for
exposure
or
nothing.
John M. Embil, MD, FRCPC
C.P.W. Warren, MB, FRCPC
Department of Medicine
University of Manitoba Health Sciences Centre
Winnipeg, Manitoba, Canada
References
1 Embil J, Warren P, Yakrus M, et al. Pulmonary illness
2
3
4
5
6
7
associated with exposure to Mycobacterium avium complex in
hot tub water: hvpersensitivitv pneumonitis or infection?
Chest 1997; 111:813-16
Kahana LM, Kay JM, Yakrus MA, et al. Mycobacterium
avium complex infection in an immunocompetent young
adult related to hot tub exposure. Chest 1997; 111:242-45
Lynch DA, Rose CS, Way D, et al. Hvpersensitivitv pneumo¬
nitis: sensitivity of high-resolution CT in a population-based
159:469-72
study. AJR 1992;
Schuyler M, Cormier MY. The diagnosis of hypersensitivity
Chest 1997; 111:534-36
pneumonitis.
Prince DS, Peterson DD, Steiner RM, et al. Infection with
avium complex in patients without predispos¬
Mycobacterium
ing conditions. N Engl J Med 1989; 321:863-68
due to
Rosenzweig DY. intracellulare-avium
Pulmonary7 mycobacterial infections
clinical fea¬
complex:
Mycobacterium
tures and course in 100 consecutive cases. Chest 1979;
75:115-19
Teirstein AS, Damsker B, Kirsclmer PA, et al. Pulmonary7
infection with Mycobacterium avium-IntraceUulare: Diagno¬
sis, clinical patterns, treatment. Mt Sinai J Med 1990; 57:
209-15
Scully RE, Mark EJ, McNeely WF, et al. Case 6-1996: case
records of the Massachusetts General Hospital. New Engl
J Med 1996; 334:521-26
9 Coleman A, Colby TV. Histologic diagnosis of extrinsic
allergic alveolitis. Am J Surg Pathol 1988; 12:514-18
8
Pulmonary Vascular Involvement in
Pulmonary Histiocytosis X
workload achieved=0.884-(0.0088XVdA^t at rest)-(0.002X
residual volume) + (0.0044XDco); r2=0.73]. We concluded that
the functional limitation in activity7 these patients experience, as
reflected by diminished exercise performance, may be due in
large part to pulmonary vascular involvement by the disease
process.
As yet, there have been no therapeutic trials with interventions
aimed at vasodilation as a primary treatment for this condition.
Our experience and that of Harari et al suggest that this might be
a useful avenue to pursue.
Robert S. Crausman, MD, FCCP
Memorial Hospital of Rhode Island
Pawtucket, Rhode Island
Talmadge E. King, Jr, MD, FCCP
National Jewish Medical and Research Center
Denver
References
1 Harari S, Brenot F, Barberis M, et al. Advanced pulmonary
histiocytosis X is associated with severe pulmonar)7 hyperten¬
sion [letter]. Chest 1997; 111:1142-43
2 Travis WD, Borok Z, Roum JH, et al. Pulmonary7 Langerhans
cell granulomatosis (histiocytosis X): a clinicopathologic study
of 48 cases. Am J Surg Pathol 1993; 17:971-86
3 Crausman RS, Jennings CA, Tuder RM, et al. Pulmonary
histiocytosis X: pulmonary function and exercise pathophysiol¬
ogy. Am J Respir Crit Care Med 1996; 153:426-35
Usefulness of Walking Test for
Arterial Oxygen Desaturation
Screening in General Population
To the Editor:
To the Editor:
We read with interest the communication by Harari et al (April
1997)1 regarding their finding of pulmonary hypertension
nally, linear regression analysis demonstrated that these param¬
eters (Vd/Vt and Deo) together explained 55% (partial r2=0.55)
ofthe variability in exercise performance ofthe group [maximum
in
a
group of severely affected patients with pulmonar)7 histiocytosis X
(PHX) who had been referred for lung transplantation. Their
the importance
findings are intriguing and add to data indicating
of the pulmonary vascular involvement in this disease. Vascular
involvement has frequently been described pathologically in
PHX. Travis and coworkers2 found evidence of vascular involve¬
ment in 80% of biopsy specimens. The pathophysiologic signifi¬
cance of this vascular involvement has received little attention.
We reported the pulmonary7 function and exercise performance
of a cohort (n=23) of less severely affected patients with PHX.3
The group demonstrated normal lung volume (total lung capac¬
ity, 90% predicted) and mildly altered spirometry7 (FEV1 77%
predicted, FEV1/FVC 80%) with a disproportionate reduction
in diffusing capacity for carbon monoxide (Deo, 59% predicted).
The exercise performance for the group was reduced (workload
at maximum exercise, 54% predicted) with an abnormal dead
space to tidal volume ratio (41%, at rest), which failed to fall with
exercise (41%, at peak exercise). This combination of a low Deo
and abnormal physiologic dead space ventilation (Vd/Vt) strongly
suggest the presence of pulmonary vascular abnormalities. Fi=
=
1714
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Patients with COPD often are hypoxic during exercise, even
though they are not hypoxic at rest,1 and this exercise-induced
hypoxemia may lead to pulmonary7 hypertension and heart fail¬
ure.2 The early diagnosis of exercise-induced hypoxemia may
facilitate early use of appropriate therapeutic approaches which,
in turn, may improve the patient's quality of life and prognosis.
To evaluate the frequency of exercise-induced hypoxemia in an
apparently healthy population, a 3-min walking test with simul¬
taneous measurement of oxygen saturation by pulse oximetry was
performed by7 360 subjects during a medical health examination.
No subject had a previous history of lung disease or abnormalities
on chest radiography. During the walking test, each subject was
equipped with a pulse oximeter and was encouraged to walk as
fast as possible. None of the subjects had hypoxemia before the
exercise test.
Forty-one (11.4%) subjects developed oxygen desaturation
disclosed that,
during the walking test. Further investigation
among these 41 subjects, there were 24 with COPD, 2 with
arthritis rheumatoid-associated lung disease, 1 with diffuse
causative
panbronchiolitis, and 4 with severe scoliosis. The
factor of exercise-induced hypoxemia could not be clarified in
10 subjects. The Hugh-Jones score and the pulse oxygen
saturation at rest3 were not significantly different between
subjects with and without oxygen desaturation (Table 1).
Communications to the Editor