Tokyo University Hospital
Correspondence to: Shinji Teramoto, MD, FCCP, Department of Geriatric Medicine, Tokyo University Hospital, 7–3-1 Hongo Bunkyo-ku, Tokyo, Japan 113-8655
To the Editor:
In a recent issue of CHEST, Lee and Lepler (April
1999)1 rationally discussed the mimicking of
hepatopulmonary syndrome (HPS) by the severe intrapulmonary shunting
that is caused by carcinoid syndrome.
HPS is caused by hypoxemia in patients with chronic liver diseases in
the absence of intrinsic lung disease,2and so
carcinoid-related intrapulmonary shunting and hypoxemia are not exactly
the same as HPS. However, HPS may occur secondary to a functional
right-to-left shunt because of intrapulmonary vascular
dilatation.3Thus, the shunting in that situation may
mimic the pathogenesis of HPS in carcinoid syndrome. Furthermore,
recent evidence suggests that nitric oxide (NO) is an important
mediator of impaired oxygenation in patients with cirrhosis
(ie, HPS).5 The increased production of NO by
metastatic carcinoid tumors in the lung may be another cause of
extraordinary vasodilation and intrapulmonary shunting, resulting in
severe hypoxemia in carcinoid syndrome.
Patients with carcinoid syndrome are known to produce the
vasoconstrictor 5-hydroxytryptamine. However, NO, a major vasodilator,
also may be produced in patients with carcinoid syndrome.6
Although carcinoid-related pulmonary shunting may be responsible for
hypoxemia in the case of the patient reported by Lee and Lepler who has
metastatic carcinoid tumors, the pathogenic mechanism of severe
hypoxemia may not be simple in carcinoid syndrome. Because many
neurohumoral vasoactive substances can be released by tumors, the
complex regulatory mechanism may work in the lungs of the patients.
Further analysis of vasodilators and vasoconstrictors may be important
to elucidate the mechanism of hypoxemia in the carcinoid syndrome.
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