ERYTHROCYTOSIS IN EMPHYSEMA.

Abstract

Marked erythrocytosis is frequently seen in hypoxia due to high altitudes and cyanotic congenital heart disease (Hurtado, Merino and Delgado, 1945) but is relatively uncommon in association with chronic respiratory failure (Baldwin, Cournand and Richards, 1949). This discrepancy has exercised a number of writers. Wilson, Borden and Ebert (1951) have proposed that bronchial infection may depress the erythropoietic response of the bone marrow in patients with chronic bronchitis and emphysema and Ratto, Briscoe, Morton and Comroe (1955) have postulated depression of erythropoiesis by carbon‐dioxide retention. Simpson (1957) found evidence of bleeding in a number of his emphysematous subjects and suggested that concealed haemorrhage may be of importance in modifying haematological changes in respiratory hypoxia.More recently, Shaw and Simpson (1961) and Lertzman, Israels and Cherniack (1962) have proposed that expansion of plasma volume accompanying respiratory failure may account for the apparent infrequency of erythrocytosis in emphysema, but the view that the erythropoietic response to hypoxia is normal in emphysema is based on evidence which is not entirely satisfactory. Thus Shaw and Simpson compared the red‐cell mass in English subjects with emphysema with that of native Peruvian Indians living at high altitudes, a comparison which assumes similarity of nutrition and incidence of conditions such as intestinal infestation. Lertzman and associates compared the red‐cell mass in respiratory failure with that in patients with hypoxia due to other causes. In the majority of these latter patients, the hypoxia was due to obesity but the red‐cell mass was expressed per kilogram of body weight rather than as a function of height or lean‐body mass. In each of these studies the red‐cell mass in emphysema varied from within the normal range to more than double this figure in patients with hypoxia of comparable severity. The fact that many chronically cyanosed emphysematous patients show no significant increase in red‐cell mass remains unexplained and warrants further attention.In the present investigation a small group of severely disabled patients was chosen for study. All suffered from chronic bronchitis and emphysema with persistent cyanosis during remission from acute pulmonary infection. Four exhibited the conventional haematological changes of secondary polycythaemia, whilst another four were similarly disabled but showed no such changes in the peripheral blood. The two groups were compared in an attempt to account for the apparent failure of erythropoietic response to hypoxia in the latter. The investigation was designed to ascertain whether the defect lay in the elaboration of erythropoietin, the humoral mediator of the hypoxic stimulus to the bone marrow, or in the response of the bone marrow to this humoral stimulus.