Erythropoietic response to hypoxaemia in diffuse idiopathic pulmonary fibrosis, as opposed to chronic obstructive pulmonary disease

Abstract

The aim of this study was to assess the erythropoietic response to hypoxaemia in patients with diffuse idiopathic pulmonary fibrosis (DIPF), and to speculate on the underlying mechanisms. Patients on an established chronic respiratory failure due to DIPF or chronic obstructive pulmonary disease (COPD) were studied. The erythropoietic response to hypoxaemia in both conditions was assessed. We studied 18 patients with DIPF and 29 patients with COPD in respiratory failure in a stable stage, free from acute infection and congestive heart failure. Blood gases, erythrocytic parameters, as well the serum levels of iron, ferritin and erythropoietin were determined. All the DIPF patients studied, apart from two, had normal or subnormal haematocrit values. The patients with COPD had an inconsistant response to hypoxaemia; 12 had normal or subnormal haematocrit values and the remaining 17 were erythraemic. The mean value of erythropoietin (EPO) in both DIPF and COPD patients was significantly higher than normal. In conclusion, patients with DIPF exhibit a lack of erythropoietic response to hypoxaemia, despite the augmented erythropoietin levels. This may reflect a defective bone marrow erythropoietic response in DIPF patients. It is suggested that the pathophysiology of DIPF underlies this mechanism.

Anemia in COPD: A Systematic Review of the Prevalence, Quality of Life, and Mortality

“…2), which suggests that at least a component of the anemia is attributable to inflammation (ie, the anemia of chronic inflammation). 22 Tassiopoulos and colleagues, 23 in 2001, were among the first to study anemia and its compensatory erythropoietic action in COPD patients. Their findings indicated an inverse correlation between the hemoglobin and erythropoietin concentrations, which suggests that in COPD patients low hemoglobin correlates with a compensatory erythropoietin response.…”

“…27,28 The mechanism whereby inflammation causes anemia is incompletely established. However, cytokines such as the IL-1, IL-6, and tumor necrosis factor (TNF-alpha), released by activated monocytes in patients with underlying inflammatory conditions, 23,29 are certainly involved. Several studies have demonstrated that these and other cytokines are associated with the appearance of anemia and may be involved in the pathogenesis by mechanisms such as blunting erythropoietin production in response to hypoxia or decreasing bone marrow responsiveness to erythropoietin.…”

“…25,30,31 Inflammatory cytokines, especially IL-1 ␤ and TNF-alpha, may induce apoptosis of red cell precursors as well as down-regulate the appearance of erythropoietin receptors on erythroid progenitor cells. 23 IL-6 is released by a number of cells in response to infection, trauma, or immunological challenge, and is a major factor in the regulation of the acute inflammatory response. The role of IL-6 in the pathogenesis of anemia first became apparent in the cancer setting, where severe anemia was found to be associated with very high levels of this and other inflammatory cytokines.…”

Anemias in chronic obstructive pulmonary disease

“…S. Tassiopoulos и соавт. [19] одни из первых оценили связь АХЗ с ХОБЛ. Первоначальная цель состояла в сравнении компенсатор-ных механизмов эритропоэза у пациентов с идиопатическим фи-брозом легких и ХОБЛ.…”

“…Однако результаты оказа-лись противоречивыми. У пациентов с ХОБЛ уровень гемоглоби-на был нормальным или сниженным, несмотря на высокие кон-центрации ЭПО в плазме [19]. Эти данные подтверждены резуль-татами другого исследования, в котором также обнаружены более высокие уровни СРБ и ИЛ-6 у больных ХОБЛ [10].…”