Перегляд вихідного коду сторінки Advanced All-inclusive Plan For CYTH4

035; figure 6) but statistical significance was lost after adjusting for differences in FEV1 (p=0.081). Differences in SGRQ scores, HAD scores, and ESS between ID and IR groups, did not reach statistical significance (mean 33.5 vs 30.1, p=0.056; median  13.5 vs 11, p=0.133 and median 8 vs 5, p=0.279, respectively). Figure?6 Box plots showing distribution of (A) Shuttle Walk Test (SWT) distance and (B) St George's Respiratory Questionnaire (SGRQ) score, by iron status in the chronic obstructive pulmonary disease (COPD) cohort. SWT distance was lower in the iron-deficient ... [http://en.wikipedia.org/wiki/PSCD4 CYTH4] Discussion This study has demonstrated a high prevalence of non-anaemic iron deficiency in COPD that may be driven by inflammation. Patients with iron deficiency were more hypoxaemic even though they did not have significantly worse airflow limitation. Such marked daytime and nocturnal hypoxaemia in the ID group was unexpected. One possible explanation arises from the essential role of iron as a cofactor in a key cellular pathway that senses hypoxia, and modulates levels of the hypoxia-inducible factor family of transcription factors.6 8 9 Tissue iron deficiency alters the effect of hypoxia on the pulmonary vasculature,8 and thus may impair physiological ventilation to perfusion matching and worsen hypoxaemia. Irrespective of the underlying mechanisms, the high prevalence of iron deficiency in COPD and the  newly identified association of iron deficiency with hypoxaemia are potentially of considerable clinical significance.  The major hormone that acts to determine iron availability and distribution is hepcidin. Serum levels of hepcidin are influenced by iron, hypoxia, erythropoietic drive and inflammation.12 The importance of inflammation in regulating iron availability in COPD is illustrated by the failure of the combination of iron deficiency and hypoxia to suppress hepcidin completely in the ID COPD group, whereas it is barely detectable in the ID healthy controls. This ��inappropriate expression�� of hepcidin is similar to that seen in the anaemia of chronic disease.24 Within the ID COPD group, despite significantly lower ferritin and MCV, anaemia was uncommon and mean haemoglobin concentration was not lower than in the IR patients. The ID group had higher EPO levels, consistent with appropriate sensing of hypoxaemia, but a failure of the marrow to respond accordingly. It appears as a tension exists here between erythropoietic drive and iron availability, with inflammation-driven, hepcidin-mediated iron sequestration constraining a rise in haemoglobin. In support of this suggestion, it was noted 50?years ago that individuals with severe lung disease tended to increment their haemoglobin only if given intramuscular iron.