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Original papers

Prevalence of anemia and its impact on mortality in patients with acute exacerbation of chronic obstructive pulmonary disease in a developing country setting

Chronic Obstructive Pulmonary Disease (COPD) is going to be the third most common cause of death worldwide. The natural course of COPD is interrupted by acute exacerbations (AECOPD) with an overall mortality rate of 10%. Anemia is a well-known independent predictor of mortality in several chronic diseases. Little is known about the impact of anemia on mortality in AECOPD. The aims of this study were to determine the prevalence of anemia in AECOPD patients and its impact on mortality in a developing country setting. We retrospectively studied 200 hospitalized patients with AECOPD (100 died in hospital and 100 survived) in Imam Khomeini teaching hospital, Urmia, Iran. Prevalence of anemia between deceased and surviving patients compared by using x-square test. Mean admission day Hb and Hct level were compared between the two groups by using Student t-test. Anemia was defined according to WHO criteria: Hb< 13 g/dl in males; Hb< 12 g/dl in females. The prevalence of anemia was significantly higher in patients who died in hospital compared to those who survived (72% vs. 49%, p=0.001 and OR= 2.68). The mean ± SD Hb level was 11.5±2.7 g/dl among deceased patients vs.13.0±2.0 g/dl among survivors (p value<0.001). The duration of hospitalization was significantly higher (p<0,001) in anemic patients (mean 13.28 days in anemic vs. 7.0 days in non-anemic patients). In bivariate correlation analysis, Hb was positively correlated with FEV1 (r=+0.210, p=0.011) and negatively with duration of hospitalization (r=-0.389, p=0.000). Anemia was common in AECOPD patients in this developing country setting and was significantly associated with in hospital mortality.
Keywords: Acute exacerbation of chronic obstructive Pulmonary Disease (AECOPD); anemia; mortality, COPD

Echocardiographic Evaluation of the Relationship Between inflammatory factors (IL6, TNFα, hs-CRP) and Secondary Pulmonary Hypertension in patients with COPD. A Cross sectional study

Background: Inflammatory mechanism appears to play a major role in the pathogenesis of various types of human pulmonary hypertension such as idiopathic PAH (IPAH) and PAH associated'' with connective tissue disease. Although we know that inflammatory factors such as IL6 and TNFα have an important role in IPAH, there is limited information about the relationship between acute phase reactants and pulmonary hypertension occurring secondary to pulmonary diseases such as chronic obstructive pulmonary diseases (COPD).
Methods: This cross-sectional study was carried out on 94 patients who had COPD. Patients with a recent history of systemic steroid and acetylsalicylic acid ( ASA) use, infection, trauma or surgery, gastrointestinal bleeding, coronary artery disease (CAD) and Hypertension were excluded. Body plethysmography and transthoracic echocardiography were done. Blood samples for each patient included were drawn for complete blood count (CBC), IL6, TNFα and highly sensitive C reactive protein (hs-CRP).
Results: Twenty patients (28.6%) had pulmonary hypertension. The difference between the mean IL6 and hs-CRP in patients with and without pulmonary hypertension was significant (7pg/ml vs. 4.4pg/ml and 13.04pg/ml vs. 3.31pg/ml) (p= 0.006 and p=0.000). There was a correlation between IL6 and mean pulmonary arterial pressure (r = 0.35, p=0.003). After adjustment for age, sex, serum Hemoglobin, Hematocrit, O2Sat, FEV1, FVC the relationship between the IL6, hs-CRP and the presence of pulmonary hypertension remained significant (p=0.022, p=0.026) .
Conclusion: Inflammatory factors such as IL6 and hs-CRP are independent risk factors for pulmonary hypertension in COPD patients.
Keywords: COPD, pulmonary hypertension, inflammatory factors, secondary

Can a simple forced inspiratory maneuver help identify subjects at risk for sleep-disordered breathing?

Application of a negative pressure has been utilized in experimental settings to demonstrate abnormal upper airways compliance. We hypothesized that a simple forced inspiratory maneuver could be used as a screening test for this abnormality in an epidemiological setting.
277 men and women, aged 30 years or more, who attended a Preventive Medicine Centre, volunteered for completing a sleep questionnaire, having standard anthropometric measurements, a non-invasive upper airways examination, and for performing an oronasal peak inspiratory maneuver.
The peak inspiratory flow (PIF) of 127 females was significantly less compared to that of the 137 males (211±47 vs. 269±59 l.min-1). PIF was significantly inversely related to age in both sexes; a positive correlation with height was found in males only. Males with enlarged soft palates had a significantly lower PIF (256±54 vs. 277±62 l.min-1 ; p=0.04). No difference in PIF was found in subjects who stated that they experienced breathing pauses during sleep. Habitual snoring males had a significantly lower PIF as compared to the non-snorers (251±59 vs. 282 ±57 l.min-1; p=0.003); after adjustment for age, this difference was borderline significant (p=0.06).
A forced inspiratory flow maneuver yielded a PIF which was different between genders, was age-dependent in both sexes, and related to height in males. PIF did not identify male subjects with breathing pauses during sleep, but was associated with a larger soft palate and was borderline decreased in habitual snoring males. The present results suggest that, with further validation, the PIF test could represent a simple means to indirectly explore upper airways compliance.
Keywords: sleep apnea, snoring, peak inspiratory flow, sceening test