PURPOSE:This study was designed to evaluate the levels of hepcidin in the serum of patients with chronic obstructive pulmonary disease (COPD).METHODS:In the study, 74 male patients (ages 45-75) in a stable period for COPD were grouped as Group I: Mild COPD (n:25), Group II: Moderate COPD (n:24), and Group III: Severe COPD (n:25). Healthy non-smoker males were included in Group IV (n:35) as a control group. The differences of hepcidin level among all the groups were examined. Also, in the patient groups with COPD, hepcidin level was compared with age, body mass index, cigarette (package/year), blood parameters (iron, total iron binding capacity, ferritin, hemoglobin, hematocrit [hct]), respiratory function tests, and arterial blood gas results.RESULTS:Although there was no difference between the healthy control group and the mild COPD patient group (P=0.781) in terms of hepcidin level, there was a difference between the moderate (P=0.004) and the severe COPD patient groups (P=0.002). The hepcidin level of the control group was found to be higher than the moderate and severe COPD patient groups. In the severe COPD patients, hepcidin level increased with the increase in serum iron (P=0.000), hct (P=0.009), ferritin levels (P=0.012), and arterial oxygen saturation (SaO2, P=0.000).CONCLUSION:The serum hepcidin level that is decreased in severe COPD brings into mind that it may play a role in the mechanism to prevent hypoxemia. The results suggest that serum hepcidin level may be a useful marker in COPD. Larger prospective studies are needed to confirm our findings between hepcidin and COPD.

Pulmonary embolism (PE) is a major cause of cardiovascular mortality and financial burden that affects the community. The diagnosis of PE can be difficult because of the nonspecific symptoms, which include cough, dyspnea, hemoptysis and pleuritic chest pain. Hereditary and acquired risk factors are associated with PE. Incidence of PE is increasing, associated with the development in the diagnostic methods. Evidence-based algorithms can help clinicians diagnose PE. Serum D-dimer level, computed tomography pulmonary angiogram (CTPA), ventilation-perfusion scintigraphy or echocardiography help to establish clinical probability and the severity of PE. Anticoagulation is the standard treatment for PE. However, thrombolytic treatment is a significant alternative in high risk of PE as it provides rapid clot resolution. This article reviews the risk factors, diagnostic algorithms, and methods of treatment in PE in the light of current information.

Serum S100B protein level is increased in patients with OSAS and may be a useful biochemical marker in those patients.

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The present study showed that central thrombus was not an independent predictor of mortality in hemodynamically stable PE patients. LMWH and UFH were similarly effective in the treatment of this patient group.