Search

Presence of high fever may cause confusion in differential diagnosis of pulmonary embolism (PE) versus pneumonia. The aim of this study is to investigate the diagnostic value of serum procalcitonin (PCT) in differential diagnosis of PE and community-acquired pneumonia (CAP). A total of 24 patients with proven PE and 22 patients with CAP were included in the study. The study population was subdivided as PE patients with fever (group 1, n = 8) and without fever (group 2, n = 16); and CAP (group 3, n = 22). Serum PCT and systemic inflammatory markers were measured at the initial diagnosis and the third day of the treatment. The relation of PCT level with the other systemic inflammatory markers was investigated in each measurement point. The initial mean serum PCT level in group 3 (2.24 ± 0.99 ng/mL) was statistically higher than group 1 (0.48 ± 0.77 ng/mL) and group 2 (0.14 ± 0.17 ng/mL; P = .000, .000, respectively). Procalcitonin level at the initial (2.24 ± 0.99 ng/mL) and the third day of treatment (0.92 ± 0.62 ng/mL) in group 3 showed a statistically significant reduction (P = .000). There were no statistically significant reduction in PCT levels by anticoagulation in groups 1 and 2 (P = .262, .119, respectively). Other systemic inflammatory markers including interleukin 6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor α (TNF-α) levels statistically significantly decreased with anticoagulant and antimicrobial therapy. This study suggested that serum PCT level may be valuable for differentiating PE patients with or without fever from patients with CAP.

The aim of this study is to evaluate the plasma total homocysteine level in patients with venous thromboembolism (VTE) and to investigate the effect of different risk factors on plasma levels. Ninety-three-patients with VTE and 37-control participants diagnosed with other than VTE were included in the study. Plasma homocysteine levels and the factors affecting plasma homocysteine levels were evaluated. Plasma homocysteine level was higher among patients with VTE compared to the controls independent from vitamin B12 and folate levels. The prevalence of hyperhomocysteinemia in VTE was 63%. Plasma homocysteine level was higher in patients with PE than deep venous thrombosis (DVT; 23 ± 13.7 vs 16 ± 5.8 μmol/L, P = .018). With regression analysis hyperhomocysteinemia was found to be associated with a 4.8-fold increased risk of VTE. Hyperhomocysteinemia is a common and possibly modifiable risk factor that should be considered when screening patients with VTE. Secondary causes of hyperhomocysteinemia especially vitamin B12 deficiency should be monitored in patients with VTE to prevent recurrences.