Numan Ekim

An Unusual Cause of Urinothorax

Urinothorax is a rare complication of blunt renal trauma, ureteral instrumentation or ureteral surgery. A leakage from the urinary tract causes urinoma, a retroperitoneal collection of fluid, which can lead to urinothorax. We report a patient with solitary kidney who underwent extracorporeal shock wave lithotripsy (ESWL) for nephrolithiasis. Four days after ESWL, she had right-sided pleural effusion which demonstrated as urinothorax. Urinoma occurring after ESWL, as in our case, is a situation that has not been reported before as a cause of urinothorax. Urinothorax should be taken into consideration in patients with pleural effusion who recently underwent ESWL.

Hyperhomocysteinemia Prevalence Among Patients With Venous Thromboembolism

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.

The role of plasminogen activator inhibitor-1 polymorphism, factor-V-Leiden, and prothrombin-20210 mutations in pulmonary thromboembolism.

Polymorphism in plasminogen activator inhibitor-1 gene is suggested to be associated with an increased risk of venous thromboembolism. The aim of this study was to investigate the association of plasminogen activator inhibitor-1 gene polymorphism and its coexistence with factor-V-Leiden and prothrombin-20210 mutations in pulmonary thromboembolism. The authors investigated plasminogen activator inhibitor-1 4G/5G polymorphism, factor-V-Leiden, and prothrombin-20210 mutations in 143 pulmonary thromboembolism patients and 181 controls. Plasminogen activator inhibitor-1 4G/4G, 4G/5G, and 5G/5G gene polymorphisms and prothrombin-20210 mutations were not different between cases and controls. Factor-V-Leiden mutation was present in 21.0% and 7.7% of the cases and controls, respectively, P = .001. Neither different plasminogen activator inhibitor-1 genotypes and 4G allele nor coexistence of the allele with factor-V-Leiden or prothrombin-20210 was associated with the risk of recurrence. As a result, plasminogen activator inhibitor-1 gene polymorphism or its concomitant presence with mentioned mutations was not found to be associated with increased risk for pulmonary thromboembolism or recurrent disease in this study.

Fever in pulmonary embolism.

This study was planned to investigate the characteristics of clinical and laboratory findings of patients with fever diagnosed as pulmonary embolism (PE) in comparison with PE patients without fever and patients with community-acquired pneumonia (CAP). Thirty-nine PE patients with fever without other identifiable causes (18 received antibiotics and 21 did not receive antibiotics) (study groups) were included in the study. 22 patients with PE without fever and 21 patients diagnosed with CAP were retrospectively selected as control groups. Daily peak body temperature, risk factors for PE, symptoms, and physical and laboratory findings at admission were recorded. Patients with CAP demonstrated higher body temperature than PE patients with fever (38.5 ± 0.6 versus 37.8 ± 0.6°C, P = 0.0001). Fever patterns were similar between the three groups of patients who had fever. The leukocyte count and the erythrocyte sedimentation rate (ESR) were slightly higher in the group of PE with fever versus PE without fever (11 465.6 ± 4229.4/mm3, 51.1 ± 34.7/mm/h versus 10 777.3 ± 4927.6/mm3, 35.2 ± 30.1/mm/h, respectively) (P > 0.05). The group of CAP showed significantly highest values of leukocyte count and ESR (15 490.5 ± 5606.3/mm3, 69.1 ± 35.9/mm per h, respectively) (P < 0.05). This study suggested that fever might accompany with PE. The presence of slight leukocytosis and increased ESR may not securely differentiate PE patients with fever from patients with CAP.

Tumor necrosis factor-alpha (TNF-α) in pleural fluids

Summary Our study was undertaken to investigate the role of tumor necrosis factor-alpha (TNF-α) at the site of disease activity in tuberculous pleuritis (TP). Concentrations of TNF-α were measured directly by radioimmunoassay (RIA) in the pleural fluid (PF) and plasma (P) of patients with TP ( n = 14), malignant effusions ( n = 18) and transudates ( n = 7). Among these three groups mean plasma levels of TNF-α were not statistically significant ( P > 0.05), but in the TP group mean levels of TNF-α in PF were significantly higher than in the cancer and transudate groups ( P P > 0.05). These results may indicate a local synthesis of TNF-α by cells within the pleural cavity in this disease.

Disseminated cryptococcosis in a human immunodeficiency virus-negative patient: a case report.

Cryptococcus neoformans is a widely distributed saprophytic fungus that may cause opportunistic infections in normal and immunocompromised individuals particularly in patients with HIV infection. Disseminated infection in HIV‐negative individuals is occasionally seen: a 57‐year‐old HIV‐negative Turkish female initially presented with enlarged mediastinal lymph nodes and a large pulmonary parenchymal nodule, eventually diagnosed with disseminated cryptococcosis and tuberculosis.

The role of thrombophilic risk factors in the severity of pulmonary thromboembolism

High plasma factor-VIIIc concentration, presence of factor‐V 1691 G‐A (FVL) and prothrombin20210A (PT20210A) mutations were shown to be significant risk factors for venous thromboembolism (VTE) and recurrent VTE. The objective of this study was to investigate the role of these thrombotic risk factors in the severity of pulmonary thromboembolism (PTE). The plasma concentrations of factor VIIIc, presence of FVL and PT20210A mutations were studied in 32 patients with PTE. Eleven of the patients had documented recurrent VTE. Lung perfusion scans were scored according to the percentage of vascular obstruction. Patients who had a pulmonary vascular obstruction score (PVOs) >50% were compared to those with PVOs<50%. There was no significant difference between the patients with PVOs >50% and those with PVOs <50%, with regard to the presence of FVL and PT20210A mutation. However, patients with PVOs >50% had a significantly higher factor-VIIIc concentration than those with PVOs <50% (factor-VIIIc levels were 253.3±29.1 International Units (IU)·dL−1 and 138.5±16.2 IU·dL−1, respectively; p<0.005). Factor-VIIIc concentrations were significantly correlated with PVOs (r=0.52, p<0.005). Patients with recurrent VTE had significantly higher factor-VIIIc concentrations than those in which it occurred for the first time (factor-VIIIc concentrations were 232.6±30.9 IU·dL−1 and 158.3±20.6 IU·dL−1, respectively; p<0.05). The authors conclude that in addition to being a risk factor for venous thromboembolism, high factor-VIIIc concentration is an important factor in the severity of pulmonary thromboembolism.

Dramatic response of a patient with pregnancy induced idiopathic pulmonary arterial hypertension to sildenafil treatment

Idiopathic pulmonary arterial hypertension (IPAH) is characterized by a progressive increase in pulmonary vascular resistance, which may lead to right ventricular failure and death. Major cardiovascular and pulmonary alterations occur during pregnancy and therefore worsen or increase the complications of pulmonary arterial hypertension (PAH). A patient diagnosed with IPAH after a successful full‐term pregnancy and cesarean section with epidural anesthesia is presented. The postoperative course was complicated by progressive dyspnea, and lower limb edema. The outcome of treatment with sildenafil during puerperium was favorable in this patient. The clinical course was complicated by an unexpected spontaneous pregnancy after primary infertility.

The Value of Serum Procalcitonin in Differential Diagnosis of Pulmonary Embolism and Community-Acquired Pneumonia

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.

Is Tissue-Plasminogen Activator Gene Polymorphism a Risk Factor for Venous Thromboembolism in Every Population?

Background: Tissue-plasminogen activator is a key protein of fibrinolytic system. In recent years the relation between t-PA, its genetic polymorphisms and arterial or venous thrombosis were investigated in different populations. The aim of this study is to investigate the role of t-PA gene polymorphism in Turkish venous thromboembolism (VTE) patients.Methods: A case-control study was performed. We investigated the t-PA insertion/deletion (I/D) polymorphism in 93 VTE patients and 146 controls without VTE. Recurrent cases and documented risk factors for PTE were recorded.Results: Cases and controls did not differ with respect to the different t-PA genotypes. The prevalence of I allele was 44.1%, 44.5% in cases and controls respectively (OR = 0.95, 95% CI: 0.78–1.24, p > 0.05). Different t-PA genotypes had no effect on recurrent disease. No gender difference was observed with respect to the different t-PA genotypes. There was no significant difference for genotype frequency between PTE patients with documented risk factors and unprovoked cases.Conclusions: In conclusion there was no association between t-PA genotype and VTE in this group of Turkish population. It was also found that genotype frequencies for t-PA in both VTE and control subjects seems different from those reported from western part of the world.Abbreviated Abstract. The aim of this study is to investigate the role of t-PA gene polymorphism in Turkish VTE patients. We investigated 93 VTE patients and 146 controls without VTE. Cases and controls did not differ with respect to the different t-PA genotypes. The prevalence of I allele was 44.1%, 44.5% in cases and controls respectively (OR = 0.95, 95% CI: 0.78–1.24, p > 0.05). Different t-PA genotypes had no effect on recurrent disease. No gender difference was observed with respect to the different t-PA genotypes. There was no significant difference for genotype frequency between PTE patients with documented risk factors and unprovoked cases. In conclusion there was no association between t-PA genotype and VTE in this group of Turkish population. It was also found that genotype frequencies for t-PA in both VTE and control subjects seems different from those reported from western part of the world.