Aspirin resistance in cerebrovascular disease and the role of glycoprotein IIIa polymorphism in Turkish stroke patients.

Aspirin resistance occurs in 5-45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P = 0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100 mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36-60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke.

[Associations between TGF-ß1 G/A and TNF-α 308 G/A gene polymorphisms with airway resistance in chronic obstructive pulmonary disease]. / Kronik obstrüktif akciger hastaliginda TGF-ß1 G/A ve TNF-α 308 G/A gen polimorfizmleri ile hava yolu direncinin degerlendirilmesi.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is an important morbidity and mortality cause all over the world. Although specific gene region has not been defined in the pathogenesis of COPD, cytokine gene polymorphisms like tumor necrosis factor-alfa (TNF-α) and transforming growth factor-beta1 (TGF-ß1) may contribute to the development of COPD. The aim of the present study was to evaluate the associations between airway resistance with TGF-ß1 G/A and TNF-α 308 G/A gene polymorphisms in COPD patients. PATIENTS AND METHODS: 264 subjects were included to the study (Group 1; 75 COPD patients, Group 2; 139 subjects with at least 10 packet year smoking history without airflow obstruction, Group 3; 50 healthy subjects). Pulmonary function tests and body plethysmography to measure airway resistance were performed to the subjects. TGF-ß1 800 G/A and TNF-α 308 G/A gene polymorphisms were evaluated. Chi-square, Anova and correlation analysis were used for statistical analysis. RESULTS: There were significant difference among COPD stages in terms of TNF-α 308 G/A polymorphism (p< 0.05). Thirteen (23.6%) stage 1 COPD patients had TNF-α 308 G/A polymorphism and the other did not have. We did not find statistically significant difference among COPD stages in terms of TGF-ß1 800 G/A polymorphism (p> 0.05). TNF-α and TGF-ß1 genotypes and TNF-a 308 G/A and TGF-ß1 800 G/A polymorphisms were not different among study groups. Moreover, no significant differences betweeen subjects with and without increased airway resistance in terms of TNF-α 308 G/A and TGF-ß1 800 G/A polymorphisms were present. CONCLUSION: These results can suggest the lack of association between TNF-α 308 G/A and TGF-ß1 800 G/A gene polymorphisms with COPD development and airway resistance in Turkish population.

Deep vein thrombosis in a child with Down syndrome: A case report.

We report on the case of iliofemoral popliteal vein thrombosis in a child with Down syndrome who had surgery for a congenital heart defect. She was readmitted to our hospital because of gastroenteritis and generalized tonic-clonic seizures at age 14 months. On the second day of hospitalization, color Doppler ultrasonography revealed right iliofemoral and popliteal vein thrombosis. She was treated successfully with intravenous fluids and low-molecular-weight heparin. No predisposing factor other than dehydration could be found in the patient. We suggest that dehydration should be kept in mind as a cause of deep-vein thrombosis in patients with severe dehydration.