A severe and common pulmonary vascular complication of liver disease is hepatopulmonary syndrome (HPS). It is a triad of liver dysfunction and/or portal hypertension, intrapulmonary vascular dilatations, and increased alveolar-arterial oxygen gradient. Prevalence varies according to various study groups from 4%-47%. While the most common presenting symptom of HPS is dyspnea, it is usually asymptomatic, and thus all liver transplant candidates should be screened for its presence. Pulse oximetry is a useful screening method, but arterial blood gas examination is the gold standard. If there is an abnormal P (A-a)O2 gradient, microbubble transthoracic echocardiography should be done for diagnosis. Outcome is unpredictable, and there is currently no effective medical therapy. The only effective therapy is considered to be liver transplantation. Complete resolution of HPS after liver transplantation is seen within a year in most HPS patients.

BACKGROUND: Pulmonary thromboembolism is a serious cardiovascular condition with considerable morbidity and mortality. Clinical studies have indicated that hyperuricemia is an independent risk factor for cardiovascular events. The aim of this study was to investigate possible value of the serum levels of uric acid (UA) in predicting 30-d pulmonary thromboembolism-related mortality. METHODS: Pulmonary thromboembolism was confirmed by computed tomography pulmonary angiography, demographic data, troponin, systolic pressure and pulse on admission, and simplified pulmonary embolism severity index assessment. UA levels were analyzed on admission. The primary end point was all-cause mortality during the first 30 d. RESULTS: A total of 337 acute pulmonary thromboembolism subjects, of whom 59% were females, were enrolled. The median (interquartile range) serum UA level was 5.35 (4.1–7.3) mg/dL. Serum UA levels of deceased subjects were higher than those of alive subjects during the study period (6.9 [4.6–10.0] mg/dL vs 5.2 [4.1–7.0] mg/dL, P = .038). In the receiver operating characteristic analysis, the area under the curve was 0.650 (CI 0.732–0.960) for UA levels for all-cause mortality. A level of serum UA ≥ 5 mg/dL showed 73% sensitivity and 88% negative predictive value for all-cause 30-d mortality. A weak correlation was determined between the UA levels and age (r = 0.25, P < .001) and any troponin (r = 0.267, P < .001). Serum UA level was an independent predictor of short-term mortality in pulmonary thromboembolism (odds ratio 1.2, P = .002). CONCLUSIONS: Serum UA levels may be a potential biomarker for predicting outcome in patients with acute pulmonary thromboembolism.

Background/Aims: The aim of the present study was to investigate whether Helicobacter pylori causes or triggers recurrent aphthous stomatitis (RAS) through cytokine gene polymorphism and/or cobalamin deficiency. Materials and Methods: Thirty-six patients with RAS and 130 patients without RAS were genotyped for IL-1β (−511C/T) and IL-6 (−174G/C) and evaluated for H. pylori infection and serum cobalamin level. Results: The patient groups according to RAS had similar rates of H. pylori gastritis and interleukin genotypes/alleles, and there was a non-significant difference between serum cobalamin levels (p>0.05). RAS patients with H. pylori gastritis showed a higher frequency (51.9%) of GC IL-6 genotype than RAS patients without H. pylori gastritis (11.1%) (p=0.036). Non-GG genotype and C allele were increased in patients without RAS and with H. pylori gastritis (p<0.05). Patients with H. pylori gastritis showed a lower value of serum cobalamin without statistical significance, although this difference was more prominent in RAS patients (p=0.07). Conclusion: The carriage of the C allele of IL-6 may lead a susceptibility to chronic gastric inflammation after contamination with H. pylori. If H. pylori infection is justified as a predisposing factor for RAS and its severity by further studies, we can speculate that subjects with genetic susceptibility to this infection may benefit from H. pylori eradication treatment with respect to RAS.