Criteria to select patients with hepatocellular carcinoma (HCC) for liver transplantation (LT) are based on tumor size and number of nodules rather than on tumor biology. The present study was undertaken to assess the role of transarterial chemoembolization (TACE) in selecting patients with tumors suitable for LT. Ninety-six consecutive patients with HCC were treated by repeatedly performed TACE, 62 of them exceeding the Milan criteria. Patients meeting the Milan criteria were immediately listed, and patients beyond the listing criteria were listed upon downstaging of the tumor following successful TACE. Fifty patients were finally transplanted. Of these 50 patients, 34 exceeded the Milan criteria. In these 96 patients, overall 5-year survival was 51.9%. However, it was 80.9% for patients undergoing LT and 0% for patients without transplantation (P Ͻ 0.0001). Tumor recurrence was primarily influenced by the control of the disease through continued TACE during the waiting time. Freedom from recurrence after 5 years was 94.5% in patients (n ϭ 39) with progression-free TACE during the waiting time. Tumor recurrence was significantly higher in patients (n ϭ 11) who after initial response to TACE progressed again before LT (freedom from recurrence 35.4%; P ϭ 0.0017). Progression-free course of TACE during the waiting time (P ϭ 0.006; risk ratio, 8.95), and a limited number of tumor nodules as assessed in the surgical specimen (P ϭ 0.025; risk ratio, 0.116) proved to be significant predictors for freedom from recurrence in the multivariate analysis. Milan criteria were without impact on recurrence. Our data suggest that sustained response to TACE is a better selection criterion for LT than the initial assessment of tumor size or number.
MD; for the AtheroGene InvestigatorsBackground-Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis. In hypothesizing an association between infectious agents and the development of atherosclerosis, we would expect a correlation to the extent of atherosclerosis. Moreover, this effect could be multiplied by the number of pathogens to which an individual had been exposed. Methods and Results-In 572 patients, IgG or IgA antibodies to herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter pylori were measured. The extent of atherosclerosis was determined by coronary angiography, carotid duplex sonography, and evaluation of the ankle-arm index. Elevated IgA antibodies against C pneumoniae (PϽ0.04) and IgG antibodies against H pylori (PϽ0.02), cytomegalovirus (PϽ0.05), and herpes simplex virus 2 (PϽ0.01) were associated with advanced atherosclerosis (Ն2 vascular regions), adjusted for age, sex, cardiovascular risk factors, and highly sensitive C-reactive protein.Infectious burden divided into 0 to 3, 4 to 5, and 6 to 8 seropositivities was significantly associated with advanced atherosclerosis, with an odds ratio (95% CI) of 1.8 (1.2 to 2.6) for 4 to 5 (PϽ0.01) and 2.5 (1.2 to 5.1) for 6 to 8 seropositivities (PϽ0.02) (adjusted). After a mean follow-up of 3.2 years, cardiovascular mortality rate was 7.0% in patients with advanced atherosclerosis and seropositive for 0 to 3 pathogens compared with 20.0% in those seropositive for 6 to 8 pathogens. Conclusions-Our results support the hypothesis that infectious agents are involved in the development of atherosclerosis.We showed a significant association between infectious burden and the extent of atherosclerosis. Moreover, the risk for future death was increased by the number of infectious pathogens, especially in patients with advanced atherosclerosis.
Background and Purpose-Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis.The extent of atherosclerosis and the prognosis of patients with atherosclerosis seem to be increased by the number of infections to which an individual has been exposed. In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the progression of carotid atherosclerosis. Methods-In 504 patients (74.9% men; age, 62.9Ϯ10 years), we measured intima-media thickness and prevalence of carotid artery stenosis. Follow-up measurements after a mean of 2.5 years were available in 427 patients (85%). Blood samples were taken, and IgG or IgA antibodies to Chlamydia pneumoniae, Helicobacter pylori, Haemophilus influenzae, Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus types 1 and 2 were measured. Statistical evaluation was performed with logistic regression procedures. Results-ElevatedIgA antibodies against C pneumoniae (PϽ0.04) and IgG antibodies against Epstein-Barr virus (PϽ0.01) and herpes simplex virus type 2 (PϽ0.04) were associated with progression of atherosclerosis (increase of intima-media thickness Ն0.1 mm/y or progression of carotid stenosis) after adjustment for age, sex, cardiovascular risk factors, highly sensitive C-reactive protein, and statin intake. Infectious burden, divided into 0 to 3, 4 to 5, and 6 to 8 seropositivities, was significantly associated with progression of atherosclerosis, with odds ratios of 1.8 (95% confidence interval, 1.1 to 2.9) for 4 to 5 and 3.8 (95% CI, 1.6 to 8.8) for 6 to 8 compared with 0 to 3 seropositivities after adjustment. Conclusions-Our results support the hypothesis that the number of infectious pathogens to which an individual has been exposed independently contributes to the progression of carotid atherosclerosis.
The different enhancement behaviors of malignant and benign breast lesions cannot be explained by MVD alone; however, a low MVD in the center of carcinoma is reflected quantitatively by a high enhancement ratio and qualitatively by rim enhancement, with an implication of adverse prognosis.
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