Stratified gray-scale median analysis and color mapping of the carotid plaque: correlation with endarterectomy specimen histology of 28 patients.

BACKGROUND AND PURPOSE: To determine whether a stratified gray-scale median (GSM) analysis of the carotid plaque combined with color mapping could predict plaque histology better than an overall GSM measurement. METHODS: Thirty-one carotid plaques derived from 28 patients undergoing carotid endarterectomy were investigated by ultrasound. GSMs of the whole plaque were used as measurement of echogenicity. A profile of the regional GSM as a function of distance from the plaque surface could be generated. Plaque pixels were further mapped into 3 different colors depending on their GSM value. RESULTS: Plaques with large calcifications presented the highest GSM values, and those with large hemorrhagic areas or with a predominant necrotic core exhibited the lowest. Fibrous plaques had intermediate GSM values. A necrotic core located in a juxtalumenal position was associated with significantly lower GSM values (P=0.009) and with a predominant red color (GSM <50) at the surface (P=0.0019). With respect to the thickness of the fibrous cap and the position of the necrotic core, the sensitivity and specificity of the predominant red color of the whole plaque was respectively 45% and 67% and 53% and 75%; considering the predominant red color of the surface, the sensitivity and specificity increased to 73% and 67% and 84% and 75%, respectively. CONCLUSIONS: The stratified GSM measurement combined with color mapping showed a good correlation with the different histopathological components and further allowed identification with good accuracy of determinants of plaque instability. This approach should be investigated in a prospective, natural history study.

S-adenosylmethionine in alcoholic liver cirrhosis: a randomized, placebo-controlled, double-blind, multicenter clinical trial.

BACKGROUND/AIM: The efficacy of S-adenosylmethionine (AdoMet) in the treatment of liver cell injury has been demonstrated in several experimental models. The aim of this study was to investigate the effects of AdoMet treatment in human alcoholic liver cirrhosis. METHODS: A randomized, double-blind trial was performed in 123 patients treated with AdoMet (1200 mg/day, orally) or placebo for 2 years. All patients had alcoholic cirrhosis, and histologic confirmation of the diagnosis was available in 84% of the cases. Seventy-five patients were in Child class A, 40 in class B, and 8 in class C. Sixty-two patients received AdoMet and 61 received placebo. RESULTS: At inclusion into the trial no significant differences were observed between the two groups with respect to sex, age, previous episodes of major complications of cirrhosis, Child classification and liver function tests. The overall mortality/liver transplantation at the end of the trial decreased from 30% in the placebo group to 16% in the AdoMet group, although the difference was not statistically significant (p = 0.077). When patients in Child C class were excluded from the analysis, the overall mortality/liver transplantation was significantly greater in the placebo group than in the AdoMet group (29% vs. 12%, p = 0.025), and differences between the two groups in the 2-year survival curves (defined as the time to death or liver transplantation) were also statistically significant (p = 0.046). CONCLUSIONS: The present results indicate that long-term treatment with AdoMet may improve survival or delay liver transplantation in patients with alcoholic liver cirrhosis, especially in those with less advanced liver disease.

Inhibition of membrane-bound hepatic 3 hydroxy-3 methyl glutaryl CoA reductase as the consequence of altered membrane fluidity.

The activity of hydroxy methyl glutaryl-CoA reductase in microsomes from rat and from human liver was inhibited in a non-competitive manner by fenofibric acid. High affinity of the microsomal preparation for the ligand allowed a one-step purification of the microsomal enzyme preparation, using a Sepharose gel coupled to the phenol analogue of fenofibric acid. Ther Arrhenius plots of partially purified hydroxy methyl glutaryl-CoA reductase in the microsomal fraction from rat liver showed that the break in the activation energy at 11 degrees C was abolished by the ligand. The results in the present study may be consistent with a modulation of membrane-bound HMG-CoA reductase activity.