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[en] Recent pathologic studies of hepatic resection and transplantation specimens have elucidated the morphologic features of the precancerous lesions and small hepatocellular carcinomas (HCCs) arising in cirrhotic livers. Small HCCs measuring less than 2 cm in diameter are of two types: vaguely nodular, well-differentiated tumors, also known as ''early'' HCCs, and distinctly nodular tumors, with histologic features of ''classic'' HCC. The precancerous lesions include dysplastic foci and dysplastic nodules. ''Classic'' small HCCs are supplied by nontriadal arteries, whereas early HCCs and dysplastic nodules may receive blood supply from both portal tracts and nontriadal arteries. The similarities in blood supply of these three types of nodular lesions result in significant overlap of findings on dynamic imaging. Nevertheless, small HCCs sometimes display characteristic radiologic features, such as ''nodule-in-nodule'' configuration and ''corona enhancement'' pattern. Moreover, various histologic features of these nodular lesions may also be related to a variety of signal intensities and attenuation coefficients, while the presence of cirrhosis is known to limit the sensitivity and specificity of any imaging modality, due to liver inhomogeneity. Because of these reasons, imaging findings of nodular lesions in cirrhotic livers are often inconclusive, emphasizing the need for a better understanding of these imaging features. (orig.)
[en] Highlights: • Plasma IL-1β levels were higher in plasma in patients with liver cirrhosis than control. • Plasma IL-18 levels were higher in plasma in patients with liver cirrhosis than control. • Plasma IL-18 were significantly positively associated with Child-Pugh classification. • NLRP3 expression were increased in the livers of patients with cirrhosis. NLRP3 inflammasome activation is involved in the mechanism of liver cirrhosis. In this study, we investigated the levels of plasma IL-1β and IL-18 and their relationship to component traits in patients with liver cirrhosis, and NLRP3 inflammasome expression in liver of patients with liver cirrhosis.
[en] Hepatocellular carcinoma (HCC) is one of the most frequently diagnosed tumour diseases throughout the world. In the vast majority of cases those affected are high-risk patients with chronic viral hepatitis and/or liver cirrhosis, which means there is a clearly identifiable target group for HCC screening. With resection, transplantation, and interventional procedures for local ablation, following early diagnosis curative treatment options are available with which 5-year survival rates of over 60% can be reached. Such early diagnosis is a reality only in a minority of patients, however, and in the majority of cases the disease is already in an advanced stage at diagnosis. One of the objects of HCC screening is diagnosis in an early stage when curative treatment is still possible. Precisely this is achieved by screening, so that the proportion of patients treated with curative intent is decisively higher. There is not yet any clear evidence as to whether this leads to a lowering of the mortality of HCC. As lower mortality is the decisive indicator of success for a screening programme the benefit of HCC screening has so far been neither documented nor refuted. Nonetheless, in large regions of the world it is the practice for high-risk patients to undergo HCC screening in the form of twice-yearly ultrasound examination and determination of AFP. (orig.)
[de]Das hepatozellulaere Karzinom (HCC) ist eine der weltweit haeufigsten Tumorerkrankungen. Es tritt in der grossen Mehrzahl der Faelle bei Hochrisikopatienten mit chronischer Virushepatitis bzw. Leberzirrhose auf, woraus sich eine klar identifizierbare Zielgruppe fuer das HCC-Screening ergibt. Mit der Resektion, der Transplantation und interventionellen lokal ablativen Verfahren stehen bei rechtzeitiger Diagnosestellung kurative Therapieoptionen zur Verfuegung, die 5-Jahres-Ueberlebensraten von >60% erreichen. Diese rechtzeitige Diagnosestellung erfolgt jedoch nur bei einer Minderzahl der Patienten, waehrend die Mehrzahl bereits eine fortgeschrittene Erkrankung aufweist. Eines der Ziele des HCC-Screenings ist die Diagnosestellung in einem fruehen, kurativ therapierbaren Stadium. Dieses wird durch das Screening erreicht, und die Rate der mit kurativem Ansatz therapierten Patienten wird so deutlich gesteigert. Ob dieses jedoch zu einer Senkung der HCC-Mortalitaet fuehrt, ist bisher nicht klar belegt. Da die Reduktion der Mortalitaet der entscheidende Erfolgsparameter eines Screeningprogramms ist, ist der Nutzen des HCC-Screenings nach evidenzbasierten Kriterien bisher weder belegt noch widerlegt. Dennoch wird das HCC-Screening von Hochrisikopatienten mittels halbjaehrlichem Ultraschall und Alfa-Fetoprotein- (AFP-)Bestimmung in weiten Teilen der Welt praktiziert. (orig.)
[en] Highlights: • HIV-HCV co-infection increases HIV/HCV RNAs levels and apoptosis in hepatocytes. • Fibrotic matrix stiffness enhances HIV/HCV RNAs and apoptosis in hepatocytes. • Apoptotic infected hepatocytes induce pro-fibrotic changes in hepatic stellate cells. HIV-HCV co-infection causes rapid progression of liver fibrosis. These outcomes to liver cirrhosis can be improved, but not stopped by specific antiviral therapies. Due to high significance of HIV-HCV interactions for morbidity and mortality in co-infected patients, our attention was attracted to the multi-component pathogenesis of fibrosis progression as the transition to end-stage liver disease development. In this study, we hypothesize that increased matrix stiffness enhances apoptosis in HCV-HIV-co-infected hepatocytes and that capturing of apoptotic bodies (AB) derived from these infected hepatocytes by hepatic stellate cells (HSC) drives the fibrosis progression. As the source of viruses, JFH1 (HCV genotype 2a) and HIV-1ADA (either purified or containing in infected macrophage supernatants) were chosen. Using Huh7.5-CYP (RLW) cells and primary human hepatocytes mono-infected with HCV and HIV or co-infected, we have shown that both HCV and HIV RNA levels were increased in co-infected cells, which was accompanied by hepatocyte apoptosis. This apoptosis was attenuated by azidothymidine treatment. The levels of both infections and apoptosis were more prominent in primary hepatocytes cultured on substrates mimicking fibrotic stiffness (24 kPa-stiff) compared to substrates mimicking healthy liver (2.4 kPa-soft). The engulfment of AB from pathogen-exposed hepatocytes activated pro-fibrotic mRNAs in HSC. Overall, the increased matrix stiffness is not only a consequence of liver inflammation/fibrosis, but the condition that further accelerates liver fibrosis development. This is attributed to the switching of HSC to pro-fibrotic phenotype by capturing of excessive amounts of apoptotic HCV- and HIV-infected hepatocytes.
[en] The fact there are increase of intrapulmonary arteriovenous shunt amount in the liver cirrhosis patient has been known since 1950. And the method of shunt amount calculation by radionuclide method using 99mTc-MAA was introduced in the middle of 1970. We measured intrapulmonary shunt amount by means of perfusion lung scan using 99mTc-MAA in the various type of liver diseases especially in chronic liver diseases and acute liver disease. The results were as followed. 1) The amount of arteriovenous intrapulmonary shunt in the total case of liver disease was 9.3±3.9%, and that of in the control group was 4.6±2.1%. 2) The amount of arteriovenous intrapulmonary shunt in the chronic liver disease was 10.8±4.4%, and that of in the acute liver disease was 7.2±2.8%. We observed significant differences between normal control group and liver disease group, and between chronic liver disease group and acute liver disease group in the amount of shunt by the nucleolide method.
[en] To determine the utility of the chemical shift technique in MRI for the detection of fact in focal hepatic lesions and to see its significance in patients with and without hepatic cirrhosis. 159 patients with 207 hepatic lesions were studied using MRI (IT). Two groups were established: a) patients with hepatic cirrhosis (n=63 with 69 lesions) and b) patients without cirrhosis (n=96 with 138 lesions). Images were obtained in phase (P) and in opposite phase (OP) with gradient echo sequences (RG). The parameter used to differentiate the lesions with fat from those without fat was the variation percentage of the intensity of the signal (VIS) between the images in P and in OP. The statistical valuation was carried out using Student's t tests and the area under the ROC curve. The chemical shift technique detected fat in 25 lesions (12%), 10 hepatocarcinomas in the patients with cirrhosis and two angiomyolipomas and 13 nodular fat infiltrations in the patients who did not have cirrhosis. The average VIS percentage in the 10 hepatocarcinomas was 174.77% (ranging from 88.64% to 369.33%) while in the remaining 59 hepatocarcinomas it was -4.03% (ranging from 12.79% to -19.10%) (p=0.003). In the patients who did not have cirrhosis the average VIS percentage of the lesions with fat was 161.23 (ranging from 19.82 to 605.78) while in the lesions without fat it was -0.41 (ranging from -18.96 to 19.52) (p=0.003). The area under the ROC curve was 1 for the VIS parameter. The chemical shift technique allowed for fat to be detected within hepatic lesions. Based on our study, a nodule with fat in a patient with hepatic cirrhosis is suspected to have hepatocarcinomas while in patients who do not suffer from cirrhosis the existence of fat in a nodule favours its bening nature. (Author) 39 refs