BACKGROUND The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia,thereby causing significant alterations in the anatomical and morphological aspects of the live...BACKGROUND The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia,thereby causing significant alterations in the anatomical and morphological aspects of the liver.This condition significantly hampers the accuracy of preoperative imaging diagnosis,while also exacerbating the complexity of surgical procedures and the likelihood of complications.CASE SUMMARY A 60-year-old female patient was admitted to the hospital presenting with recurring epigastric pain accompanied by a high fever.The patient had a history of cholecystectomy,although the surgical records were not accessible.Based on preoperative imaging and laboratory examination,the initial diagnosis indicated the presence of intrahepatic calculi,abnormal right liver morphology,and acute cholangitis.However,during the surgical procedure,it was observed that both the left and right liver lobes exhibited evident atrophy and thinness.Additionally,there was a noticeable increase in the volume of the hepatic caudate lobe,and the original bilioenteric anastomosis was narrowed.The anastomosis underwent enlargement subsequent to hepatectomy.As a consequence of the presence of remaining stones in the caudate lobe,the second stage was effectively executed utilizing ultrasound-guided percutaneous transhepatic catheter drainage.Following the puncture,three days elapsed before the drain tip inadvertently perforated the liver,leading to the development of biliary panperitonitis,subsequently followed by pulmonary infection.The patient and her family strongly refused operation,and she died.CONCLUSION The hepatic atrophy-hypertrophy complex induces notable alterations in the anatomical structure,thereby posing a substantial challenge in terms of imaging diagnosis and surgical procedures.Additionally,the long-term presence of hepatic fibrosis changes heightens the likelihood of complications arising from puncture procedures.展开更多
Background and Aims:The aim was to establish a liver venous deprivation(LVD)model in rats,compare hepatic hypertrophy between LVD and associated liver partition and portal vein ligation for staged hepatectomy(ALPPS),a...Background and Aims:The aim was to establish a liver venous deprivation(LVD)model in rats,compare hepatic hypertrophy between LVD and associated liver partition and portal vein ligation for staged hepatectomy(ALPPS),and explore the underlying mechanisms.Methods:The LVD or extended-LVD(e-LVD)group received portal vein ligation(PVL)combined with hepatic vein ligation(HVL).The ALPPS or eALPPS group received PVL plus parenchyma ligation.Liver regeneration was assessed by measuring the liver weight and performing pathological analysis.Liver functions and the sphingosine kinase 1(SPHK1)/sphingosine-1-phosphate(S1P)/sphingosine-1-phosphate receptor 1(S1PR1)pathway were also investigated.Results:All future liver remnants(FLRs)in the ALPPS,e-ALPPS,LVD,and e-LVD groups exhibited significant hypertrophy compared with the control group.The LVD and e-LVD procedures induced similar liver hypertrophy than that in the corresponding ALPPS groups.Furthermore,the LVD and e-LVD methods led to obvious cytolysis in the venous-deprived lobes as well as a noticeable increase in serum transaminase levels,while no necrosis was observed in the ALPPS and e-ALPPS groups.SPHK1/S1P/S1PR1 pathway were distinctly activated after operation,especially in congestive/ischemic livers.Conclusions:We describe the first rat model of LVD and e-LVD with simultaneously associated HVL and PVL.Compared with the ALPPS technique,the LVD or e-LVD procedure had a comparable overall effect on the hypertrophy response and a stronger effect on liver function.The SPHK1/S1P/S1PR1 pathway was involved in the LVD-or ALPPS-induced liver remodeling.展开更多
BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing l...BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing liver segments.This study aimed to determine the effects of transcatheter arterial embolization(TAE)on tumor volume and liver regeneration in a rabbit VX2 tumor model.METHODS:Twenty-three rabbits underwent subcapsular tumor implantation with a VX2 tumor.Two weeks after implantation,18 rabbits were used for TAE experiments,5were for sham controls.Tumor response and liver regeneration response of the embolized cranial and non-embolized caudal liver lobes were assessed by CT volumetry,liver to body weight index,and the amount of proliferating hepatocytes.RESULTS:All super-selective arterial tumor embolization procedures were performed successfully.Despite embolization,the tumor volume increased after an initial steady state.The tumor volume after embolization was smaller than that of the sham group,but this difference was not significant.Massive necrosis of the tumor,however,was seen after embolization,without damage of the surrounding liver parenchyma.There was a significant atrophy response of the tumor bearing cranial lobe after super-selective arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized,caudal lobe.This regeneration response was confirmed histologically by a significantly higher number of proliferating hepatocytes on the Ki-67 stained slides.CONCLUSIONS:Super-selective,bland arterial coil embolization causes massive necrosis of the tumor,despite increase of volume on CT scan.Atrophy of the tumor bearing liver lobe is seen after arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized lobe,despite absence of histological damage of the tumor-surrounding liver parenchyma.展开更多
Recent nationwide clinico-epidemiological surveys in Japan showed that the occurrence of cardiomyopathies was most frequently seen in the age of sixties, and that cardiomyopathies are important causes of heart failure...Recent nationwide clinico-epidemiological surveys in Japan showed that the occurrence of cardiomyopathies was most frequently seen in the age of sixties, and that cardiomyopathies are important causes of heart failure in the elderly. Viral infection was conventionally considered to cause myocarditis, which resulted in the development of dilated cardiomyopathy. Recent studies suggest that hepatitis C virus (HCV) is involved in the development of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in addition to myocarditis. Furthermore, left ventricular aneurysm represents the same morbid state not only after myocardial infarction but also after myocarditis. There were wide variations in the frequency of detection of HCV genomes in cardiomyopathy in different regions and in different populations. Major histocompatibility complex class Ⅱ genes may play a role in the susceptibility to HCV infection, and may influence the development of different phenotypes of cardiomyopathy. If in fact the myocardial damage is caused by HCV, it might be expected that interferon (IFN) administration would be useful for its treatment. Hepatitis patients receiving IFN treatment for hepatitis were screened by thallium myocardial scintigraphy, and an abnormality was discovered in half of the patients. Treatment with IFN resulted in a disappearance of the image abnormality. It has thus been suggested that mild myocarditis and myocardial damage may be cured with IFN. We have recently found that high concentrations of circulating cardiac troponin T are a specific marker of cardiac involvement in HCV infection. By measuring cardiac troponin T in patients with HCV infection, the prevalence of cardiac involvement in HCV infection will be clarified. We are proposing a collaborative work on a global network on myocarditis/cardiomyopathies due to HCV infection. (J Geriatr Cardiol 2004;1(2):83-89. )展开更多
文摘BACKGROUND The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia,thereby causing significant alterations in the anatomical and morphological aspects of the liver.This condition significantly hampers the accuracy of preoperative imaging diagnosis,while also exacerbating the complexity of surgical procedures and the likelihood of complications.CASE SUMMARY A 60-year-old female patient was admitted to the hospital presenting with recurring epigastric pain accompanied by a high fever.The patient had a history of cholecystectomy,although the surgical records were not accessible.Based on preoperative imaging and laboratory examination,the initial diagnosis indicated the presence of intrahepatic calculi,abnormal right liver morphology,and acute cholangitis.However,during the surgical procedure,it was observed that both the left and right liver lobes exhibited evident atrophy and thinness.Additionally,there was a noticeable increase in the volume of the hepatic caudate lobe,and the original bilioenteric anastomosis was narrowed.The anastomosis underwent enlargement subsequent to hepatectomy.As a consequence of the presence of remaining stones in the caudate lobe,the second stage was effectively executed utilizing ultrasound-guided percutaneous transhepatic catheter drainage.Following the puncture,three days elapsed before the drain tip inadvertently perforated the liver,leading to the development of biliary panperitonitis,subsequently followed by pulmonary infection.The patient and her family strongly refused operation,and she died.CONCLUSION The hepatic atrophy-hypertrophy complex induces notable alterations in the anatomical structure,thereby posing a substantial challenge in terms of imaging diagnosis and surgical procedures.Additionally,the long-term presence of hepatic fibrosis changes heightens the likelihood of complications arising from puncture procedures.
基金supported by the Fundamental Research Funds for the Central Universities (NO.2042020kf0124)the National Natural Science Foundation of China (NO.82001940).
文摘Background and Aims:The aim was to establish a liver venous deprivation(LVD)model in rats,compare hepatic hypertrophy between LVD and associated liver partition and portal vein ligation for staged hepatectomy(ALPPS),and explore the underlying mechanisms.Methods:The LVD or extended-LVD(e-LVD)group received portal vein ligation(PVL)combined with hepatic vein ligation(HVL).The ALPPS or eALPPS group received PVL plus parenchyma ligation.Liver regeneration was assessed by measuring the liver weight and performing pathological analysis.Liver functions and the sphingosine kinase 1(SPHK1)/sphingosine-1-phosphate(S1P)/sphingosine-1-phosphate receptor 1(S1PR1)pathway were also investigated.Results:All future liver remnants(FLRs)in the ALPPS,e-ALPPS,LVD,and e-LVD groups exhibited significant hypertrophy compared with the control group.The LVD and e-LVD procedures induced similar liver hypertrophy than that in the corresponding ALPPS groups.Furthermore,the LVD and e-LVD methods led to obvious cytolysis in the venous-deprived lobes as well as a noticeable increase in serum transaminase levels,while no necrosis was observed in the ALPPS and e-ALPPS groups.SPHK1/S1P/S1PR1 pathway were distinctly activated after operation,especially in congestive/ischemic livers.Conclusions:We describe the first rat model of LVD and e-LVD with simultaneously associated HVL and PVL.Compared with the ALPPS technique,the LVD or e-LVD procedure had a comparable overall effect on the hypertrophy response and a stronger effect on liver function.The SPHK1/S1P/S1PR1 pathway was involved in the LVD-or ALPPS-induced liver remodeling.
文摘BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing liver segments.This study aimed to determine the effects of transcatheter arterial embolization(TAE)on tumor volume and liver regeneration in a rabbit VX2 tumor model.METHODS:Twenty-three rabbits underwent subcapsular tumor implantation with a VX2 tumor.Two weeks after implantation,18 rabbits were used for TAE experiments,5were for sham controls.Tumor response and liver regeneration response of the embolized cranial and non-embolized caudal liver lobes were assessed by CT volumetry,liver to body weight index,and the amount of proliferating hepatocytes.RESULTS:All super-selective arterial tumor embolization procedures were performed successfully.Despite embolization,the tumor volume increased after an initial steady state.The tumor volume after embolization was smaller than that of the sham group,but this difference was not significant.Massive necrosis of the tumor,however,was seen after embolization,without damage of the surrounding liver parenchyma.There was a significant atrophy response of the tumor bearing cranial lobe after super-selective arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized,caudal lobe.This regeneration response was confirmed histologically by a significantly higher number of proliferating hepatocytes on the Ki-67 stained slides.CONCLUSIONS:Super-selective,bland arterial coil embolization causes massive necrosis of the tumor,despite increase of volume on CT scan.Atrophy of the tumor bearing liver lobe is seen after arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized lobe,despite absence of histological damage of the tumor-surrounding liver parenchyma.
文摘Recent nationwide clinico-epidemiological surveys in Japan showed that the occurrence of cardiomyopathies was most frequently seen in the age of sixties, and that cardiomyopathies are important causes of heart failure in the elderly. Viral infection was conventionally considered to cause myocarditis, which resulted in the development of dilated cardiomyopathy. Recent studies suggest that hepatitis C virus (HCV) is involved in the development of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in addition to myocarditis. Furthermore, left ventricular aneurysm represents the same morbid state not only after myocardial infarction but also after myocarditis. There were wide variations in the frequency of detection of HCV genomes in cardiomyopathy in different regions and in different populations. Major histocompatibility complex class Ⅱ genes may play a role in the susceptibility to HCV infection, and may influence the development of different phenotypes of cardiomyopathy. If in fact the myocardial damage is caused by HCV, it might be expected that interferon (IFN) administration would be useful for its treatment. Hepatitis patients receiving IFN treatment for hepatitis were screened by thallium myocardial scintigraphy, and an abnormality was discovered in half of the patients. Treatment with IFN resulted in a disappearance of the image abnormality. It has thus been suggested that mild myocarditis and myocardial damage may be cured with IFN. We have recently found that high concentrations of circulating cardiac troponin T are a specific marker of cardiac involvement in HCV infection. By measuring cardiac troponin T in patients with HCV infection, the prevalence of cardiac involvement in HCV infection will be clarified. We are proposing a collaborative work on a global network on myocarditis/cardiomyopathies due to HCV infection. (J Geriatr Cardiol 2004;1(2):83-89. )
