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症例は66歳，女性．検診でC型肝炎を指摘され精査目的で当院受診．腹部エコーで肝S7-8に径４cmの辺縁高エコー，内部低エコーの腫瘤を認めた．Dopplerでは内部に血流を認めなかった．造影CTでは造影される乳頭状結節を伴う嚢胞性腫瘤を認めた．MRIでは腫瘤内部はT1強調像で低信号，T2強調像で高信号を呈し，造影MRIでは造影される乳頭状結節を認めた．肝嚢胞腺癌を否定できず手術を施行した．肝右上区域に肝外突出性の腫瘤を認め，横隔膜に癒着していた．肝右上区域切除・同部横隔膜合併切除を施行した．切除標本では内部に泥状物質の貯留を認め腫瘤壁は不均一に肥厚していた．病理所見では腫瘤は厚い線維層で被覆され，その内側にほぼ完全に壊死した層を認めた．一部に非壊死部を認め，銀染色で壊死以前には何らかの腫瘍性病変の存在が示唆された．良悪性の鑑別困難な肝嚢胞性腫瘤では自然壊死した腫瘍も考慮すべきであると思われた．

Objective: Hepatitis C virus (HCV) RNA titer and HCV genotype are considered to be major determinants of the outcome of interferon monotherapy. To clarify whether interferon monotherapy is really effective in patients with the appropriate viral parameters, we prospectively examined these parameters and treated the patients with interferon monotherapy. Methods: Sixty-four patients with an HCV RNA titer 100 kIU/ml and genotype 1 were also enrolled as controls. All patients were treated with 10 megaunits of interferon-α2b every day for 2 weeks and then 3 times a week for 24 weeks. Results: Of the 64 patients with either HCV RNA 100 kIU/ml and genotype 1 were virologic sustained responders (p < 0.001). Conclusion: Our current study showed that the patients with HCV RNA

Patient age and gender may be associated with response to peginterferon alpha plus ribavirin, the current standard of care (SOC) for chronic hepatitis C genotype 1. We queried whether there was an association between age, gender, and treatment response to SOC in Japanese patients infected with hepatitis C virus (HCV) genotype 1. Between 2006 and 2009, HCV-infected Japanese patients treated with peginterferon alpha-2b plus ribavirin for 48 weeks were enrolled. Patients were allocated into four groups according to age and gender, and epidemiological data and treatment outcomes were retrospectively analyzed. HCV RNA was measured with COBAS AMPLICOR HCV Monitor Test v. 2.0. The overall sustained virological response (SVR) rate was 49.8%: patients aged ≤65 and >65 years, 50.9 and 44.0%, respectively; male and female, 56.5 and 39.0%. SVR rates of SOC against HCV genotype-1 females aged >65 years (19.0%) were inferior to those in males aged >65 years (57.8%) in Japan. Multivariate logistic regression analysis showed that SVR was attained independently of adherence 80/80/80 in all groups. Adherence to medication is also a key factor for the eradication of HCV in patients aged >65 years. As the SVR rate of patients aged ≤65 years was similar to that of patients aged >65 years, SOC could be useful for treating some of the elderly patients.

Advanced chronic hepatitis C patients with sustained virolological response by antivirals remain at risk for hepatocellular carcinoma (HCC). We investigated the incidence of HCC during and immediately after peginterferon-alfa-2a and ribavirin (RBV) treatment in patients with chronic hepatitis C in Japan. HCC was detected in 8 of 238 patients during and after these treatments (mean follow-up period: 572 ± 252 days). In conclusion, occurrence of HCC is not a rare event during and immediately after peginterferon-alfa-2a plus RBV treatment. In cases with cirrhosis, higher α-fetoprotein levels, old age, or a previous history of HCC treatment, clinicians should be especially alert for the possible development of HCC during and immediately after peginterferon-alfa-2a and RBV treatment. Clinicians should regularly check for the possible development of HCC even in chronic hepatitis C patients under treatment.

The current standard treatment for patients infected with hepatitis C virus (HCV) of genotype 2 is the combination of peginterferon (PEG-IFN) plus ribavirin (RBV) for 24 weeks.We assessed the sustained virological response (SVR) rates in HCV genotype 2-infected Japanese patients in relation to the duration of treatment.Between 2006 and 2009, among 147 patients with HCV genotype 2-infection in Chiba Prefecture, 138 consecutive patients were finally enrolled. Twenty-one, 97 and 20 patients were treated with PEG-IFN-alfa 2b plus RBV for 16, 24 and 48 weeks, respectively. Epidemiological data and treatment outcomes were retrospectively evaluated. HCV RNA was measured with COBAS AMPLICOR HCV Monitor Test v. 2.0.The overall SVR rate was 82.6% (114 of 138): treatment-naïve patients, 86.4% (89 of 103); patients with history of previous treatment, 71.4% (25 of 35). Patients treated for 16, 24 and 48 weeks obtained SVR rates of 66.6% (14 of 21), 86.5% (84 of 97) and 80.0 (16 of 20), respectively.The SVR rates of PEG-IFN-alfa 2b plus RBV in Japanese patients were similar to those in previous studies. Combination treatment for 24 weeks for some patients infected with HCV genotype 2 may be superior to that for 16 weeks. More precise patient selection will be needed to shorten the combination treatment.

Summary. Extremely low levels of serum hepatitis C virus (HCV) RNA can be detected by COBAS TaqMan HCV test. To investigate whether the COBAS TaqMan HCV test is useful for measuring rapid virological response (RVR) and early virological response (EVR) to predict sustained virological response (SVR), we compared the virological response to PEG-IFN-alfa 2a plus RBV in 76 patients infected with HCV genotype 1 when undetectable HCV RNA by the COBAS TaqMan HCV test was used, with those when below 1.7 log IU/mL HCV RNA by COBAS TaqMan HCV test was used, which corresponded to the use of traditional methods. Among the 76 patients, 28 (36.8%) had SVR, 13 (17.1%) relapsed, 19 (25.0%) did not respond, and 16 (21.0%) discontinued the treatment due to side effects. The positive predictive values for SVR based on undetectable HCV RNA by COBAS TaqMan HCV test at 24 weeks after the end of treatment [10/10 (100%) at week 4, 21/23 (91.3%) at week 8 and 26/33 (78.7%) at week 12] were superior to those based on

The clinical features of 86 cases of idiopathic portal hypertension, the equivalent of hepatoportal sclerosis in the United States and of noncirrhotic portal fibrosis in India, are presented. This disease is characterized by overt splenomegaly with pancytopenia, portal hypertension, and relatively mild abnormalities in liver function tests. Although differential diagnosis from liver cirrhosis is not always easy, liver histology, laparoscopy, portography, hepatic venography, and measurement of wedged hepatic vein pressure are useful in diagnosis. Prognosis is relatively benign if variceal bleeding is controlled or prevented, and the disease does not progress to cirrhosis. The etiology is still undetermined, but the liver pathology characterized by occlusive changes of the intrahepatic portal radicles, portal and peripheral fibrosis, and irregularly distributed parenchymal atrophies suggests some sort of portal venopathy that causes decreased portal perfusion of peripheral liver parenchyma. These patients with idiopathic portal hypertension were compared with 63 cases of cirrhosis with splenomegaly and 80 cases of cirrhosis without splenomegaly. There was some similarity in hematologic findings between idiopathic portal hypertension and cirrhosis with splenomegaly, but the basic disease process seemed distinctly different. The cause of marked splenomegaly does not seem to be simply congestion, and remains an enigma.

従来の経皮経肝的門脈造影法(旧法)に新たにPTC針やSheath等を用いることによって,門脈への穿刺を安全且つ高い成功率で行い,さらに各種カテーテルの交換を極めて容易に施行しうる改良法(新法)を考案した.各種肝疾患133例に新・旧両法を施行しその各々の成功率,合併症,方法の相違点を検討し得られた門脈像から各門脈流域静脈の位置,分岐角度等をX線的に検討した.成功率は旧法で59.9%であったが新法では90.3%と向上した.一方合併症は両法を通じて胆道造影が28例(21.1%)と最も多く術後開腹術を必要とした例は1例(0.8%)であった.X線的に検討した側副血行路を含む門脈流域静脈の分岐・合流位置及びその角度等を参考にすれば,各静脈(特に側副血行路)への超選択的造影や採血等がさらに容易になり門脈圧亢進症においてその病態生理の研究や閉塞術の治療等に有用と思われる.

Two patients are described in whom percutaneous transhepatic catheterization of the portal vein for a hemodynamic study demonstrated a continuous reversed blood flow in the portal vein, entering into a large collateral. The measurements made of blood pressure in the superior mesenteric, splenic, and left gastric veins, and of ammonia, immunoreactive insulin, and C-peptide in blood taken from these and peripheral veins all indicated reversed portal vein blood flow. The evidence for retrograde portal vein blood flow was obtained in only 2 of 203 patients with cirrhosis in whom portal hemodynamics were studied by the same procedure. Thus, spontaneous reversal of portal vein blood flow does occur, but very rarely.

We studied the direction of blood flow in the splenic vein, using a combined ultrasonic system consisting of an electronic sector scanner and a pulsed Doppler flowmeter, in 21 patients with a large spontaneous splenorenal shunt demonstrated by angiography. Pulsed Doppler flowmetry revealed hepatofugal flow in the splenic vein in all 11 patients with chronic spontaneous hepatic encephalopathy, and hepatopetal flow in 10 patients without encephalopathy. In the former, hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt was corroborated by the venogram obtained after superior mesenteric arteriography. In 5 patients without a history of hepatic encephalopathy, superior mesenteric arteriography demonstrated hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt. Pulsed Doppler flowmetry, however, revealed hepatopetal flow in all of these patients, suggesting that the angiographic finding of hepatofugal flow may have represented an artifact.

To study the effects of intra- and extrahepatic portal-systemic shunts on insulin degradation, 11 patients with liver cirrhosis and 7 noncirrhotic patients with liver disease were studied with percutaneous transhepatic catheterization. Insulin levels in portal and peripheral blood were measured simultaneously for 1-2 hr after intravenous administration of glucose. The degrees of intra- and extrahepatic portal-systemic shunting were measured with this technique using 131I-macroaggregated albumin and 99mTc-macroaggregated albumin. The amount of insulin secreted and insulin degraded were assessed from the areas under blood concentration curves for portal and peripheral blood. Insulin degradation was significantly reduced in cirrhotics compared to noncirrhotics with liver disease, although there was no difference in the amount of insulin secreted between these two groups. It was also correlated significantly with the degree of intrahepatic shunting but not with the degree of extrahepatic shunting. These results suggest that intrahepatic shunting plays an important role in the reduction of insulin degradation in cirrhosis.

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.

1. 経静脈ブドウ糖負荷後,門脈血インシュリンはほぼ2分,15分から90分に頂値をもつ二相性の分泌を示した.末梢静脈血インシュリンもほぼ二相性の分泌を示した.2. 耐糖能の示標であるKG値は,門脈血IRI AUC060によって表わされたインシュリン分泌量より(門脈血IRI AUC060―末梢静脈血IRI AUC060)によって表わされたインシュリン消費量とより強い相関を示した.3. (門脈血IRI AUC060―末梢静脈血IRI AUC060)/(門脈血IRI AUC060)×100で表わされるインシュリン除去率は肝内短絡率と有意の相関を示したが,肝外短絡率とは相関しなかった.以上より肝内短絡発生に基づく,インシュリン代謝の減少は,慢性肝疾患,特に肝硬変患者にみられる耐糖能低下の成因の重要な1つの因子と考えられる.

To study the effects of habitual alcohol intake on the latency period for the development of liver cirrhosis and hepatocellular carcinoma (HCC), 158 patients with cirrhosis and 79 with HCC were analyzed with respect to age at the time of diagnosis. They were classified into four groups based on hepatitis B surface antigen (HBsAg) in serum, and the history of intake of more than one small bottle of Japanese "sake" or an equivalent per day for more than 10 years. The average age of HBsAg positive male cirrhotics with a drinking habit (n = 10) was 38.8 years, 10.5 years younger than that of those without a drinking habit (n = 8) (P less than 0.05). The average age of HBsAg negative cirrhotics with a drinking habit (n = 97) was 47.9 years, eight years younger than that of those not drinking (n = 36) (P less than 0.001). There was no significant difference in the laboratory data between these groups. The average age of the HBsAg positive HCC patients with a drinking habit (n = 20) was 48.9 years, nine years younger than that of those without a drinking habit (n = 12) (P less than 0.05). The average age of HBsAg negative male HCC cases with habitual intake of more than 126 ml of ethanol per day was 51.0 years (n = 8), ten years younger than that of nondrinking male HCC cases (n = 11) (P less than 0.05). These data suggest that habitual alcohol intake may promote the development of liver cirrhosis and HCC, especially in HBsAg carriers.

This is the report of a 50-year-old man with a more than 20-year history of chronic progressive portal-systemic encephalopathy. Liver tests were normal except for increased serum ammonia and indocyanine green plasma retention. The liver pathology was compatible with idiopathic portal hypertension or noncirrhotic portal fibrosis, demonstrating localized surface nodularity and portal fibrosis. Percutaneous transhepatic catheterization of the portal vein revealed near top normal portal vein pressure and a large shunt connecting the left gastric or superior mesenteric vein and the left renal vein. Presumably, the patient had portal hypertension in the past and formation of a short, large-caliber shunt between the portal system and the renal vein effectively decompressed the portal circulation.

A total of 141 patients with hepatocellular carcinoma were examined by selective celiac and hepatic arteriography. In 7 the so-called "thread and streaks" sign or its equivalent was observed along the vertebral column at the level of the diaphragm where the hepatic veins enter the inferior vena cava. Extensive tumor growth in the hepatic vein and invading the vena cava was confirmed by autopsy in 3 and hepatic venography in 1.