[Alcoholic steatohepatitis (ASH). 4. Therapy and follow-up].
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Fatty Liver, Alcoholic↗
Biomedical subjects
Yoshiyuki Yamagishi
Publications and source records attributed to Yoshiyuki Yamagishi.
[A case of intrahepatic cholangiocarcinoma effectively treated by hepatic arterial infusion chemotherapy].
The patient was a 50-year-old woman who suffered from gastric discomfort. She was first diagnosed as intrahepatic cholangiocarcinoma with hepatic, paraaortic lymphnodal and bone metastasis. Initial systemic chemotherapy using gemcitabine (GEM) and 5-FU failed to control the disease activity. Then she was given GEM and cisplatin (CDDP) combination chemotherapy. The response was assessed as stable disease (SD), but grade 4 leukopenia was seen. Then systemic therapy using GEM, and hepatic arterial infusion therapy with CDDP, l-leucovorin and 5-FU were continued biweekly. Partial response (PR) was achieved six months later, and her disease status was maintained as SD. This hepatic arterial infusion chemotherapy would be safe and feasible as therapy for inoperable intrahepatic cholangiocarcinoma.
Antineoplastic Combined Chemotherapy Protocols↗
[Alcoholic liver diseases and hepatitis virus C in Japan].
Recently incidence of alcoholic liver disease (ALD) has been increasing in Japan associated with an increase in alcoholic beverage consumption. There have been a large number of reports about the relationship between alcohol and hepatocarcinogenesis, but it remains controversial. In the present study, we addressed the recent trend in incidence of ALD including liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in heavy drinkers in Japan. We carried out nation-wide survey by asking for the hospitals that are approved by the Japanese Society of Gastroenterology for recent aspects of in-patients with ALD. Except for HCC, percentage of ALD without viral hepatitis is more than 70%, which is increased when compared to the national survey carried out in 1992. In alcoholic LC patients, those who did not have viral hepatitis were 81%. However, the percentage of HCC without viral hepatitis was 34% of all of the heavy drinkers with HCC. Regarding the case in our university hospital, 138 cases (32%) of 432 patients with HCC were heavy drinkers. However, regarding in our general hospital, 15 cases of 23 patients with HCC (61%) were heavy drinkers. In conclusion, since the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers.
Alcohol Drinking↗
Herbal cardiotonic pills prevent gut ischemia/reperfusion-induced hepatic microvascular dysfunction in rats fed ethanol chronically.
AIM: Cardiotonic Pill (CP), an oral herbal medicine that includes Danshen (Salviae Miltiorrhizae), Panax notoginseny and Dyroblanops aromatica gaertn, has been clinically used for vascular diseases such as occlusive vasculitis, coronary diseases, atherosclerosis, and cerebral infarction. The main component, Salviae Miltiorrhizae, has been reported to prevent cerebral and intestinal reperfusion injury. However, little is known about the effect of CP on hepatic microcirculation. Thus, this study aimed to determine whether CP could affect hepatic microvascular dysfunction elicited by gut ischemia/reperfusion (I/R) in rats fed ethanol chronically. METHODS: Male Wistar rats were pair-fed with a liquid diet containing ethanol or isocaloric control diet for 6 wk. After laparotomy, one lobe of the liver was examined through an inverted intravital microscope. The rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Rhodamine-6G-labeled leukocytes in the sinusoids were observed 90 min after the onset of superior mesenteric artery occlusion. Plasma tumor necrosis factor (TNF)-alpha and endotoxin levels were measured 1 h after the onset of reperfusion. Plasma alanine aminotransferase (ALT) activities were measured 6 h after the onset of reperfusion. In another set of experiments, CP (0.8 g/kg, intragastrically) was administered 1 and 24 h before the onset of ischemia. RESULTS: In control rats, gut I/R elicited increases in the number of stationary leukocytes, and plasma TNF-alpha and endotoxin levels and plasma ALT activities. These changes were mitigated by pretreatment with CP. In ethanol-fed rats, the gut I/R-induced increases in the number of stationary leukocytes, plasma endotoxin levels and ALT activities were enhanced. Pretreatment with CP attenuated the enhancement of gut I/R-induced responses by chronic ethanol consumption. CONCLUSION: These results suggest that CP prevents the gut I/R-induced hepatic microvascular dysfunction and hepatocellular injury. A reduction of inflammatory responses such as TNF-alpha production via reduction of blood endotoxin levels appears to be involved in the mechanisms. Chronic ethanol consumption enhances gut I/R-induced hepatic microvascular and hepatocellular injury. CP also attenuates an enhancement of gut I/R-induced responses by chronic ethanol consumption via the reduction of blood endotoxin levels.
Animals↗
Value of computed tomography-derived estimated liver volume/standard liver volume ratio for predicting the prognosis of adult fulminant hepatic failure in Japan.
BACKGROUND AND AIMS: The prognosis of fulminant hepatic failure (FHF) has been improved but is still unsatisfactory, and liver atrophy has been reported as a poor prognostic factor for this disease. The aim of this study was to assess the clinical value of the estimated liver volume (ELV) compared to the standard liver volume (SLV) in patients with FHF. METHODS: Estimated liver volume of 24 adult patients with FHF receiving artificial liver support (ALS) was measured by using computed tomography. Actual liver weight (ALW) was measured if possible, and the calculated ELV/SLV ratio was compared to the ALW/SLV ratio and the ALW/BW (bodyweight) ratio. Sequential ELV/SLV ratios during the clinical course were analyzed in relation to the prognosis. RESULTS: The ELV/SLV ratio was significantly correlated with both the ALW/SLV and ALW/BW ratios. The mean ALW/SLV ratio of patients who underwent living donor liver transplantation (LDLT) was 0.59 +/- 0.17. The mean ELV/SLV ratio at the time of starting ALS (day 0) in the patients who survived (group 1) was 1.081 +/- 0.183, but that of cases who underwent LDLT or died without LDLT (group 2) was 0.764 +/- 0.255. The mean ELV/SLV ratios were 1.084 +/- 0.222 and 0.650 +/- 0.195 in groups 1 and 2, respectively, 5 days after starting ALS (day 5). Among the group 2 patients, those who had no liver atrophy on day 0 had a significantly decreased ELV/SLV ratio on day 5. CONCLUSIONS: These results suggest that the ELV/SLV ratio is a very useful objective marker to estimate liver atrophy and this marker reflects the prognosis of FHF patients very well.
Adult↗
[A case of advanced gastric cancer with lymphangitis carcinomatosa after operation of Krukenberg tumor treated by TS-1 plus CPT-11 as third-line chemotherapy].
Chemotherapies for recurrent gastric cancer have not yet been established. Here we report a case of type 4 gastric cancer associated with lymphangitis carcinomatosis which became refractory to the previous chemotherapies. The case was a 40-year-old woman. She had been diagnosed with gastric cancer after a Krukenberg tumor operation. Chemotherapies (TS-1 plus CDDP as first-line, and TS-1 plus taxanes as second-line) were performed, and a partial response was achieved. Disease activity has been well controlled until this time. Since recurrence of left pleural effusion and lymphangitis carcinomatosis was recognized, we changed the chemotherapy TS-1 plus CPT-11. Pleural effusion decreased and lymphangitis carcinomatosis improved. The serum CA 19-9 level rose transiently after CPT-11 administration, and tended to fall at the second week of chemotherapy. However, the patient died 2 years 4 months after the onset. TS-1 plus CPT-11 combination chemotherapy would be effective for lymphangitis carcinomatosis and also useful as third-line chemotherapy for recurrent gastric cancer.
Adult↗
Japanese herbal medicine, Saiko-keishi-to, prevents gut ischemia/reperfusion-induced liver injury in rats via nitric oxide.
AIM: To determine whether Saiko-keishi-to (TJ-10), a Japanese herbal medicine, could protect liver injury induced by gut ischemia/reperfusion (I/R), and to investigate the role of NO. METHODS: Male Wistar rats were exposed to 30-min gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment. Plasma tumor necrosis factor (TNF) levels and alanine aminotransferase (ALT) activities were measured. TJ-10 1 g/(kg.d) was intragastrically administered to rats for 7 d. A NO synthase inhibitor was administered. RESULTS: In control rats, gut I/R elicited increases in the number of stationary leukocytes, and plasma TNF levels and ALT activities were mitigated by pretreatment with TJ-10. Pretreatment with the NO synthase inhibitor diminished the protective effects of TJ-10 on leukostasis in the liver, and the increase of plasma TNF levels and ALT activities. Pretreatment with TJ-10 increased plasma nitrite/nitrate levels. CONCLUSION: TJ-10 attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential hepatocellular injury via enhancement of NO production.
Animals↗
Hepatocellular carcinoma in heavy drinkers with negative markers for viral hepatitis.
Alcohol has been known to be associated with an increased risk of cancer. We investigated the characteristics of hepatocellular carcinoma (HCC) in heavy drinkers with negative serum markers for viral hepatitis (non-B, non-C) to determine whether ethanol enhances the development of HCC in Japanese patients with or without serum markers for viral hepatitis. Among the 432 HCC cases seen at our hospital between 1995 and 2000, 26 patients had negative serum markers (non-B, non-C) and were heavy drinkers. The mean patient age at the time of HCC diagnosis was [Formula: see text] years. The mean total ethanol intake was [Formula: see text] kg. Most of the patients also had liver cirrhosis (LC), although the frequency was significantly higher in non-B, non-C, heavy drinkers HCC cases than in non-B, non-C, non-alcoholic HCC cases. Among the hepatitis C virus (HCV)-positive cases, the mean age at the time of HCC diagnosis was lower in heavy drinkers; this trend was not seen in HBV-positive cases. In HCC cases with heavy drinking, a high frequency of gastrointestinal (oropharynx, esophagus, stomach, colon and anal) cancers was seen. As for the aldehyde dehydrogenase-2 (ALDH2) genotype, the frequency of normal homozygotes was 87.5% in heavy drinkers with HCC and the frequency of heterozygotes was 12.5%; the frequency of heterozygotes was 58.3% in alcoholics with esophageal cancer. More than half of the non-B, non-C, heavy drinkers HCC cases had a normal range of serum alpha-fetoprotein (AFP) levels. These results indicate that heavy drinking enhances HCV-related hepatocarcinogenesis. Whether or not ethanol is directly involved in hepatocarcinogenesis remains controversial, but LC may progress HCC in heavy drinkers even if their serum markers for HBV (including tissue) or HCV are negative. Therefore, close observation, including radiographic examinations, is recommended for non-B, non-C, heavy drinkers with LC. In HCV-positive cases, abstinence or a reduction in daily ethanol intake is recommended.
Journal Article↗
[A case of recurrent pleural effusion and positive cytology of advanced gastric cancer treated by TS-1 plus weekly taxane as second-line chemotherapy].
A second-line chemotherapy for advanced gastric cancer has not been established. We report a case of good response in a 39-year-old woman who had recurrent pleural effusion and positive cytology of type 4 gastric cancer and was treated with TS-1, a DPD inhibitory fluoropyrimidine, in combination with weekly taxane. After a partial response for type 4 gastric cancer from the treatment with 2 courses of TS-1 plus low-dose cisplatinum (CDDP), followed by outpatient chemotherapy with TS-1 alone or TS-1 plus weekly CDDP, left pleural effusion appeared and CA19-9 increased during the 7th course of the chemotherapy. Cytology of the effusion was class IV. The patient was treated with a course of TS-1 (120 mg/day, day 1-21) plus paclitaxel (50 mg/m2, day 1, 8) followed by 2 week washout. In the following courses, paclitaxel was replaced with docetaxel (30 mg/m2, day 1 and 8) and the course was continued in the outpatient setting. After 2 courses, the left pleural effusion disappeared and remained absent after 6 courses. Gastric biopsy showed no cancer cells and abdominal CT showed no recurrence. Serum CA19-9 doubled 1 week after taxane treatment and decreased gradually week by week during the course. This case suggests that a combination of TS-1 and taxane is effective against recurrent pleural effusion of advanced gastric cancer and useful as a second-line chemotherapy.
Adult↗
Low-dose ethanol attenuates gut ischemia/reperfusion-induced liver injury in rats via nitric oxide production.
BACKGROUND AND AIMS: The acute administration of low-dose ethanol was demonstrated to attenuate liver injury elicited by gut ischemia/reperfusion (I/R). Nitric oxide (NO) has been found to be a modulator of adhesive interactions between leukocytes, platelets, and endothelial cells, but there has been much controversy about the effects of ethanol on NO regulation. The objective of this study was to investigate the role of NO in ethanol-reduced hepatic microvascular dysfunction elicited by gut I/R. METHODS: Male Wistar rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment and non-perfused sinusoids (NPS). Plasma alanine aminotransferase (ALT) activities were measured 6 h after the onset of reperfusion. In another set of experiments, ethanol (10%, 1 g/kg) was administered before ischemia. RESULTS: Gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma ALT activities; all of which were attenuated by pretreatment with ethanol or an NO donor. Gut I/R caused the apoptosis of hepatocytes, which was prevented by pretreatment with ethanol. Pretreatment with an NO synthase inhibitor diminished the protective effects of ethanol. The administration of ethanol increased plasma nitrite/nitrate levels. CONCLUSION: These results suggest that low-dose ethanol attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential liver injury by increasing sinusoidal NO levels.
Alanine Transaminase↗
National survey of hepatocellular carcinoma in heavy drinkers in Japan.
BACKGROUND: The major cause of hepatocellular carcinoma (HCC) in the general Japanese population is an infection related to hepatotropic viruses, especially hepatitis virus C (HCV). Even in heavy drinkers, the major cause of HCC is HCV infection. However, HCC without viral infection has been reported in heavy drinkers. Alcohol has been also reported to be associated with an increased risk of cancer. In this study, we investigated aspects of HCC pathogenesis in heavy drinkers in Japan. METHODS: Questionnaires were sent to 1,350 hospitals authorized by the Japanese Society of Gastroenterology. The questionnaires asked about the number of inpatients with the different types of alcoholic liver diseases, admitted to each hospital between 1998 and 2001. RESULTS: The percentage of heavy drinkers among all admitted patients with liver diseases or liver cirrhosis was approximately 15%. Of the patients with alcoholic liver cirrhosis, the cirrhosis was derived from alcohol alone in 61% and from alcohol plus a virus in 39% of patients. Furthermore, the percentage of patients with alcoholic liver cirrhosis caused by alcohol alone and who did not have HCC was 80%. However, the percentage of HCC patients who tested negative for viral hepatitis serum markers was 27% of the total number of heavy drinkers admitted for HCC. A study mainly on liver cirrhosis performed in the early 1990's demonstrated that the alcohol-alone group accounted for 44% of admitted patients with alcoholic liver cirrhosis and 18% of heavy drinkers admitted for HCC. CONCLUSIONS: Because the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers. Radiographical examination is recommended even in patients with alcoholic liver cirrhosis who test negative for serum markers of viral hepatitis.
Adult↗
Hemophagocytic syndrome associated with fulminant hepatitis A: a case report.
A 37-year-old man had a sore throat and pyrexia since January 1999. He was treated at a nearby hospital, but not improved. Jaundice was indicated there, and the patient was referred transferred to our hospital, where he was admitted for treatment with a diagnosis of severe acute hepatitis with acute renal failure. Thereafter the patient was revealed to have had a past history of heavy drinking, and he underwent the treatment with a diagnosis of acute fulminant hepatitis due to hepatitis A virus (HAV). He showed a tendency toward improvement. During the course, however, viral associated hemophagocytic syndrome (VAHS) developed. Various treatments were conducted, but it was not improved, and the patient died on Hospital Day 66. On pathologic autopsy, remarkable hepatosplenomegaly associated with marked bone marrow abnormalities compatible with VAHS was observed. Aspergillus abscesses were also observed in many organs, and they were considered as an adverse reaction to potent immunosuppressive therapy. Since there have been only a few reports on HAV-related VAHS, discussing VAHS related to HAV, the present case was considered valuable.
Adult↗
[Recent progress in alcoholic liver diseases].
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Alcohol Drinking↗
[Alcoholic liver diseases in Japan and modification by hepatitis virus].
Recently incidence of alcoholic liver disease (ALD) has been increasing in Japan associated with an increase in alcoholic beverage consumption. There have been a large number of reports about the relationship between alcohol and hepatocarcinogenesis, but it remains controversial. In this review, we addressed 1) the recent trend in incidence of ALD including severe alcoholic hepatitis (SAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in heavy drinkers in Japan, and 2) the characteristics of HCC in heavy drinkers with negative serum markers for viral hepatitis. We carried out nation-wide survey by asking for the hospitals that are approved by the Japanese Society of Gastroenterology for recent aspects of in-patients with ALD. Except for HCC, percentage of ALD without viral hepatitis is more than 70%, which is increased when compared to the national survey carried out in 1992. Percentage of alcoholic LC without positive markers for viral hepatitis was 61% and alcohol plus virus group was 39%. Furthermore, in alcoholic LC patients without HCC, those who did not have viral hepatitis were 80%. However, the percentage of HCC without viral hepatitis was 27% of all of the heavy drinkers with HCC. Regarding our own cases, subjects were 432 HCC patients who were admitted to our hospital since 1995. There were 296 cases (68.5%) of HCV-positive, 70 cases (16.2%) of HBV-positive, 27 cases (6.3%) of both HCV- and HBV-positive. Thirty-nine cases (6.7%) were negative for serum markers for viral hepatitis. Among them, 13 cases (3.0%) were not heavy drinkers (non-B, non-C, non-alcohol) and 26 cases (6.0%) were heavy drinkers (non-B, non-C, heavy drinkers). Twenty-five of these 26 (96.2%) cases had cirrhosis. In conclusion, since the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers. Radiographic examinations at an appropriate interval for HCC are recommended, even in cases with alcoholic liver cirrhosis who are negative for serum markers of viral hepatitis, to ensure the early diagnosis of HCC.
Alcohol Drinking↗
[A case of liver abscess with septic thrombophlebitis of the portal vein and superior mesenteric vein caused by Streptococcus milleri].
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Humans↗
Role of ICAM-1 in chronic ethanol consumption-enhanced liver injury after gut ischemia-reperfusion in rats.
Intercellular adhesion molecule-1 (ICAM-1) has been implicated in the hepatic microvascular dysfunction elicited by gut ischemia-reperfusion (I/R). Although the effects of chronic ethanol (EtOH) consumption on the liver are well known, it remains unclear whether this condition renders the hepatic microcirculation more vulnerable to the deleterious effects of gut and/or hepatic I/R. The objectives of this study were to determine whether chronic EtOH consumption alters the severity of gut I/R-induced hepatic microvascular dysfunction and hepatocellular injury and to determine whether ICAM-1 contributes to this response. Male Wistar rats, pair fed for 6 wk a liquid diet containing EtOH or an isocaloric control diet, were exposed to gut I/R. Intravital video microscopy was used to monitor leukocyte recruitment in the hepatic microcirculation, the number of nonperfused sinusoids (NPS), and plasma concentrations of endotoxin and tumor necrosis factor-alpha. Plasma alanine aminotransferase (ALT) levels were measured 6 h after the onset of reperfusion. In control rats, gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma endotoxin, tumor necrosis factor-alpha, and ALT. In EtOH-fed rats, the gut I/R-induced increases in NPS and leukostasis were blunted in the midzonal region, while exaggerated leukostasis was noted in the pericentral region and terminal hepatic venules. Chronic EtOH consumption also enhanced the gut I/R-induced increase in plasma endotoxin and ALT. The exaggerated responses to gut I/R normally seen in EtOH-fed rats were largely prevented by pretreatment with a blocking anti-ICAM-1 monoclonal antibody. In conclusion, these results suggest that chronic EtOH consumption enhances gut I/R-induced hepatic microvascular dysfunction and hepatocellular injury in the pericentral region and terminal hepatic venules via an enhanced hepatic expression of ICAM-1.
Alanine Transaminase↗
Ethanol modulates gut ischemia/reperfusion-induced liver injury in rats.
Whereas both ethanol and gut ischemia/reperfusion (I/R) are known to alter hepatic microvascular function, little is known about the influence of ethanol consumption on the hepatic microvascular responses to I/R. The objective of this study was to determine whether acute ethanol administration exacerbates the hepatic microvascular dysfunction induced by gut I/R. Rats were exposed to gut ischemia for 30 min followed by reperfusion. Intravital videomicroscopy was used to monitor leukocyte recruitment and the number of nonperfused sinusoids (NPS). Plasma alanine aminotransferase (ALT), tumor necrosis factor-alpha (TNF-alpha), and endotoxin concentrations were monitored. In separate experiments, ethanol was administered 15 min or 24 h before gut ischemia. In control rats, gut I/R increased the number of stationary leukocytes and NPS. It also elevated the plasma ALT, TNF-alpha, and endotoxin with a corresponding increase in intestinal mucosal permeability. Low-dose ethanol consumption 15 min before gut ischemia blunted the gut I/R-induced leukostasis and elevations in plasma TNF-alpha and ALT. However, high-dose ethanol consumption aggravated the gut I/R-induced increases in leukostasis and increases in plasma endotoxin and ALT. When ethanol was administered 24 h before, high-dose ethanol aggravated the gut I/R-induced hepatocellular injury, but low-dose ethanol did not have any effects on it. These results suggest that low-dose ethanol consumption shortly before gut ischemia attenuates the hepatic inflammatory responses, microvascular dysfunction, and hepatocellular injury elicited by gut I/R, whereas high-dose ethanol consumption appears to significantly aggravate these gut I/R-induced responses.
Alanine Transaminase↗
[Intensive therapy for fulminant hepatic failure: importance of co-operation between physicians of internal medicine and transplantation surgery].
We followed up the patients with fulminant hepatic failure who admitted in our hospital and investigated clinical problems raised in the patients who underwent living-related liver transplantation (LRLT). Among 15 patients with fulminant hepatic failure 6 were managed without LRLT and 3 patients survived, and the survival rate was 50%. Other 9 patients received LRLT, and 2 of these 9 died with their complications after the transplantation. Thus the survival rate by LRLT in fulminant hepatic failure was 77.8%. Brain CT scan examination showed severe brain edema in a patient and the edema did not improve after LRLT. Another patient suffered from development of fungal infection in her lungs after LRLT. We suspected the presence of subclinical infection in the preoperation period. The recovery from brain edema and the existence of subclinical infection are mostly difficult to evaluate but are very important for obtaining a good output. These results suggest that LRLT is a promising procedure for treatment of fulminant hepatic failure but a close cooperation between physicians of internal medicine and transplantation surgery from preoperative management until postoperative period is necessary.
Acute Disease↗