Changes in physical activity level during hospitalization in patients with stroke and those with fracture: a prospective longitudinal study.

[Purpose] To examine changes in physical activity levels between admission and discharge in patients hospitalized after stroke and fracture. [Participants and Methods] Patients with stroke (n=36) or fracture (n=41) wore an accelerometer during the daytime for three days after admission and before discharge. Physical activity was divided into sedentary behavior (SB), light-intensity (LIPA), and moderate-to-vigorous (MVPA), and then compared between hospital admission and discharge using the Wilcoxon signed-rank test. The characteristics of patients with or without changes in SB during hospitalization were compared using the Mann-Whitney U test. [Results] The median LIPA time in patients after stroke and fracture increased from 107.5 and 106.7 minutes on admission to 122.0 and 127.3 minutes at discharge, and the median MVPA time increased from 2.7 and 0.7 minutes on admission to 4.2 and 2.7 minutes at discharge, respectively. In particular, LIPA in non-therapy time increased for patients both after stroke and fracture. No differences in characteristics were observed between with or without changes in SB regardless of differences in diagnoses. [Conclusion] These findings indicate that while physical activity levels increased during hospitalization, they remained below World Health Organization recommendations for MVPA, and patient characteristics alone may not account for increased activity levels.

Medium-chain triglyceride supplementation under a low-carbohydrate formula is a promising therapy for adult-onset type II citrullinemia.

BACKGROUND: Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver. Citrin deficiency causes neonatal intrahepatic cholestasis (NICCD), which usually resolves within the first year of life. However, small numbers of adults with citrin deficiency develop hyperammonemic encephalopathy, adult-onset type II citrullinemia (CTLN2), which leads to death due to cerebral edema. Liver transplantation is the only definitive therapy for patients with CTLN2. We previously reported that a lactose (galactose)-restricted and medium-chain triglyceride (MCT)-supplemented formula is notably effective for patients with NICCD. Citrin deficiency may impair the glycolysis in hepatocytes because of an increase in the cytosolic NADH/NAD+ ratio, leading to an energy shortage. MCT administration can provide energy to hepatocytes and was expected to have a good effect on CTLN2. METHODS: An MCT supplementation therapy under a low-carbohydrate formula was administered to five patients with CTLN2. Four of the patients had episodes of hyperammonemic encephalopathy, and one patient had postprandial hyperammonemia with no symptoms. RESULTS: One of the patients displaying hyperammonemic encephalopathy completely recovered with all normal laboratory findings. Others notably improved in terms of clinical and or laboratory findings with no hyperammonemic symptoms; however, the patients displayed persistent mild citrullinemia and occasionally had postprandial mild hyperammonemia most likely due to an irreversible change in the liver. CONCLUSIONS: An MCT supplement can provide energy to hepatocytes and promote hepatic lipogenesis, leading to a reduction in the cytosolic NADH/NAD+ ratio. MCT supplementation under a low-carbohydrate formula could be a promising therapy for CTLN2 and should also be used to prevent CTLN2 to avoid irreversible liver damage.

The anti-apoptotic effect of fucoxanthin on carbon tetrachloride-induced hepatotoxicity.

This study evaluated the anti-apoptotic activity of fucoxanthin in carbon tetrachloride (CCl(4))-induced hepatotoxicity. An in vitro study using the 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay clearly demonstrated an attenuation of CCl(4)-induced hepatotoxicity with fucoxanthin. This effect was dose-dependent; 25 µM was more effective than 10 µM of fucoxanthin for attenuating the hepatotoxicity induced by 5 mM of CCl(4). Acute CCl(4)-hepatotoxicity in rats, with numerous cells positive for the terminal deoxynucleotidyl - transferase (TdT) -mediated deoxyuridine triphosphate-digoxigenin (dUTP) nick-end labeling (TUNEL) stain were seen in the pericentral area of the hepatic lobule. Oral pretreatment of CCl(4)- injected rats with fucoxanthin significantly reduced hepatocyte apoptosis. Fucoxanthin was immunohistochemically shown to increase heme oxygenase-1 expression in the cultured liver cells of Hc cells and TRL1215 cells. By oral pretreatment of CCl(4)-injected rats with fucoxanthin, the hepatic heme oxygenase-1 protein levels were significantly increased compared to those not pretreated with fucoxanthin. Heme oxygenase-1 mRNA expression after CCl(4 )injection was higher in the CCl(4)+fucoxanthin group than in the CCl(4 )group, although the difference was not significant. The findings suggest that fucoxanthin attenuates hepatocyte apoptosis through heme oxygenase-1 induction in CCl(4)-induced acute liver injury.

[A case of hepatitis E differentially diagnosed from drug-induced liver injury].

A woman in her seventies was admitted because of general fatigue and liver dysfunction (ALT 2565 IU/l). She was diabetic and, 2 months ago, began eating kikuimo (Jerusalem artichoke) containing inulin, which is thought to decrease blood sugar level. Although tests showed no evidence of acute infection of HAV, HBV, HCV, EBV and CMV, a drug-induced lymphocyte stimulation test using kikuimo extract was positive. She was first diagnosed with drug-induced liver injury according to the Japanese diagnostic criteria for the disease. After a non-eventful recovery, her serum was found to be positive for hepatitis E-antibody and RNA (genotype 3), indicating recent, autochthonous infection of HEV. The patient might have been misdiagnosed with drug-induced liver injury unless the serum test for HEV had been performed. We believe that HEV screening is mandatory for accurate diagnosis of hepatitis E and drug-induced liver injury.

Hepatocellular carcinoma in extremely elderly patients: an analysis of clinical characteristics, prognosis and patient survival.

AIM: To identify the clinical and prognostic features of patients with hepatocellular carcinoma (HCC) aged 80 years or more. METHODS: A total of 1310 patients with HCC were included in this study. Ninety-one patients aged 80 years or more at the time of diagnosis of HCC were defined as the extremely elderly group. Two hundred and thirty-four patients aged > or = 50 years but less than 60 years were regarded as the non-elderly group. RESULTS: The sex ratio (male to female) was significantly lower in the extremely elderly group (0.90:1) than in the non-elderly group (3.9:1, P < 0.001). The positive rate for HBsAg was significantly lower in the extremely elderly group and the proportion of patients negative for HBsAg and HCVAb obviously increased in the extremely elderly group (P < 0.001). There were no significant differences in the following parameters: diameter and number of tumors, Child-Pugh grading, tumor staging, presence of portal thrombosis or ascites, and positive rate for HCVAb. Extremely elderly patients did not often receive surgical treatment (P < 0.001) and they were more likely to receive conservative treatment (P < 0.01). There were no significant differences in survival curves based on the Kaplan-Meier methods in comparison with the overall patients between the two groups. However, the survival curves were significantly worse in the extremely elderly patients with stage I/II, stage I/II and Child-Pugh grade A cirrhosis in comparison with the non-elderly group. The causes of death did not differ among the patients, and most cases died of liver-related diseases even in the extremely elderly patients. CONCLUSION: In the patients with good liver functions and good performance status, aggressive treatment for HCC might improve the survival rate, even in the extremely elderly patients.

Pilot clinical trial of the use of alpha-tocopherol for the prevention of hepatocellular carcinoma in patients with liver cirrhosis.

Patients with chronic hepatitis C virus (HCV) infection often develop liver cirrhosis and hepatocellular carcinoma (HCC). The purpose of this study was to test the chemopreventive effect of alpha-tocopherol on hepatocarcinogenesis in patients with liver cirrhosis and a history of HCV infection. Eighty-three patients with liver cirrhosis and with positive history of HCV infection were divided at random into two groups. Forty-four patients were treated with alpha-tocopherol (Vit E group) while the other 39 were followed as controls. The clinical background (gender, age, and laboratory data) was similar in the two groups. Serum levels of alpha-tocopherol, albumin, alanine aminotransferase (ALT), and total cholesterol and platelet count were measured serially over a period of five years. The mean serum concentration of alpha-tocopherol was low in both groups at entry and was significantly higher in the Vit E group than in the control group one month after treatment. Platelet count, serum albumin, ALT, and total cholesterol were not different between the two groups during the five-year period. Cumulative tumor-free survival and cumulative survival rate tended to be higher in the Vit E group than in controls, albeit statistically insignificant. The serum level of alpha-tocopherol was low in patients with liver cirrhosis and positive for HCV. Although the administration of alpha-tocopherol normalized the level one month later, it could neither improve liver function, suppress hepatocarcinogenesis, nor improve cumulative survival. Patients treated with alpha-tocopherol tended to live longer without development of HCC but the difference was not statistically significant.

Severe manifestation of acute hepatitis A recently found in Gunma, Japan.

BACKGROUND: The incidence of acute hepatitis A infection in Japan peaked 10 years ago and has been decreasing since then. However, an increase in severe cases of the disease has been documented recently. We experienced an outbreak in 1998-1999, and compared the clinical features of the disease in 1998-1999 (recent outbreak) and in 1987-1988 (past outbreak) in our prefecture (Gunma). METHODS: Forty patients with acute hepatitis A were admitted to nine Gunma hospitals from October 1998 to September 1999. Their clinical features were compared with those of 100 patients with acute hepatitis A admitted to the same hospitals in 1987-1988. RESULTS: Both outbreaks occurred mostly during the winter-spring season. Secondary familial infection was significantly decreased in the recent outbreak. Patients in the recent outbreak were 7 years older than those in the past outbreak. Laboratory findings, such as serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and prothrombin time, were worse in the recent than in the past outbreak. Severe-type hepatitis and fulminant hepatitis occurred in 5 patients (12.5%) in the recent outbreak but in only 2 patients (2.0%) in the past outbreak. CONCLUSIONS: Clinical data and manifestations were more severe in the recent outbreak than in the past outbreak of acute hepatitis A. It is important to be aware of hepatitis A virus infection and to take into account the available vaccination against hepatitis A virus in Japan.

A case of amebic liver abscess complicated by hemobilia due to rupture of hepatic artery aneurysm.

We report the case of a 51-year-old man with hepatic amebic abscess complicated by hepatic artery aneurysm. The patient first presented with peritonitis caused by perforating appendicitis. Surgical treatment resolved peritonitis but Entamoeba histolytica was detected in the colonic mucosa. Subsequently, liver abscess developed and the size of the abscess increased gradually after surgery in spite of continued treatment with metronidazole. Brown pus was drained from the abscess but 13 days after the drainage process the patient complained of right upper abdominal pain and the drained fluid became blood-colored and stool became tarry in color. Enhanced computed tomography showed a hepatic artery aneurysm that had ruptured into the liver abscess and duodenoscopy revealed bleeding from the ampulla of Vater. Transcatheter arterial embolization with several steel coils was successfully performed which resulted in cessation of bleeding from the ampulla of Vater. The patient was discharged without any complications five weeks after rupture of the aneurysm. Our case demonstrates rupture of the hepatic artery aneurysm as a rare complication of amebic liver abscess and the effectiveness of interventional embolotherapy in this condition.