Satoaki Mima

Treatment of gastric fundal varices by balloon-occluded retrograde transvenous obliteration

Although less common than oesophageal varices in portal hypertension, gastric fundal varices carry a higher mortality rate when they rupture. They are less amenable to sclerotherapy. We have developed a minimally invasive balloon‐occluded retrograde transverse obliteration (B‐RTO) procedure to treat gastric fundal varices. B‐RTO involves inserting a balloon catheter into an outflow shunt (gastric‐renal or gastric‐vena caval inferior) via the femoral or internal jugular vein. Blood flow is then blocked by inflating the balloon, and 5% ethanolamine oleate iopamidol is injected in a retrograde manner. The embolized gastric varix subsequentlyl disappears. B‐RTO was performed in 32 patients with gastric varices. Follow‐up endoscopies were performed at intervals of 2–4 months for an average observation period of 14 months. Eradication of the varices has been confirmed in 31 of 32 patients. No recurrence occurred in any patients in the follow‐up period. There were no significant changes in liver function after the procedure. We conclude that B‐RTO is a safe and effective procedure for the treatment of gastric fundal varices.

HEPATITIS C VIRUS IS FREQUENTLY COINFECTED WITH SERUM MARKER-NEGATIVE HEPATITIS B VIRUS: PROBABLE REPLICATION PROMOTION OF THE FORMER BY THE LATTER AS DEMONSTRATED BY IN VITRO COTRANSFECTION

Patients with hepatitis C have been reported occasionally to be coinfected with serum marker‐negative (silent) hepatitis B virus (HBV). The frequency and significance of such coinfection were investigated. Thirty patients with hepatitis C virus (HCV) infections (10 acute, 10 chronic, 10 cirrhotic) were selected randomly; the acute cases were without serum hepatitis B surface antigen (HBsAg) and anti‐hepatitis B core IgM, and the chronic cases were without HBsAg. A nested polymerase chain reaction for the X open reading frame was used to amplify HBV DNA in serum, and immunoperoxidase staining was carried out on liver biopsy specimens. Nucleotide sequencing was carried out to characterize the amplified HBV DNAs. In order to clarify the possibility that the silent HBV mutant promotes HCV replication in the liver, the full‐length HCV RNA and the cloned silent HBV DNA dimer were cotransfected into an established cell line, HuH‐7, and the amount of secreted HCV RNA was quantified serially. The target HBV DNA was amplified in 26 (86.7%) of the 30 patients. Subsequent direct nucleotide sequencing in 9 selected patients revealed an 8‐nucleotide deletion, characteristic of a silent HBV mutant. Immunostaining revealed hepatitis B surface antigen in 15 (50.0%). Cotransfected silent HBV DNA augmented the secretion of HCV RNA by up to 5‐fold in comparison with HCV RNA transfection alone. In conclusion, HCV is coinfected frequently with the silent HBV mutant and the latter probably promotes the replication of the former in the liver. J. Med. Virol. 52:399–405, 1997.

Mass screening for hepatocellular carcinoma: Experience in Hokkaido, Japan

Abstract Mass screening for liver cancer based mainly on abdominal ultrasound was begun in major cities of Hokkaido, Japan, in November 1981, to enable early detection and treatment of hepatocellular carcinoma (HCC). Serum alpha‐fetoprotein levels were also measured to minimize false negative studies. Examinees included those who sought liver disease screening as well as high risk individuals: hepatitis B surface antigen carriers and those with a past or current liver disease, history of blood transfusion, family history of liver cancer, and more recently those with positive anti‐hepatitis C antibodies. The examination was carried out on each Saturday and Sunday as one round, and by February 1992 48 rounds had been performed. A total of 8090 individuals were investigated, and HCC was detected in 91 with a detection rate of 1.12%. This rate was 1.6% among 5684 individuals who were selected for high risk. Cumulative rates of survival among these patients were 79.0% at 1 year, 43.8% at 3 years, 19.3% at 5 years and 15.4% at 7 years. These survival rates were comparable with those for the patients with HCC diagnosed during follow‐up of chronic liver disease and treated at our hospital. The cost for detecting one HCC patient in this programme was ¥ 2 660 000 (∼US

Detection of precore/core-mutant hepatitis B virus genome in patients with acute or fulminant hepatitis without serological markers for recent HBV infection

25 000), which was less than those for some other types of cancer in a similar setting. Considering the high detection rate in this programme, we feel that similar programmes should be encouraged and supported.

Expression pattern of a newly recognized protein, LECT2, in hepatocellular carcinoma and its premalignant lesion

To confirm the possibility that some hepatitis B virus (HBV) variants do not induce HB s antigen (HBsAg), anti-HB core antibody (anti-HBc) and anti-HBc IgM in a transient infection, polymerase chain reaction (PCR) was performed in 20 patients with acute hepatitis and 7 patients with fulminant hepatitis. Patients were diagnosed with non-A, non-B hepatitis by serological markers at admission. PCR successfully amplified the precore/core gene in 5 (25%) of the patients with acute hepatitis and 2 (29%) of the patients with fulminant hepatitis. Subsequent sequencing revealed frequent mutations including precore-defects in the precore/core gene.

Ursodeoxycholic acid (UDCA) therapy for autoimmune hepatitis

Leukocyte cell‐derived chemotoxin 2 (LECT2) is a recently isolated protein and has been shown to be synthesized by human hepatocytes. All hepatocytes show diffuse immunostaining for LECT2 within the cytoplasm. In the present study, an attempt was made to clarify the expression pattern of LECT2 in nine cases of low‐grade malignant hepatocellular carcinoma (LGM‐HCC) and five cases of advanced HCC and 19 cases of premalignant lesion, termed atypical hyperplasia (AH), using the indirect immunoperoxidase technique. Variable spotty to coarsely diffuse staining in the majority of cells, a mixture of positively staining and negatively staining areas, and essentially negative staining was observed within the cellular cytoplasm of AH, LGM‐HCC and advanced HCC, respectively. The expression of LECT2 became weaker with the progression of multistep hepatocarcinogenesis. The data clearly demonstrate that LECT2 becomes essentially negative in full‐blown HCC cells and that the histological distinction between AH and LGM‐HCC is valid. It also seems likely that LECT2 is related to hepatocyte growth.

Probable implication of mutations of the X open reading frame in the onset of fulminant hepatitis B

Abstract To assess the efficacy of ursodeoxycholic acid (UDCA) in autoimmune hepatitis we administered UDCA (600 mg/day, orally) to four patients who had autoimmune hepatitis refractory to treatment with prednisolone alone (20 mg every other day). During the treatment, serum levels of alanine aminotransferase (ALT) normalized and we were able to taper the dose of prednisolone to 5 mg every other day. The results indicate that UDCA administered concomitantly with very low doses of prednisolone may prove effective in patients who have autoimmune hepatitis.