Hitoshi Sugaya

Minimal change oesophagitis: a disease with characteristic differences to erosive oesophagitis

Background : The majority of gastro‐oesophageal reflux disease (GERD) seems to be non‐erosive reflux disease. Nonerosive reflux disease includes minimal change oesophagitis (whitish or reddish, oedematous change and erosion that is not regarded as mucosal break) and no endoscopic abnormalities.

Fulminant B hepatitis in a surface antigen and hepatitis B DNA-negative patient with diffuse large B-cell lymphoma after CHOP chemotherapy plus rituximab

The reactivation of hepatitis B in patients who are hepatitis B carriers is a well-known and often fatal complication of chemotherapy [1]. The current recommendations are that patients who are positive for hepatitis B surface (HBs) antigen should receive antiviral prophylaxis prior to chemotherapy [2,3] or should be carefully monitored when they receive cytotoxic or immunosuppressive therapy [4]. For HBs antigen-negative patients with evidence of previous hepatitis B virus (HBV) infection, however, the data are still insufficient to provide information on the incidence of HBV reactivation [5]. We experienced an individual with resolved HBV infection (i.e. HBs antigen-negative, anti-hepatitis B core (HBc) antibody-positive), in whom fatal reactivation of hepatitis B developed following chemotherapy that included rituximab for lymphoma. A 54-year-old man was diagnosed as stage IV diffuse large B-cell lymphoma in July 2005. Prior to chemotherapy, he was negative for HBs antigen. He had neither a past history nor a family history of liver diseases. He received CHOP (cyclophosphamideþdoxorubicineþ vincristineþdexamethasone) plus rituximab (R-CHOP). We occasionally added etoposide, ifosfamide, and methotrexate to that regimen. Seven courses of combination chemotherapy were completed in November 2005, and complete remission was accomplished. During the treatment for lymphoma, liver dysfunction was not demonstrated. In October 2005, during the chemotherapy period, the titers of HBs antigen (CLIA), anti-HBc antibody (CLIA), and HBV DNA (PCR) were 50.05 IU/ml, 10.8 S/CO, and 52.6 log10 copies/ml, respectively. In December 2005, when the chemotherapy was completed, HBs antigen was still 50.05 IU/ml, the titer of anti-HBc antibody was 10.5 S/CO, and the HBV DNA level was increased to 3.3 log10 copies/ml. The genotype of HBV was type C. In February 2006, he developed malaise and loss of appetite. He was admitted to our hospital in March 2006, when serum levels of aspartate aminotransferase, alanine aminotransferase, and total bilirubin were elevated to 622 IU/l, 531 IU/l, and 2.1 mg/dl, respectively. The titers of HBs antigen, anti-HBc antibody, and HBV DNA were 250 IU/ml, 8.2 S/CO, and [mt]7.7 log10 copies/ml, respectively. Anti-HBs antibody and IgM antibody to HBc antigen yielded negative results. Exacerbation of HBV infection was diagnosed and we initiated lamivudine at a daily dose of 100 mg to prevent HBV proliferation on the 1st day of admission. On the 8th day of admission, plasma exchange was introduced since fulminant hepatic failure developed

Serum and tissue PIVKA-II expression reflect the biological malignant potential of small hepatocellular carcinoma.

A sensitive method for measuring the serum level of protein-induced by vitamin K absence or antagonist II (PIVKA-II) has become so widely available that it is now used for the clinical diagnosis of small hepatocellular carcinoma (HCC). It is known that serum PIVKA-II can be a prognostic indicator for HCC, but there have been no detailed investigations concerning the tissue expression of PIVKA-II. The present study assessed the relationship between serum or tissue PIVKA-II and the biological malignant potential of HCC. The subjects were 25 patients with histologically confirmed HCC, that were solitary and 3 cm or less in diameter. Tissue PIVKA-II was detected by immunostaining using MU-3 as the primary antibody. The biological malignant potential of the tumors was evaluated on the basis of the Ki-67 labeling index of HCC cells and the tumor arterial vascularity assesed by angiography and CO(2) enhanced ultrasonography. The recurrence-free period after treatment was also evaluated. Among the 25 patients, eight were positive for tissue PIVKA-II. Serum PIVKA-II levels were significantly higher in the tissue PIVKA-II-positive patients compared with the negative patients, but serum and tissue PIVKA-II expressions were not consistently parallel. Tumor cell proliferation was closely correlated with the tissue PIVKA-II expression, while the recurrence-free period was correlated with the serum PIVKA-II level. Tumor arterial vascularity showed a strong correlation with the expression of both serum and tissue PIVKA-II. In conclusion, serum and tissue PIVKA-II expression reflect the biological malignant potential of HCC and thus may be useful indicators for the prognosis of small HCC.

A case of gallbladder carcinoma producing both α-fetoprotein (AFP) and carcinoembryonic antigen (CEA)

SummaryA 73-year-old woman with gallbladder carcinoma infiltrating to the liver presenting high serum values of AFP and CEA was reported. Serum values of AFP and CEA were remarkably high (165,000 ng/ml and 1,070 ng/ml). Immunohistochemically the tumor cells were stained for AFP and CEA by the PAP method. Serum AFP subfraction was analyzed by crossed immunoaffinoelectrophoresis with lentil lectin and concanavalin A, which showed most of the serum AFP bound to both lentil lectin and concanavalin A. As a case of gallbladder carcinoma presenting a high serum value of AFP is rare, it may imply a diagnostic challenge.

A case report of leiomyosarcoma originating in the ligamentum teres of the liver

SummaryA case of leiomyosarcoma that appeared to have originated in the ligamentum teres hepatis of a 66-year-old female has been presented. The case was suspected of leiomyosarcoma originating in the ligamentum teres of the liver from the findings by preoperative examinations, and definitely diagnosed as such in a laparotomy and by histological examination of the resected tissue specimen.

The diagnostic value of laparoscopy on focal hepatic lesions

SummaryWe compared laparoscopy with other diagnostic methods (abdominal angiography, CT, US, etc.) for the diagnosis of focal hepatic lesions.The rate of correct diagnosis by laparoscopy combined with needle biopsy was 81 % (30 of 37 cases).Although the area of liver surface which is visible through laparoscopy is limited, this procedure is considered useful in the following situations: (a) to confirm the diagnosis in combination with needle biopsy of the observed lesion, (b) to perform needle biopsy with safety and accuracy under laparoscopic guidance, (c) to detect minute lesions not detected by other methods, when the lesion is identified by observation during laparoscopy.Finally, laparoscopic examination provided substantial information guiding surgical treatment.RésuméLa laparoscopie a été comparée à d’autres méthodes d’investigation (angiographie abdominale, tomodensitométrie computée, ultrasonographie, etc.) dans le diagnostic de lésions hépatiques focales.Le taux de diagnostic correct obtenu par la combinaison laparoscopie-biopsie à l’aiguille a été de 81 % (30 sur 37 cas).Bien que la surface du parenchyme hépatique visible en laparoscopie soit limitée, cet examen s’est avéré utile dans les situations suivantes:a)pour confirmer un diagnostic, en conformité avec la biopsie à l’aiguille au niveau de la lésion observée;b)pour exécuter la biopsie à l’aiguille avec sûreté et précision sous guidance laparoscopique;c)Pour objectiver des lésions minuscules, non détectées par d’autres méthodes, lorsque ces lésions sont identifiées par l’observation laparoscopique. Enfin, l’examen laparoscopique fournit des informations essentielles dans la conduite du traitement chirurgical.

The diagnostic value of pneumoperitoneogram for splenomegaly in chronic liver diseases

SummaryThe splenic enlargement is an important symptoms of portal hypertension, and various attempts have been made to objectively describe it. But, endoscopic diagnosis for splenomegaly in chronic liver diseases may be sometimes difficult for these uncharacteristic appearances.The pneumoperitoneography was performed in 141 chronic liver diseases just before laparoscopic procedure, size and form of the spleen on X-ray film were measured and analysed.We have compared these results with the laparoscopic findings (the gross appearance of liver and spleen, the degree of portal hypertension, etc.), the patterns on scintigram and the histological findings of the liver.There were fairely good correlation between the splenic findings on radiogram and above factors, especially the size of the spleen was gradually increased according to the degree of portal hypertension and the fibrous change of the liver specimens.In conclusion, the findings of spleen on pneumoperitoneogram were valuable for diagnosis of splenomegaly in chronic liver diseases.

Identification of the Prelinitis Condition in Gastric Cancer and Analysis of TGF-β, TGF-β RII and pS2 Expression

In the present study, we performed an immunohistochemical examination of the expression of transforming growth factor-β (TGF-β), TGF-β type II receptor (TGF-β RII) and a trefoil peptide, pS2, in the several types of gastric cancer. The TGF-β:TGF-β RII ratios of IIc-like type and Ménétrier type closely resembled that of linitis type. pS2 was intensely expressed in cytoplasm of the superficial and foveolar epithelium, as well as in scirrhous type gastric cancers which retained the gastric or intestinal phenotype. However, pS2 expression was significantly (p < 0.05) reduced in linitis type gastric cancers (1 of 6; 17%) when compared with other scirrhous types of gastric cancers (13 of 22; 59%). A decrease in the TGF-β:TGF-β RII ratios in linitis type, IIc-like type and Ménétrier type gastric cancers may be associated with the fibrosis seen in these types of cancer. Furthermore, reduction of pS2 expression in linitis type gastric cancer may represent a dedifferentiation of the cancer from gastric or intestinal phenotype. Judging by the expression patterns of TGF-β, TGF-β RII and pS2, it is possible that IIc-like type and Ménétrier type gastric cancers are precursor lesions of linitis type gastric cancer.

A case of idiopathic portal hypertension after renal transplantation

SummaryA case of idiopathic portal hypertension (IPH) developing after renal transplantation is reported. A 33-year-old Japanese male who had undergone renal transplantation 8 years previously was transferred to our hospital because of hematemesis from ruptured esophageal varices. He had no history of any liver disease before the renal transplantation, but had a history of receiving blood transfusion. Abdominal computed tomography (CT) and ultrasonography revealed marked splenomegaly and collateral channels, but no obliteration which might cause portal hypertension in the hepatic or portal vein. No findings suggestive of hepatitis or liver cirrhosis were found either macroscopically on laparoscopy or by liver biopsy. Light microscopic study of the liver biopsy specimen showed mild periportal fibrosis, inconspicuous portal branches in the most peripheral tracts, but no pseudolobule formation or piecemeal necrosis. However collagen deposition was found in the perisinusoidal space and partly in intercellular space on electron microscopy. We consider that the development of portal hypertension in this case is responsible for the collagen deposition, which may be related to the administration of azathioprine after renal transplantation. There are few reports on IPH after renal transplantation, and it is stressed that a lower amount of azathioprine than previously reported may induce IPH under such conditions.

Marked atrophy of the right lobe seen in idiopathic portal hypertension confirmed by laparoscopy

A 70‐year‐old‐male was hospitalized for the treatment of esophageal varices and close examination of the liver. Blood chemistry tests revealed mild liver dysfunction. Abdominal ultrasound and computed tomography scan revealed marked atrophy of the right and quadrate lobes of the liver without abnormalities of the biliary system. Abdominal angiography revealed marked atrophy of the right lobe of the liver, without obliteration in the portal venous system, but it could not be determined whether the atrophy was congenital or secondary. Subsequently performed laparoscopy revealed marked atrophy of the anterior segment of the right lobe and quadrate lobe with the whitish scarred edge demarcating the border between the edge and neighboring liver parenchyma. The liver surface appeared to be undulant, but non‐cirrhotic. These findings suggest secondary lobar atrophy of the liver, without cirrhosis. Liver biopsy of the left lobe showed the findings to be compatible with idiopathic portal hypertension (IPH), and we diagnosed IPH based on these findings and hepatic lobar atrophy was attributable to IPH. There have been few reports of cases with hepatic lobar atrophy associated with IPH, and the mechanism of atrophy is unclear. We report a case of IPH with marked liver atrophy in which laparoscopy is a decisive means whether liver atrophy is congenital or secondary.