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Use of a standard open stent or self-expanding metal stent for patients with malignant dysphagia is associated with a risk of gastroesophageal reflux especially when placed across the esophagogastric junction. We report 3 cases of malignant esophageal stenosis treated with a long cover-type Niti-STM stent with an antireflux mechanism. Case 1: A 87-year-old man presented with dysphagia due to esophageal cancer at the middle thoracic esophagus. Two months after surgery using a standard open stent, the dysphagia relapsed because of tissue overgrowth. Case 2: A 73-year-old woman presented with lung cancer and severe dysphagia due to enlarged mediastinal lymph nodes. Case 3: A 66-year-old man presented with dysphagia due to esophageal cancer at the lower thoracic esophagus. All 3 patients received an antireflux stent across the esophagogastric junction. In cases 1 and 2, dysphagia was relieved immediately without complications. In case 3, the patient experienced severe reflux and chest pain associated with stent placement and could not ingest any solid food. We conclude that the antireflux stent may be useful for palliation in patients with severe malignant esophageal obstruction; however, patients should be informed about the risk of failure to prevent reflux.

A 78-year-old man presented to our hospital with lung abnormality on his chest radiograph. Computed tomography (CT) showed a mass and obstructive pneumonia in the right upper lobe of the lung. The mass was diagnosed as a pulmonary adenocarcinoma with a bronchoscopy (cT4N2M0, Stage IIIB). CT also revealed multiple hepatic tumors, which were diagnosed as hepatocellular carcinoma (HCC) by dynamic CT and gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid enhanced magnetic resonance imaging(EOB-MRI). First, we treated the lung cancer with a combination of cisplatin and pemetrexed (PEM), but it caused renal dysfunction. Carboplatin (CBDCA) and PEM combination chemotherapy was administered, and not only the lung cancer but also the HCCs decreased in size. There are few reports of synchronous double cancers of HCC and primary lung cancer, and the treatment is not established. We report that platinum-containing anticancer drugs such as CBDCA may be effective against synchronous double cancers of HCC and lung cancer.

There is insufficient evidence for the pre-operative use of chemoradiotherapy (CRT) in treatment of advanced rectal cancers, and its efficiency and safety are unclear. However, it has recently been suggested that a new class of carcinostatic agents are more effective during preoperative CRT. Under the National Comprehensive Cancer Network (NCCN) guidelines, 5-FU and capecitabine have been recommended as the standard drugs for use during combination chemoradiotherapy. The Japanese Society for Cancer of Colon and Rectum (JSCCR) guidelines for 2014 also recommend the use of both drugs during preoperative CRT. We report a case of rectal cancer, which was successfully treated with radical resection and neoadjuvant chemoradiotherapy.

A standard treatment for primary peritoneal carcinoma has not been established to date. We describe a case in which this cancer was successfully treated by use of paclitaxel and carboplatin chemotherapy.An 80-year-old woman who presented with abdominal distension and right upper abdominal pain was diagnosed with massive ascites and an omentum tumor via abdominal computed tomography and magnetic resonance imaging (MRI); her ovaries were normal-sized. Serum levels of the tumor marker CA125 were above normal (170 U/mL), and aspiration cytology showed the presence of adenocarcinoma cells. Despite several examinations, the primary tumor was not detected. The patient underwent exploratory laparotomy and was diagnosed with primary peritoneal carcinoma. She received combination chemotherapy consisting of paclitaxel and carboplatin. Serum CA125 levels returned to normal, and an MRI showed no evidence ofa tumor.Paclitaxel and carboplatin combination chemotherapy is effective for treatment of primary peritoneal adenocarcinomas.

Background: The aim of this study was to clarify the clinical significance of reddish markings appearing on the surface of the liver. Methods: Subjects were patients with Hepatitis B virus-related (n = 232) or Hepatitis C-related (n = 246) chronic liver disease. Reddish lesions were obtained from this population using punch biopsy (n = 30) or wedge biopsy (n = 4), then studied histopathologically. In addition, the incidence and macroscopic forms of reddish markings in each laparoscopic stage for the 478 subjects were examined to determine when reddish markings appeared. Results: Reddish markings on the liver surface appeared only after the appearance of hepatic parenchymal destruction subjacent to the liver capsule, rather than with the appearance of piecemeal necrosis in the portal area. Moreover, following expansion of necrotic hepatic parenchyma subjacent to the liver capsule and distortion of hepatic lobular architecture in this lesion, net-like or hemorrhagic fleck-like reddish markings appeared. Therefore, this was recognized as changes at the liver capsule, such as capillary proliferation and dilatation, and blood flow changes in both the capsule and hepatic parenchymal lesions subjacent to the liver capsule. With regards to timing, reddish markings were most frequently observed in the transition to liver cirrhosis. After the appearance of reddish markings on the liver surface, chronic hepatitis rapidly progressed to liver cirrhosis. Conclusion: Reddish markings correspond to hepatic parenchymal destruction subjacent to the liver capsule, and not to piecemeal necrosis. Reddish markings appear in the transition to liver cirrhosis and might offer a useful marker of the progression to liver cirrhosis.

The patient was an 87-year-old woman who was diagnosed with atrial fibrillation, which was treated with an anticoagulant, and with chronic kidney disease. The patient was diagnosed as having liver dysfunction and lower cholangiocellular carcinoma (cStage I) on ultrasonography and magnetic resonance cholangiopancreatography. Since it was impossible to perform curative resection owing to the patient's decreased cardiac and renal function, we performed palliative endoscopic retrograde biliary drainage (ERBD) with a plastic stent (PS), and the patient was discharged 11 days later. However, the patient was readmitted because of fever (38.0°C) and vomiting 124 days after ERBD. We assumed that the patient had developed cholangitis due to PS obstruction. Moreover, her blood culture was positive for Klebsiella pneumoniae. We were unable to replace the PS as the tumor had increased in size and hemorrhage from the papilla of Vater continued after the stent had been removed. The signs of inflammation improved after treatment of sepsis with antibiotics and immunoglobulins, and we performed percutaneous transhepatic cholangio drainage( PTCD) and eventually inserted a percutaneous transhepatic biliary endoprosthesis (PTBE) with an expandable metallic stent (EMS). The patient died 2 months later; no stent occlusion was observed. Our experience suggests that endoscopic biliary stents should be selected bearing in mind the patency of the stent and the prognosis.

A 67-year-old woman with complaints of cough and dyspnea was admitted; her chest radiographs and computed tomography (CT) scans revealed pulmonary carcinomatous lymphangitis. Endoscopic examination revealed advanced gastric cancer and the patient was treated with a combination of 40 mg/m2 docetaxel, administered on day 1, and S-1 100 mg/body/day, administered for 14 days followed by a 7-day interval, as 1 course despite her performance status( PS) being grade 3. After 2 courses of chemotherapy, CT showed that the carcinomatous lymphangitis had improved, and the patient was discharged with PS of grade 0. We report that combination chemotherapy with docetaxel and S-1 might be effective for the treatment of advanced gastric cancer with carcinomatous lymphangitis of the lung in patients with a poor systemic condition.

OBJECTIVES To investigate the prevalence and relative titre of TT virus (TTV) DNA, and to examine the relationship between the extent of TTV viraemia and the immune status among 144 patients with HIV infection; 178 age- and sex-matched healthy individuals were also studied. METHODS TTV DNA was detected quantitatively by two distinct polymerase chain reaction (PCR) methods [untranslated region (UTR) and N22]. UTR PCR detects all TTV genotypes, and N22 PCR can primarily detect four major TTV genotypes (1-4). RESULTS Using UTR PCR and N22 PCR, respectively, TTV DNA was detected significantly more frequently in HIV-infected patients than in controls (99 versus 91%, P < 0.001; 56 versus 27%, P < 0.0001), and the relative titre (10N/ml) was significantly higher in HIV-infected patients [4.5 +/- 1.2 (mean +/- SD) versus 3.1 +/- 0.9, P < 0.0001; 2.6 +/- 1.5 versus 1.5 +/- 0.9, P < 0.0001]. Age, sex, co-infection with hepatitis B or C virus, and risk factors for HIV transmission did not appear to be significant factors associated with the titre of TTV viraemia. However, the titre of TTV DNA was significantly higher in HIV-infected patients with AIDS (P < 0.0001), those with low CD4 T cell count (P < 0.0001), or those with high HIV viral loads (P = 0.0047). CONCLUSION TTV is highly prevalent and high-titred in HIV-infected patients. The TTV viral load may reflect the degree of immune status of these immunocompromised hosts.

It remains unclear whether the hepatitis C virus genotype is associated with the severity and outcome of HCV-related liver disease. The aim of this study was to determine whether hepatitis C virus genotype influenced the risk of developing hepatocelMar carcinoma. Two hundred and sixty nine patients who had chronic hepatitis C and cirrhosis without hepatocellular carcinoma were studied. The stage and activity of hepatitis were determined at laparoscopy and patients were followed up until the development of hepatocellular carcinoma or for a maximum of 16 years. Hepatitis C virus genotypes were determined by a genotyping enzyme-linked immunosorbent assay. A cross-sectional study revealed that the prevalence of hepatitis C virus genotype 1 increased and that of genotype 2 decreased with the progression of liver disease (pc 0.01). A follow-up study using the Kaplan-Meier method showed that hepatocellular carcinoma occurred more frequently in patients with hepatitis C virus genotype 1 (p

RNA of recently reported, putative non-A to E hepatitis virus designated GB virus C (GBV-C) was determined by reverse-transcription polymerase chain reaction in sera from 231 Japanese patients with primary hepatocellular carcinoma. GBV-C RNA was detected in 21 patients (9% of the total), including two of the 23 patients (8%) with markers of hepatitis B virus infection, 11 of the 114 patients (10%) with markers of hepatitis C virus infection, seven of the 86 patients (8%) with markers of both hepatitis B and C virus infections, and one of the eight patients (13%) without such markers. These results indicate that the contribution of GBV-C infection to the development of hepatocellular carcinoma would be small either by itself or in cooperation with hepatitis B and C viruses.

The entire nucleotide sequence was determined for eight hepatitis B virus (HBV) genomes from three symptom-free carriers, two patients with chronic persistent hepatitis and one patient with chronic active hepatitis, who were positive for antibody to hepatitis B e antigen (HBeAg). The two patients with chronic persistent hepatitis were tested again after they developed chronic active or fulminant hepatitis, making a total of eight samples. Six had a point mutation in the preC region prohibiting the encoding of HBeAg precursor, while the remaining two had a deletion of 8 or 21 nucleotides within the X gene upstream of the preC transcription initiation sites which would affect the X gene and the putative preC/C promoter. Most genomes from the three symptom-free carriers and the two patients with chronic persistent hepatitis, with HBV DNA levels of 10(2)-10(3)/ml, had deletion, frameshift mutation, initiation failure or a premature stop codon, rendering them replication-incompetent. In contrast, such mutations were rarely seen in HBV genomes from the two patients with chronic persistent hepatitis after they had developed active or fulminant hepatitis and from the patient with chronic active hepatitis, all of whom had vigorous HBV replication with serum HBV DNA from 10(6) to 10(9)/ml. Unique mutations for amino acid changes were more frequent in HBV genomes with a higher replicative activity. These results indicate two kinds of HBV genomes with an HBeAg-minus phenotype, one with defects seriously affecting viral replication and the other without such defects, which would account for different clinical profiles in carriers with antibody to HBeAg.

A 28-year-old woman was admitted to our hospital with abdominal pain. Abdominal CT scan demonstrated a well-demarcated heterogeneous lipid tumor about 8 cm in diameter anterior to the stomach. Abdominal ultrasonography (US) revealed a low echoic mass without enhancement of vascular images. We made a diagnosis of the lipoma, but not excluding the possibility of a liposarcoma, or the torsion of a tumor. We performed an operation to remove the tumor. Finally the tumor was diagnosed as a lipoma of the lesser omentum with torsion of the pedicle. This is the third reported case of torsion of a lipoma. In addition, this case is considered as the first such case of lipoma of the lesser omentum.

To investigate the duration of fecal shedding and changing loads of hepatitis E virus (HEV) in feces and serum from patients with acute HEV infection, HEV RNA was quantitated in periodic serum and fecal specimens obtained from 11 patients with sporadic acute hepatitis E. All 11 patients had detectable HEV RNA in serum at admission, with the highest viral load being 1.9 × 10 3 to 1.7 × 10 7 copies/ml, and HEV viremia lasted until days 17 to 48 (mean, 28.3) after the onset of hepatitis. Even at the initial examination on days 10 to 29 (mean, 17.6), the HEV load in fecal supernatant was less than 5.7 × 10 4 copies/ml for 10 of the 11 patients, while for the remaining patient (patient 1) it was markedly high, 2.0 × 10 7 copies/ml on day 22. In addition, although HEV RNA in fecal supernatant continued to be positive until days 14 to 33 (mean, 22.4) for patients 2 to 11, that for patient 1 was detectable even on day 121. HEVs in fecal specimens obtained on days 22, 24, 26, 28, and 30, but not day 121, from patient 1 grew efficiently in PLC/PRF/5 cells, reaching the highest titer of up to 10 7 copies/ml in culture medium on day 50 postinoculation. The HEV genome recovered from patient 1 had 29 unique nucleotides that were not seen in any of the 25 reported HEV isolates of the same genotype over the entire genome, with six amino acid substitutions in the ORF1 protein.

Objective: Hepatitis B virus (HBV) genotypes B and C are predominant in Japan. Previously, we reported that approximately 9% of HBV carriers in the Ehime area of western Japan were infected with genotype D (HBV/D) and their sequences closely related. Recently, serum samples from 3 patients with chronic HBV/D infections living in Tokyo and the surrounding area became available for testing. The purpose of this study was to determine whether the HBV/D isolates from these different areas of Japan are closely related. Methods: Of the 3 Tokyo area patients infected with HBV/D, 2 had chronic hepatitis, and 1 had hemophilia with a history of frequent coagulation factor injections. The complete HBV/D genome sequences of each were determined, and compared with those of subjects from the Ehime area. Results: All 3 HBV/D sequences had a genomic length of 3,182 bases, and the hepatitis B surface antigen subtype was ayw3. Phylogenetic analysis revealed that the 1 of the HBV/D isolates was closely related to the isolates from Ehime Prefecture, while 1 was similar and 1 was clearly distinct. Conclusion: Our results indicate that HBV/D infections in Japan are heterogeneous.

To investigate the prevalence of hepatitis B virus (HBV) genotypes and characteristics of HBV isolates among Japanese patients infected with human immunodeficiency virus type 1 (HIV), serum samples collected between September 1990 and March 2002 from 471 HIV-infected patients (age, 38.8 ± 11.4 [mean ± standard deviation] years; male, 90%) were tested for hepatitis B surface antigen (HBsAg) and HBV DNA. Positivity for HBsAg and HBV DNA was seen in 42 patients (8.9%), 41 of whom had contracted HIV infection through sexual activity and 1 had hemophilia. Genotypes of HBV were determined by comparative and phylogenetic analyses of the S gene sequence (396 nucleotides [nt]). The distribution of HBV genotypes among the 42 HBV-viremic patients was: A (50%), B (5%), C (24%), D (5%), E (2%), H (10%), A plus D (2%), A plus G (2%). The hemophilia patient had HBV genotype D. Genotypes E, G, and H which had not been reported in Japan, were found in one patient each who had traveled to Zambia, the US, and South America, respectively. Genotypes A and D, which are rare in Japan, were found in patients who had no history of traveling abroad. The entire genome of the HB-JI411 (genotype E [3,212 nt]), HB-JI444G (genotype G [3,248 nt]), and HB-JI260 (genotype H [3,218 nt]) isolates had the highest identity of 98.3%, 99.9%, and 98.5%, respectively, with reported HBV isolates of the same genotype. Most Japanese patients coinfected with HIV and HBV had HBV genotypes that are found rarely or had not been reported in Japan. J. Med. Virol. 76:24–32, 2005. © 2005 Wiley-Liss, Inc.

TT virus (TTV) has not yet been cultured or visualized. We attempted to recover and visualize TTV-associated particles from the serum samples and feces of infected humans. Serum samples were obtained from 7 human immunodeficiency virus (HIV)-infected patients. Three patients had a high TTV DNA titer (10(8) copies/ml), three had a low TTV DNA titer (10(2) copies/ml), and one was negative for TTV DNA. Fecal supernatant was obtained from a different TTV-infected subject. The serum samples were fractionated by high-performance liquid chromatography, and TTV DNA-rich fractions were subjected to floatation ultracentrifugation in cesium chloride. Virus-like particles, 30-32 nm in diameter, were found in the 1.31-1.33 g/cm(3) fractions from each of the three serum samples with high TTV DNA titer, but not in any fraction from the four serum samples that either were negative for TTV DNA or had low TTV DNA titer. The TTV particles formed aggregates of various sizes, and immunogold electron microscopy showed that they were bound to human immunoglobulin G. Similar virus-like particles with a diameter of 30-32 nm banding at 1.34-1.35 g/cm(3) were visualized in fecal supernatant with TTV genotype 1a by immune electron microscopy using human plasma containing TTV genotype 1a-specific antibody.

Markers of GB virus C (GBV-C) and hepatitis C virus (HCV) were sought in 80 patients before and after they underwent BMT in a metropolitan hospital in Tokyo between 1990 and 1996. RNA of GBV-C was detected in 14 (18%) patients before BMT. Of the 55 patients who had been transfused, 14 (25%) possessed GBV-C RNA at a frequency significantly higher than in the 25 untransfused patients who were all negative (P < 0.01). HCV RNA was detected in three of the 55 (5%) transfused patients, but in none of the 25 untransfused patients. Sera at 3 months after BMT were available for 57 patients. GBV-C RNA persisted in all 10 patients who were infected before BMT, while it was detected in five of the remaining 47 (11%) patients who were not. However, persistent and/or ongoing GBV-C infection had no appreciable influence on patient morbidity or mortality. Two of the 57 patients were positive for HCV RNA before BMT and this persisted after BMT in both. HCV RNA became positive in eight of the remaining 55 (15%) patients who were negative before BMT. Of the 14 patients who received transfusions screened by the first-generation test at BMT, seven (50%) became positive for HCV RNA, a rate significantly higher than the one of 41 (2%) patients who received transfusions screened by the second-generation test (P < 0.001). These results indicate that BMT patients are at increased risk of GBV-C infection transmitted by transfusions received before and at the time of BMT, and that the risk of HCV infection has decreased after the implementation of the second-generation anti-HCV test.

We examined the prevalence of hepatitis A virus (HAV) and hepatitis E virus (HEV) infections among 280 Japanese patients infected with human immunodeficiency virus type 1 (HIV) and among 1,000 apparently healthy blood donors as a control. The prevalence of antibody to HAV was significantly higher among the HIV-infected patients than among the healthy donors (25.4% vs. 19.0%, P=0.025). When restricted to subjects aged

Electron microscopic and virological studies of marmoset liver tissue with acute infection of hepatitis A virus (HAV), especially in the earlier stages of infection, were carried out to characterize the maturation process of HAV. Four marmosets were inoculated intravenously with HAV suspension and sacrificed 1 week, 2 weeks, 3 weeks and 4 weeks after inoculation respectively. Hepatitis A antigen (HAAg) in 10% liver homogenates of marmosets was examined by radioimmunoassay and a large amount of HAAg was detected in the liver homogenate of two marmosets sacrificed 2 weeks and 3 weeks after inoculation respectively. The histodiagnosis of the marmoset sacrificed 2 weeks after HAV inoculation was normal. However, many clusters of virus-like particles about 27 nm in diameter, in both "solid" and "empty" forms were found, mainly in vesicles of Kupffer cells by electron microscopy. In the animal that developed mild hepatitis 3 weeks after inoculation HAV-like particles were found in vesicles of hepatocytes by electron microscopy. By immune electron microscopy using peroxidase-conjugated anti-hepatitis A antibody, HAAg was detected on the particles present within the cytoplasmic vesicles of Kupffer cells or hepatocytes and on the surrounding membrane of the vesicles which contained HAV-like particles.

Electron microscopic studies of the morphology of hepatitis B surface antigen (HBsAg) produced by PLC/PRF/5 cells in vitro were carried out. Aggregates of 20-nm spherical particles in 3-day culture supernatants were observed by immune electron microscopy (IEM). Aggregates of tubular structures were found with IEM in the extracts of the cells. Tubular structures 18 to 22 nm in diameter were seen by electron microscopy (EM) in the cisternae of the endoplasmic reticulum in 2-3% of the cells. The tubular structures in the cytoplasm and extracts of PLC/PRF/5 cells resembled those observed in the hepatocytes of human carriers of hepatitis B virus (HBV). Intracellular localization of HBsAg in PLC/PRF/5 cells by direct peroxidase-conjugated antibody staining was observed on the tubular structures and the cisternal wall, which contained these structures. Rotation technique analysis indicated that the tubular structures were composed of 11 or 12 subunits.

症例は70歳,女性.腹部腫瘤を主訴として入院.腹部CT, Echo,腹腔動脈造影などの検査,および腹腔鏡下腫瘍生検による癌部組織診断が乳頭管状腺癌であったことより,胆嚢癌とその肝内転移と診断した.入院時よりalpha-fetoprotein (AFP)値ならびにcarcinoembryonic antigen (CEA)値が共に異常高値を示し,crossed immuno-affinoelectrophoresisによるAFPのレクチン親和性の分析では,本症例のAFPパターンがyolk sac型を呈していた.Methotrexate (MTX), 5-fluorouracil (5-FU) sequential療法を5クール施行することによって,AFP値74,000ng/ml→8,600ng/ml, CEA値3,500ng/ml→326ng/mlと改善,さらに触診およびCTで腫瘤の縮小を確認し,本療法の有効性を確認した.AFPおよびCEAの局在は,酵素抗体法での検索で,原発巣と肝転移巣の腫瘍細胞の一部に証明されたが,肝転移巣周辺の非癌部肝組織には証明されなかった.従ってAFP値ならびにCEA値の高値は,腫瘍細胞自体の産生によるものと考えられた.

Two sera obtained from four healthy blood donors, which caused non-A, non-B post-transfusion hepatitis in two recipients, were experimentally inoculated into nine marmosets. Three of seven marmosets developed acute hepatitis characterized by the elevation of serum concentrations of glutamic pyruvic transaminase (GPT) and/or isocitric dehydrogenase (ICD) 8-11 weeks after inoculation. Four of seven showed histopathological changes of acute hepatitis in liver biopsy specimens during the biochemically acute phase. In electron microscopic examination, attached membrane-like structures, which consisted of two-unit membranes of two neighboring endoplasmic reticula with electron-dense material between them, were noted in cytoplasm of hepatocytes during the acute phase of hepatitis. Furthermore, acute-phase sera obtained from two animals were inoculated into four additional marmosets, and non-A, non-B hepatitis was successfully passaged in two of them. The results of this study indicate that certain species of marmoset monkeys are susceptible to human non-A, non-B hepatitis agents and provide a useful animal model for non-A, non-B hepatitis.

Fecal extracts of hepatitis A (HA) patients were selected for the presence of hepatitis A virus (HAV) by radioimmunoassay (RIA) and immune electron microscopy (IEM). When FL and Vero cells were inoculated with fecal extracts containing HAV, development of hepatitis A antigen (HAAg) was evident in the cytoplasm of the two cell lines by the indirect immunofluorescence (IF) test. The antigen was detectable in the cells 12 hr postinoculation (pi), and reached a plateau within two days pi. FL cell cultures inoculated with a specimen containing HAV were harvested and passaged four times. During the passages, efficient production of HAAg was confirmed in the infected cultures by three different serological tests: The indirect IF test, RIA using fixed cells, and RIA by the sandwich method. At the second and fourth passages, HAV particles were recovered in abundance from infected FL cell cultures by IEM. Throughout these experiments, no cytopathic effect (CPE) was discernible in the cultures.