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We report a case of self-limited colitis in cytomegalovirus (CMV) infection in an immunocompetent adult. A 22-year-old man developed a high fever and diarrhea. Laboratory data revealed an increased number of lymphocytes and liver damage. Enzyme immunoassays for anti-virus antibodies revealed that the patient was recently infected with CMV and rubella. Colonoscopy revealed severe erosive and edematous mucosa that resembled ulcerative colitis (UC). The symptoms, laboratory data and colonoscopic findings improved without any medical treatment. This case indicates that UC-like self-limited colitis can occur in an immunocompetent individual during the course of CMV infection.

We examined the production of prostanoids, specifically prostaglandin (PG) I 2 and thromboxane (TX) A 2 , in cultured rat hepatic sinusoidal endothelial cells treated with antithrombin (AT) III. When cells were treated for 3 h with various concentration of AT III, production of 6-keto-PGF 1α (a stable metabolite of PG I 2 ) increased significantly and in a dose-dependent manner, compared with production by untreated cells. In terms of kinetics, significant increases were noted at 3 h (20.13 ± 1.38 pg/ml), 4 h (21.23 ± 0.63 pg/ml) and 24 h (36.58 ± 4.93 pg/ml) with AT III (300 μg/ml) stimulation, compared with production by the untreated cells (10.29 ± 1.21, 10.34 ± 1.66 and 22.64 ± 2.59 pg/ml, respectively). Moreover, this production was significantly reduced with increasing concentrations of heparin. On the other hand, TX B 2 (a stable metabolite of TX A 2 ) production was unaffected by AT III treatment. These data suggest that AT III may ameliorate the liver damage or disturbances in the sinusoidal microcirculation by stimulating the PG I 2 production of hepatic sinusoidal endothelial cells.

症例は37歳の女性. 1986年11月日光過敏,蝶形紅斑,抗核抗体陽性,抗DNA抗体陽性から全身面エリテマトーデスと診断され, prednisolone投与を受けた。1989年10月から両下肢脱力感出現し精査加療目的に同年12月当科入院した.抗核抗体2,560倍,抗cardiolipin抗体陽性で,頭部CT上多発性脳梗塞が認められ, PSL 40mg/日の投与を開始した.症状改善傾向にあるも患者は服薬を中止し, 1990年4月退院した.同年5月,両下肢の対麻痺,胸椎11番以下の全知覚障害と膀胱直腸障害が出現し再入院した. aCLは高力価であり,抗リン脂質抗体が強く関与した横断性脊髄障害を合併したものと考え,血漿交換療法,副腎皮質ステロイド剤パルス療法,大量γ-globulin療法,免疫抑制剤投与を行い, aCL価は低下したが,神経症状はほとんど改善しなかった.早期の治療が横断性脊髄障害の諸症状の改善に重要である.

A 57-year-old woman was admitted to the hospital because of obstructive jaundice. Abdominal computed tomography and ultrasonography showed a homogeneous mass 7cm in diameter at the head of the pancreas. Gamma-scintigraphy showed uptake in the head of the pancreas. Histological diagnosis was obtained by endoscopic ultrasoundscopy-fine needle aspiration (EUS-FNA). The pathological and immunohistochemical studies showed diffuse lymphoma with large B-cells. We experienced a rare case of pancreatic malignant lymphoma and EUS-FNA was usefull in the diagnosis.

A 30-years-old Japanese woman with a liver tumor was found to have congenital absence of the portal vein (CAPV). Both three-dimensional CT and angiography revealed that the superior mesenteric vein and splenic vein flowed into inferior vena cava and there was us portal vein, CAPV is an extremely rare congenital anomaly and liver tumor. Most cases on diagnosed in childhood, although this case was found in on adult. We reviewed the literature on reported CAPV cases.

A 53-year-old woman who had been diagnosed with rheumatoid arthritis was found to have thrombocytopenia, splenomegaly, and gastric varices. She was diagnosed as having idiopathic portal hypertension on the basis of liver biopsy and angiography. Treatment with prednisolone was not sufficiently effective for thrombocytopenia. After transabdominal devascularization with splenectomy, thrombocytopenia subsided and gastric varices disappeared. In this case, the autoimmune mechanism as well as hypersplenism was suspected of being involved in the mechanism of thrombocytopenia.

Progressive destruction of the intrahepatic bile ducts in patients with primary biliary cirrhosis (PBC) is thought to be mediated by cytotoxic T cells which recognize certain epitopes, such as the pyruvate dehydrogenase complex (PDC). To clarify the T-cell repertoire in PBC, we analyzed T-cell receptor (TCR) Vbeta-chain messages expressed in peripheral blood mononuclear cells (PBMCs) stimulated with PDC and in liver biopsy specimens. PBMCs from 12 PBC patients and 6 healthy controls were examined. The TCR Vbeta repertoires of unstimulated PBMCs and PBMCs stimulated with PDC purified from bovine heart were analyzed, using the reverse transcriptase-polymerase chain reaction (RT-PCR) and single-strand conformation polymorphism (SSCP). Liver biopsy specimens from 5 PBC patients were also analyzed. In the PBC patients, several different T-cell clones, some of which showed the same mobility, were evident in both the PDC-stimulated and unstimulated PBMCs, as demonstrated by SSCP analysis. In addition, TCR clonality of infiltrating lymphocytes in the liver was also observed in PBC patients, showing common clonal T-cell accumulation with that seen in PBMCs stimulated with PDC. These data indicate that common clonal T-cell accumulation specific for PDC may be present in both peripheral PBMCs and the liver of patients with PBC.

We investigated the production of interleukin-8 (IL-8) and chemotactic activity released from Chang liver cells subjected to long-term treatment with ethanol (Et) and subsequent stimulation with tumor necrosis factor-alpha (TNF-alpha). Chang liver cells were cultured in the presence of 5, 50 or 100 mmol/l Et for 4 weeks and then treated with recombinant TNF-alpha (1, 10, 100 U/ml). The culture supernatants were assayed for IL-8 using a sandwich ELISA and chemotactic activity was measured using a chemotactic chamber. Total RNA was also extracted from these cells and IL-8 mRNA was assayed by RT-PCR. In addition, TNF-receptor expression on the Et-treated cells was analyzed by flow cytometry. IL-8 levels in supernatants of cells stimulated with 100 U/ml of TNF-alpha for 48 h rose significantly with increasing concentrations of Et and values obtained were as follows: 4,918 +/- 244.4 pg/ml at 0 mmol/l Et, 5,335 +/- 266.2 pg/ml at 5 mmol/l Et, 8,726 +/- 873.4 pg/ml at 50 mmol/l Et and 9,134 +/- 866.0 pg/ml at 100 mmol/l Et. The chemotactic activity also increased with increasing concentrations of Et and was almost completely suppressed by anti-IL-8 antibody. Using semiquantitative analysis of radioactivity of IL-8 mRNA using a 32P gamma ATP-labeled primer for IL-8 mRNA, Et-treated cells were shown to have markedly higher levels of radioactivity than untreated cells. In addition, TNF-receptor expression was significantly higher in cells treated with 100 mmol/l Et. These data suggest that long-term Et treatment of Chang liver cells stimulated with TNF-alpha may enhance transcription of the IL-8 gene with up-regulation of the TNF receptor.

Background/Aims: The aim of this study was to assess the effect of interleukin-6 (IL-6) on the proliferation of hepatocytes and to study the interaction between IL-6 and hepatocyte growth factor (HGF) in vivo . Methods: IL-6 was injected at a dose of 200 μg/mg subcutaneously into rats every day for 14 days. Liver and blood samples were obtained at 1, 3, 7 and 14 days during IL-6 administration. Hepatocyte proliferative activity of sera was measured using 3 H-thymidine incorporation into cultured rat hepatocytes. To evaluate the proliferative activity of the hepatocytes in tissue sections, hepatic DNA content and immunostaining of the liver tissue sections for proliferating cell nuclear antigen (PCNA) were performed. Plasma HGF levels were measured using specific EIA. In addition, total RNA was extracted from the liver and expression of HGF mRNA was detected by RT-PCR. Results: The DNA contents of liver taken from IL-6-treated rats were increased during IL-6 administration compared with untreated rats. Sera taken from IL-6-treated rats at various intervals during administration also significantly increased 3 H-thymidine incorporation by cultured rat hepatocytes compared with sera from untreated rats, suppressing 3 H-thymidine incorporation at day 1 and 3 by anti-HGF antibody. IL-6 itself did not increase 3 H-thymidine incorporation. Increased expression of PCNA in these hepatocytes was noted from 1 day after IL-6 administration, and at 14 days, the number of PCNA-positive cells was sevenfold greater than in the livers of untreated rats. However, plasma HGF levels showed a peak at day 1, decreased gradually from day 3, and became undetectable by day 14. HGF mRNA expression in livers of IL-6-treated rats was suppressed from day 3 to day 14 of IL-6 administration. Conclusions: These data show that IL-6 induces an early phase of liver cell growth in vivo and suggest that an increase level of HGF mediates this effect.