Japanese Journal of Clinical Immunology
Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300
Volume 23, Issue 1
Displaying 1-8 of 8 articles from this issue
  • Akira Ishiguro
    2000 Volume 23 Issue 1 Pages 1-11
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
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  • Hirotoshi Kikuchi
    2000 Volume 23 Issue 1 Pages 12-21
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    A fundamental feature of inflammation includes angiogenesis, adhesion of leukocytes to vascular endothelium, and entry of leukocytes into inflamed tissues. Recent studies have suggested that angiogenesis and cellular adhesion may be mutually linked processes. Both basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) have been shown to facilitate angiogenesis. However, their roles in the expression of adhesion molecules on the endothelial cells have not been clarified. The current studies therefore examined the effect of bFGF and VEGF on the expression of vascular cell adhesion molecule-1 (VCAM-1) on human umbilical vein endothelial cells (HUVEC) stimulated with tumor necrosis factor α (TNF-α).
    HUVEC (1×104/well) were incubated in a 96 well microtiter plate with culture medium containing endothelial cell growth supplement (ECGS) for 24h. After the incubation, culture medium was replaced by ECGS free culture medium with or without TNF-α (10ng/ml), bFGF (10ng/ml) and VEGF (10ng/ml), and the culture was further carried out for addi-tional 24h. The expression of VCAM-1, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA and the proliferation of HUVEC was measured by MTT colorimetric assay. Soluble VCAM-1 (sVCAM-1) in the supernatants were assessed by ELISA. Although, both bFGF and VEGF supported the proliferation of HUVEC, bFGF, but not VEGF, selectively suppressed the expression of VCAM-1 on HUVEC stimulated with TNF-α. The expression of ICAM-1 and E-selectin induced by TNF-α was not inhibited by either bFGF or VEGF.
    In addition, bFGF also decreased the levels of sVCAM-1 in the supernatants of TNF-α stimulated HUVEC. The data indicate that bFGF, but not VEGF, suppresses the production of VCAM-1 by HUVEC under stimulation with TNF-α. These results therefore suggest that angiogenic cytokines bFGF and VEGF play different roles in the regulation of the expression of adhesion molecules on endothelial cells under inflammation.
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  • Motohisa Yamamoto, Hiroki Takahashi, Tsunenori Mizukoshi, Rieko Muraka ...
    2000 Volume 23 Issue 1 Pages 22-29
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    A 68-year-old man noticed severe oral dryness and a submandibular swelling. Sjögren's syndrome (SS) was diagnosed based on microscopic findings of a labial salivary gland biopsy although both anti-SS-A and anti-SS-B antibodies were negative. In addition, hypergammaglobulinemia (IgG 7940mg/dl) and hypocomplementemia were pointed out and he was admitted to our department. On admission cervical, mediastinal, and abdominal lymph nodes swelling were detected together with enlargement of lacrimal and salivary glands. Lymphoproliferative disorders associated with SS were highly suspected. Biopsied specimens of his lacrimal gland and cervical lymph node disclosed neither malignant cells nor monoclonal proliferation of lymphocytes. An administration of corticosteroids caused rapid diminution in size of lacrimal glands, salivary glands, and lymph nodes. Both lacrimation and salivation recovered, and hypergammaglobulinemia and hypocomplementemia returned to normal after treatment. The characteristics of this case were an atypical onset in an elderly man, the negativity of anti-SS-A and anti-SS-B antibodies, and reversiblity of dryness by corticosteroid treatment. These findings suggest that the pathogenesis of this case may be different from typical SS.
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  • Michi Tanaka, Ayako Nakajima, Akira Suwa, Takashi Yamada, Takahiro Suz ...
    2000 Volume 23 Issue 1 Pages 30-36
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    We report a case with rheumatoid arthritis and hypersensitivity pneumonitis. A 66-year-old female was admitted to our hospital because of fever, cough, and progressive dyspnea on October 10, 1997. She had a history of rheumatoid arthritis from 1987 and was treated with cyclophosphamide when she developed pulmonary symptoms in September 1997. On admission arthritis was subsided. Fine crackles on ausculation of lung, hypoxia, ground-glass appearance on chest X-ray were detected. The computed tomography of the chest disclosed diffuse interstitial shadow with patchy destruction of alveolar structures. Bronchoalveolar lavage demonstrated an increase in lymphocytes with predominance of suppressor-cytotoxic T cell subset (CD 8+). The histopathological examination of transbronchial lung biopsy showed interstitial inflammation with marked predominance of lymphocyte with intraalveolar exudate. Her condition got better and she discharged without definitive diagnosis and treatment for her respiratory symptoms. Eight hours after she went back home, she suddenly presented high fever and cough and gradually developed dyspnea. She was readmitted 5 days after the previous discharge. Although no specific precipitin antibody against various microorganisms was detected in her sera, the diagnosis of hypersensitivity pneumonitis was made. Thirty mg per day of prednisolone was resolved her symptoms promptly.
    There was no reported case with hypersensitivity pneumonitis and rheumatoid arthritis of other collagen diseases. The clinical course that arthritis and pulmonary symptoms appeared alternatively is of considerable intrest to investigate for the pathogenesis of these two immune disorders.
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  • Keigo Ikeda, Masakazu Matsushita, Soichiro Ando, Iwao Sekigawa, Noboru ...
    2000 Volume 23 Issue 1 Pages 37-42
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    Recent reports have indicated that antiphospholipid antibodies (aPL) are related to other clinical manifestations such as cardiac valve lesions and hemolytic anemia besides the major clinical features of antiphopholipid syndrome (APS), including thrombocytopenia, and recurrent fetal demise. We recently encountered a case of multiple hormonal deficiencies in the pituitary gland and hypothyroidism associated with an APS. Hypopituitarism of the patient had occurred after her delivery and a magnetic resonance imaging (MRI) examination disclosed “empty sella” of the hypophysis, so she was thought to have Sheehan's syndrome. There has been a few reports describing the relationship between aPL and endocrine disorders. aPL-related onset of these diseases may be more frequent than is generally appreciated.
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  • Shingo Nakayamada, Yoshiya Tanaka, Kazuyoshi Saito, Toshiyuki Ota, Sum ...
    2000 Volume 23 Issue 1 Pages 43-48
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    A 66-year-old non-hemophiliac man developed widely spreaded hematoma in soft tissues around neck. On the day of admission, he was nearly choked by the giant hematoma which markedly compressed trachea. Initially, to keep air way, an intratracheal intubation using a fiber scope was carried out. Coagulation studies revealed a marked prolongation of activated partial thromboplastin time (129 seconds, control: 24.9-33.2), a diminished activity of factor VIII (less than 1%) and a significant increase of factor VIII inhibitor titer (60 Bethesda unit/ml). We thereby diagnosed coagulopathy related to acquired inhibitor against factor VIII.
    The general combination therapy of intravenous infusion of both prothrombin complex concentrates and activated prothrombin complex concentrates, prednisolone and plasma exchange successfully stopped expansion of the giant hematoma. However, because the titer of factor VIII inhibitor remained increased and the activity of factor VIII was continued to reduced, cyclosporin was additionally administrated. As a result, the titer of factor VIII inhibitor was markedly improved, but the reduced activity of factor VIII was continued and re-bleeding around neck was observed. We thereby administered steroid pulse therapy, which resulted in complete remission of the disease activity and recovery of factor VIII activity.
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  • Yukiko Fukumoto, Hajime Hosoi, Ayumi Kawakita, Shigeki Yamamoto, Shinj ...
    2000 Volume 23 Issue 1 Pages 49-56
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    We report A case of Sjögren's syndrome complicated with MALT (mucosa-associated lymphoid tissue lymphoma) in childhood. Additionally, Helicobacter pylori infection into the gastric mucosa was highly suspected in this case. A 13-year-old girl suffering from multiple joint pain had received treatment as Juvenile Rheumatic Arthritis with no clinical improvement until introduction to our hopital. On admission to our hospital, high levels of serum anti-SSA and anti-SSB (80.2 and 16.1 holds, respectively) were detected. Minor salivary gland biopsy showed a typical histological finding for Sjögren's syndrome as infiltrating lymphocytes around the excretory ducts. Computed tomography and 67Gallium scintigraphy showed a gastric tumor, and it was diagnosed as primary gastric B-cell MALT lymphoma by the histopathological findings. Additionally, Helicobacter pylori infection into the gastric mucosa was highly suspected. Recently it is emphasized that infection of Helicobacter pylori is related with gastric MALT lymphoma. There has been no reports of children who have Sjögren's syndrome associated with malignant lymphoma. Taken together, Helicobacter pylori infection superimposed with Sjögren's syndrome might accelerate clinical course in our particular case.
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  • Akio Mimori, Hiroyuki Nara, Naoko Kaneko, Yuko Shirota, Akira Takeda, ...
    2000 Volume 23 Issue 1 Pages 57-63
    Published: February 29, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    Clinical profiles and the treatment process of three female patients with systemic sclerosis (cases 1, 2, and 3) complicated by thrombotic microangiopathic hemolytic anemia (TMHA) were described. Thrombocytopenia preceded renal damage and hypertension in cases 1 and 2, although the chronological relationship between these parameters were unknown in case 3. Plasma exchange therapy using fresh frozen plasma was beneficial in cases 1 and 2. Cases land 3 presended with delirium and fluctuating psychosis, respectively. Early detection of thrombocytopenia and insidious hemolysis might be essential for starting effective plasmapheresis treatment in a part of patients with scleroderma kidney who present with thrombotic thrombocytopenic purpura (TTP) like disorder.
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