Japanese Journal of Clinical Immunology
Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300
Volume 23, Issue 5
Displaying 1-6 of 6 articles from this issue
  • Yoshinao Muro
    2000 Volume 23 Issue 5 Pages 425-434
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
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  • Toshio Miyawaki, Hirokazu Kanegane, Takeshi Futatani
    2000 Volume 23 Issue 5 Pages 435-444
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
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  • Takako Miyamae, Syoko Nakasima, Noriaki Tomono, Masaaki Mori, Masaaki ...
    2000 Volume 23 Issue 5 Pages 445-453
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    We experienced two infants with polyarteritis nodosa (PN). The symptoms started with high fever and skin rash, which were similar to those of Kawasaki disease (KD). However, the involvement of central nervous system and lung, such as distension of large fontanel, stridor and mild disturbance of consciousness, occurred and the systemic vasculitis resulted in hypoalbuminemia and severe generalized edema. They flared up twice or three times during the long clinical courses. Finaly, both had multiple giant coronary aneurysms and lung fibrosis.
    The clinical courses of these patients were different from those of KD in that; (1) the severity of vasculitis, (2) the wide-spread nature of the vasculitis, and (3) the chronic and recurrent clinical course.
    It is very difficult to distinguish PN from severe KD in the early stage of the diseases especially in infancy. But in the cases intractable to high-dose γ-globulin therapy and plasma exchange, it is needed to suspect PN and to induce more aggressive immunosuppres-sive therapy, such as methylprednisolone pulses and cyclophosphamide pulse therapy as soon as possible.
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  • Kiyotaka Kawauchi, Toshie Ogasawara, Masako Yasuyama
    2000 Volume 23 Issue 5 Pages 454-461
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    Malignant lymphoma is a major cause of hemophagocytic syndrome (HPS), in which reactive macrophages, phagocytic red blood cells, white blood cells, and platelets proliferate in bone marrow, liver, and spleen. In contrast to T/NK-cell lymphoma-associated hemophagocytic syndrome (T/NK-LAHS), few cases of B-LAHS have been reported; thus, the clinical characterization of B-LAHS remains to be established. We describe here four cases of B-LAHS that include the following features: (1) HPS was the initial presentation; (2) bone marrow involvement with large-cell lymphomas was noted in all cases, despite lack of remarkable lymphadenopathy; (3) no active infection with Epstein-Barr virus as the etiological agent was confirmed; (4) except for the spleen in one case, primary site of lymphoma could not be determined; and (5) serum IL-6, soluble IL-2 receptor, and IFN-γ-but not TNF-α and IL-1 β-, were significantly elevated. Such characteristics are peculiar to and different from those usually seen in B-cell lymphoma, suggesting that B-LAHS is a unique clinical entity among B-cell lymphomas.
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  • Akiko Aoki, Hirotomo Kenmochi, Eri Hagiwara, Shigeru Ohno, Atsuhisa Ue ...
    2000 Volume 23 Issue 5 Pages 462-469
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    A 53-year-old woman was admitted to our hospital in May 1999, because of progressive dyspnea and liver dysfunction. She had been receiving the replacement therapy of thyroid hormone for thirteen years and suffering from Raynaud's phenomenon for 9 years. She experienced exertional dyspnea and sicca symptom for 3 years, and had an episode of syncope 4 months before admission. An echocardiogram showed dilation of the right ventricle, tricuspid regurgitatiton and the estimated mean pressure of the pulmonary artery was higher than 120mmHg. She was diagnosed as having severe pulmonary hypertension (PH) complicated with primary Sjogren's syndrome and primary biliary cirrhosis without portal hypertension She was treated with anticoagulant (warfarin) and oral prostagrandin I2 (prostacyclin). However, right heart failure and jaundice gradually progressed and she suddenly died in December 1999. At autopsy, the heart was enlarged with right ventricular hypertrophy. Small arteries and arterioles in the lung showed concentric intimal proliferation and severe plexogenic vascular disease. Deposition of immunoglobulin was not observed in the pulmonary arteries. Since the prognosis of PH is poor, it is important to analyze the etiology of the disease for the development of the treatment.
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  • Youichi Motegi, Toshiyuki Yamada, Akihiro Morikawa
    2000 Volume 23 Issue 5 Pages 470-473
    Published: October 31, 2000
    Released on J-STAGE: February 13, 2009
    JOURNAL FREE ACCESS
    Concentrations of serum amyloid A protein (SAA) were measured in patients with hemophagocytic syndrome (HPS). There was a significant correlation between SAA and ferritin (p=0.0003), while there was no significant correlation between C-reactive protein (CRP) and ferritin. These results indicate that SAA could be a useful clinical marker for activity of HPS.
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