1,721,057 research outputs found

    New pathogenetic insights into the sarcoid granuloma

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    Although the most important enigma of sarcoidosis, ie, its etiology, remains an unsolved problem, the past few years have seen remarkable advances in understanding general immunologic and molecular aspects of the mechanisms leading to granuloma formation in sarcoidosis. It is now clear that during the sarcoid inflammatory process several cytokines are secreted at sites of disease activity; in addition, high affinity receptors for cytokines participating in the granuloma development have been recently identified. This article provides a detailed description of recent data that have clarified cellular interactions governing the dynamics of granuloma formation in sarcoidosis. Together, these new results provide important insights that can refocus efforts at developing immunotherapeutic methods of inhibiting cytokine production at sites of granuloma formation

    Chronic obstructive pulmonary disease (COPD): new insights on the events leading to pulmonary inflammation

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    The presence of a heterogeneous infiltrate of macrophages, neutrophils and CD8+ Tc1 cells is a characteristic feature in the lung of patients with chronic obstructive pulmonary disease (COPD). This paper points out the contribution of different inflammatory cells and mediators to the pathogenesis and natural history of COPD. We will comment on data suggesting that CD8 cytotoxic T cells with an activated Tc1 phenotype migrate from the secondary lymphoid tissue to pulmonary tissue damaged by smoke or infective agents. On the basis of the knowledge of the pathophysiology of immunologic events, drugs that can potentially block the inflammation leading to the disability of COPD are being investigated. Long-term study in a large number of patients with COPD will be needed to verify the impact of a number of anti-inflammatory compounds in this increasingly common disease

    [Plummer-Vinson syndrome: etiopathogenetic considerations and description of a case].

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    Dalla descrizione di un caso di Plummer-Vinson con importante stenosi esofagea nascono considerazioni circa l'eziopatogenesi di tale sindrome

    [Juvenile rheumatoid arthritis appearing after hepatitis. Causal or casual relationship].

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    High fever, spleen and lymph node enlargement, and joint pains that assumed the character of rheumatoid arthritis in the ensuing months were noted after a viral hepatitis episode in a 21-year-old woman. Serious anaemia and myocarditis also appeared when the picture was at its worst. A lymphoma was suspected, and the spleen and some abdominal lymph nodes were removed. These displayed signs of intense follicular reaction unaccompanied by atypia. The possibility that juvenile rheumatoid arthritis may be triggered by hepatitis is examined
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