INTERNE GENEESKUNDE Small bowel angioedema due to acquired C1 inhibitor deficiency: a case report and overview. Oostergo T, Prins G, Schrama YC, Leeuwenburgh I. Eur J Gastroenterol Hepatol. 2012 Dec 18. [Epub ahead of print] PMID: 23255023. Acquired angioedema is a rare disorder caused by an acquired deficiency of C1 inhibitor. It is characterized by nonpitting, nonpruritic subcutaneous or submucosal edema of the skin, or of the respiratory or gastrointestinal tract. When localized in the gastrointestinal tract, it can cause severe abdominal pain, mimicking an acute surgical abdomen, or chronic recurrent pain of moderate intensity. We report a case of a 48-year-old man presenting with recurrent episodes of hypotension and abdominal pain. Computed tomography of the abdomen showed edema of the small bowel. The first determinations of C1 inhibitor level and activity, measured in a symptom-free period, were normal. Repetition of the laboratory tests in the acute phase, however, showed a low C1 inhibitor level. Further diagnostic work-up indicated an acquired C1 inhibitor deficiency caused by a monoclonal gammopathy. He was treated with tranexamic acid as prophylaxis for his frequent attacks and to date, he has remained symptom free. Acquired C1 inhibitor deficiency is a rare cause of angioedema and is, among others, related to autoantibodies and abnormal B-cell proliferation, for example monoclonal gammopathy. The diagnosis of acquired C1 inhibitor deficiency is made on the basis of the medical history and on the level and activity of plasma C4, C1q, and C1 inhibitor. In case of high suspicion and a normal C1 inhibitor activity, it is recommended to repeat this test during an angioedema attack. Early diagnosis is important for the treatment of severe, potentially life-threatening attacks and to start prophylactic treatment in patients with frequent or severe angioedema attacks. Local and systemic cytokine profiles in non-severe and severe community-acquired pneumonia. Paats MS, Bergen IM, Hanselaar WE, Groeninx van Zoelen EC, Hoogsteden HC, Hendriks RW, Van der Eerden MM. Eur Respir J. 2012 Dec 20. [Epub ahead of print]. PMID: 23258791. Local inflammatory responses in community-acquired pneumonia (CAP) remain insufficiently elucidated, especially in patients with non-severe CAP. In this study we determined local and systemic cytokine responses in CAP patients and correlated these with disease severity and other clinical parameters.Levels of interleukin (IL)-6, IL-8, IL-10, IL-1β, tumour necrosis factor (TNF)α, interferon (IFN)γ, IL-22, IL-17A and IL-4 were determined in bronchoalveolar lavage (BAL) fluid and serum of 20 CAP patients upon admission and 10 healthy individuals. Systemic cytokine levels were also measured on days 7 and 30.In BAL fluid of CAP patients, levels of IL-6, IL-8, and IFNγ were significantly increased compared with healthy individuals, but no correlations with disease severity were found. Systemic levels of IL-6, IL-10 and IFNγ were significantly higher in severe CAP patients than in non-severe CAP patients and healthy individuals. Moreover, these cytokines showed a significant correlation with the pneumonia severity index (PSI). In the total group of CAP patients systemic IL-8 and IL-22 levels were also increased compared with healthy individuals.We therefore conclude that IL-6, IL-10 and IFNγ are important cytokines in CAP, although differences in disease severity upon admission are only reflected by systemic levels of these cytokines. 39 WETENSCHAPPELIJK jaarverslag 2012 Pagina 38
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