MDL 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. 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. Barrett’s esophagus and esophageal adenocarcinoma are common after treatment for achalasia. Leeuwenburgh I, Scholten P, Calje TJ, Vaessen RJ, Tilanus HW, Hansen BE, Kuipers EJ. Dig Dis Sci: 2012 nov 22, Epub. DOI 10.1007/s10620-012-2157-9. PMID: 23179142 66 Achalasia is characterized by esophageal aperistalsis and impaired relaxation of the lower esophageal sphincter (LES). This contrasts with an insufficient LES, predisposing to gastro-esophageal reflux and Barrett’s esophagus. The co-incidence of achalasia and BE is rare. Pneumatic dilatation (PD) may lead to gastro-esophageal reflux, Barrett’s esophagus development, and esophageal adenocarcinoma. AIMS: To determine the incidence of Barrett’s esophagus and esophageal adenocarcinoma in achalasia patients treated with PD. METHODS: We performed a single-center cohort follow-up study of 331 achalasia patients treated with PD. Mean follow-up was 8.9 years, consisting of regular esophageal manometry, timed barium esophagram, and endoscopy. RESULTS: Twenty-eight (8.4 %) patients were diagnosed with Barrett’s esophagus, one at baseline endoscopy. This corresponds with an annual incidence of Barrett’s esophagus of 1.00 % (95 % CI 0.62-1.37). Hiatal herniation was present in 74 patients and 21 developed Barrett’s esophagus compared to seven of 257 patients without a hiatal hernia. Statistical analysis revealed a hazard ratio of 8.04 to develop Barrett’s esophagus if a hiatal hernia was present. Post-treatment LES pressures were lower in patients with Barrett’s esophagus than in those without (13.9 vs. 17.4 mmHg; p = 0.03). Two (0.6 %) patients developed WETENSCHAPPELIJK jaarverslag 2012 Pagina 65
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