Case Report www.thelancet.com Vol 390 November 4, 2017 2119 A 34-year-old housewife, in the 15th week of her frst pregnancy, was referred to the Romanian Hereditary Angioedema Centre in January, 2015, because she was worried about potential risks to her pregnancy from symptoms she had had for the past 20 years. At age 14 years she began experiencing recurrent swelling of her limbs that would resolve spontaneously after 2–3 days. Over the next few years she started to develop genital and then recurrent facial swelling, each episode lasting 3–4 days. One episode of facial oedema was accompanied by swallowing and breathing difculties. Her mother also had a history of similar symptoms. At age 20 years she started to have abdominal colicky episodes, associated with nausea and vomiting. During one of her frst abdominal attacks the patient underwent an appendectomy, during which a surprisingly large amount of peritoneal fuid was evacuated, although no infammation or perforation was found on examination of the appendix. Her abdominal symptoms became more frequent from the age of 28 years, with recurrent episodes of colicky pain associated with nausea, vomiting, and occasionally diarrhoea, with no peripheral oedema or respiratory symptoms. She repeatedly attended the emergency department during such attacks, and her medical records showed that on each occasion her abdomen was distended, with difuse tenderness to palpation and shifting dullness, but examination of the head, neck, chest, limbs, and skin was unremarkable. Review of her medical fles showed that tests (including complete blood count, fbrinogen level, prothrombin time, thrombin time, platelet count, serum chemistry test, erythrocyte sedimentation rate, stool antigen test for Helicobacter pylori, thyroid hormone tests, thyroid- stimulating hormone test, thyroperoxidase antibodies, and allergy tests) were all within normal limits, and electrocardiography and chest radiography were normal. Abdominal ultrasound, performed several times during the abdominal attacks, showed ascites, but ultrasound and CT scan of the abdomen during asymptomatic periods were unremarkable. Because of the recurrent nature of her colicky pain, she decided together with a surgeon to undergo a laparoscopic investigation during such an attack at the age of 29 years. The laparoscopy, performed 12 h after the onset of abdominal pain, showed difuse mucosal oedema and erythema of the intestinal wall and, again, a large amount of peritoneal fuid (fgure, video). Examination of the fuid showed that it was serous and sterile, although we could not fnd in her notes whether it had been tested for albumin, protein, or abnormal biochemistry. At the time, no apparent explanation for the ascites was provided. During this period she was diagnosed as having idiopathic ascites, functional diarrhoea, irritable bowel syndrome, and dyspepsia, and was treated with proton- pump inhibitors, analgesics, and intravenous fuids. At age 33 years, during an episode of facial swelling, the family physician referred her to an allergist, who tested her for C4 and C1 inhibitor. C4 was 0·056 g/L (normal range 0·15–0·57 g/L), C1-inhibitor functional assay was 17% (70–130%), and C1-inhibitor antigen was 5 mg/L (210–390 mg/L), all of which confrmed a diagnosis of hereditary angio-oedema due to C1 inhibitor esterase defciency. At the time of referral to our centre she was taking no regular medication. We started treatment with C1 inhibitor concentrate for her recurrent attacks, and she had no angio-oedema attacks during the pregnancy. She had a planned caesarean section by patient choice, with C1-inhibitor concentrate cover. She had no symptoms of hereditary angio-oedema postoperatively. The baby was healthy and had normal C1-inhibitor values. 6 months later she had an episode of angio- oedema afecting the upper airway, which improved within 1 h of starting C1-inhibitor concentrate. At last follow-up in January, 2017, she had been symptom-free for the previous 3 months. Recurrent abdominal attacks lasting 2–3 days, with or without associated cutaneous oedema, are a common feature of hereditary angio-oedema due to C1-inhibitor defciency, seen in more than 90% of patients. 1,2 Recurrent ascites is found during attacks, with normalisation in asymptomatic periods. Severe abdominal attacks can mimic an acute abdomen, and patients are often seen in Recurrent ascites: a need to evaluate for hereditary angio-oedema Gabriella Gábos, Daniela Dobru, Enikő Mihály, Noémi Bara, Cătălin Dumitrache, Ramona Popa, Valentin Nădășan, Dumitru Moldovan Lancet 2017; 390: 2119–20 Gastroenterology Department (G Gábos MD, Prof D Dobru MD), and Allergy-Immunology Department (E Mihály MD, D Moldovan MD), Mureș County Hospital, Târgu Mureș, Romania; University of Medicine and Pharmacy, Târgu Mureș, Romania (Prof D Dobru, V Nădășan MD, D Moldovan); Romanian Network for Hereditary Angioedema, Romania (G Gábos, Prof D Dobru, E Mihály, N Bara MD, V Nădășan, D Moldovan); Surgery Department, Regina Maria Military Emergency Hospital, Brașov, Romania (C Dumitrache MD); and Allergy-Immunology Department, MedLife, Brașov, Romania (R Popa MD) Correspondence to: Dr Gabriella Gábos, Gastroenterology Department, Mureș County Hospital, Târgu Mureș 540103, Romania gabriellagabos@yahoo.com See Online for video A Figure: Ascites and intestinal oedema in hereditary angio-oedema Laparoscopic view during an episode of recurrent abdominal hereditary angio-oedema, showing swollen hyperaemic bowel foating in serous ascites. See Online for video