A 31-year-old woman was admitted to the Internal Medicine Department of our hospital in 2008 for unquantified weight loss and vomiting of uncertain duration. The patient did not report any other device-related symptoms. During admission, a complete biochemical study, complete blood count and thyroid function were normal. Infectious pathology was ruled out, with various serological tests, determination of parasites in faeces, etc., all of which were negative. The presence of digestive pathology was also ruled out, specifically malabsorptive symptoms (upper gastrointestinal endoscopy (EDA), anti-gliadin and anti-endomysial antibodies, duodenal biopsy: normal). The gastro-oesophagoduodenal study showed dilatation of the second duodenal portion in relation to extrinsic compression, suggestive of aorto-mesenteric clamp; the diagnosis was confirmed by performing a CT angiography of the mesenteric artery. The patient was also assessed by psychiatry, ruling out the presence of an eating disorder.

With the diagnosis of Wilkie syndrome, she was referred to the Nutrition Department in November 2009. She reported a normal weight of 56 kg. At that time she weighed 43.9 kg and her body mass index (BMI) was 16.7 kg/m2. Initially, nutritional management was attempted with dietary modifications, postural measures and prescription of supplements, without improvement; although at no time in the evolution of the patient did she present with retention stomach or hydroelectrolyte alterations. In January 2010, at 42.6 kg, a feeding tube was provisionally placed in order to attempt nutritional recovery through the administration of enteral nutrition (EN). Digestive tolerance was good and she did not present refeeding syndrome, increasing her weight to 50 kg (BMI: 19). At that time, an attempt was made to reintroduce natural foods, but the vomiting reappeared, so a new oesophagogastroduodenal study was performed, with similar findings to the diagnosis. In view of this situation, in agreement with the patient, the General Surgery Department was consulted and surgical treatment was proposed. A duodenojejunostomy was performed. Oral tolerance after surgery was initially problematic in relation to gastric hypotonia, and treatment with prokinetics was necessary. Two months after the operation the patient was completely asymptomatic, with a weight of 50 kg, oral tolerance was good and the barium study showed a stomach with normal morphology and emptying and good passage of contrast through the duodenojejunostomy. To date, the patient has lost weight again (45 kg). She denies the existence of digestive symptoms, and states that she feels thin and wishes to regain her lost weight; but refuses to take nutritional supplements, as well as any medical tests and re-evaluation by the Psychiatry Service.

