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Objective Anorexia nervosa (AN) is associated with one of the highest mortality rates of any psychiatric disorder but limited mortality data were reported for those with extremely severe malnutrition. This study aimed to estimate standardized mortality ratio (SMR), investigate predictive factors of mortality and causes of death among a sample of patients with AN admitted to a specialized clinical nutrition unit (CNU) because of extremely severe malnutrition. Methods Between 11/27/1997 and 01/15/2014, vital status was determined for 384 patients admitted for AN at the first time in the CNU. Sociodemographic, anamnestic, and clinical data were collected. We calculated the SMR. Univariate and multivariate Cox regression analyses were performed to identify mortality predictors. Results Crude mortality rate was 11.5%. (44 deaths) and SMR 15.9 [CI 95% (11.6-21.4)], 5.2 years post inpatient treatment. Mortality predictors at the time of hospitalization were as follows: older age, occurrence of an in-hospital suicide attempt, transfer to medical intensive care unit and the following somatic complications: frank anemia, dysnatremia, infectious and cardiac complications. Other predictors of mortality were: past or present history of discharge against medical advice, hematological comorbidities (not related to AN). A longer inpatient length of stay was a protective factor. Conclusion Very severely malnourished patients with AN hospitalized in a medical unit because of extremely severe somatic issues have a medium-term mortality rate higher than the general population and even higher than patients in tertiary specialized ED units. This study highlights predictive factors of mortality that will help clinicians in recognizing and managing patients at risk of death.

International audience; Background and aims: The clinical nutrition-eating disorders-unit in Raymond Poincaré Hospital is a reference center for the management of severe malnutrition and its complications in patients with anorexia nervosa (AN). The purpose of this study is to specify socio-demographic, anamnesic and clinical characteristics of AN patients hospitalized for extreme malnutrition, to identify types and prevalence of medical complications presented during their hospitalization for refeeding and the evolution of patients nutritional status. Methods: Demographic, clinical and paraclinical data of 354 severely malnourished AN patients were collected, during their first hospitalization in the unit, between November 1997 and January 2014, through medical records. The prevalence of medical complications was compared between the 2 AN subtypes (restricting and binging-purging). Results: 339 patients were female and mean age was 28.7 ± 10.7 years old. Duration of AN was 9.5 ± 9 years, 173 (48.9%) patients had a restricting AN subtype. BMI at admission was 12.2 ± 1.6 kg/m2, 280 (79.3%) patients had already been hospitalized for AN in other hospitals before. Psychiatric comorbidities were present in 168 (47.5%) patients. Associated somatic comorbidities concerned 70 (19.8%) patients. Outcomes during hospitalization were marked by 4.1 ± 3.9 kg weight gain on 36.9 ± 30.5 days. Enteral nutrition was provided in 304 (85.9%) patients. Main medical complications during hospitalization were: anemia (79%), neutropenia (53.9%), hypertransaminasemia (53.7%), osteoporosis (46.3%), hypokalemia (39.5%), hypophosphatemia (26%), hypoglycemia (13.8%), infectious complications (24.3%), cardiac dysfunction (7.1%), and proven gelatinous bone marrow transformation (6.5%). Hypokalemia was more frequent in binging-purging subtype. Lympho-neutropenia and hypertransaminasemia were more frequent in restricting subtype. During their hospitalization, 35 (10%) patients were referred to medical intensive care unit and 5 patients died. Conclusions: AN patients hospitalized for severe malnutrition in a specialized clinical nutrition unit have severe and frequent medical complications. Psychiatric comorbidities are also frequent and could complicate medical care. A specialized and multidisciplinary management of these patients is therefore essential.

Background: The question of where to hospitalize extremely malnourished patients with anorexia nervosa (AN) is a real dilemma. On one hand, psychiatrists have to deal with severe medical complications that are not within their competences and that justify hospitalization in an internal medicine ward. On the other hand, medical doctors have to face psychic decompensations that would justify admission to a psychiatric ward. In this context, we share our experience of management of severely malnourished AN adult patients in a transdisciplinary specialized eating disorders (ED) unit, referral center for AN associated with somatic severity.Method: First, we described the modalities of care proposed to patients with AN hospitalized in the medical unit. Intensive medical care, both somatic and psychiatric, are provided thanks to a transdisciplinary therapeutic program, where objectives are to: medically stabilize the patient, initiate progressive refeeding and start supportive psychotherapy before being transferred to a psychiatric ED unit. Secondly, we conducted a retrospective descriptive study that included all adult patients with AN admitted for the first time to the unit, between November 1997 and January 2014, for severe malnutrition and/or complications of the ED. Objective was to specify patients characteristics: demographic, nutritional status, history of ED, care pathway. Finally we discussed the value of such a unit.Results: Among a cohort of 386 adult patients with AN (21 males and 365 females) admitted for the first time in the unit, mean age was 29.4 (± 11.5) years, mean BMI was 12.7 (± 2.2) kg/m². Before being supported in the unit, 78.2% of patients had already been hospitalized in other hospitals. Mean length of stay was 35.2 days. Patients were clinically serious and unstable because of life-threatening somatic complications due to a low BMI. During hospital stay, a temporary transfer to medical intensive care unit was necessary for 25.6% of patients. Average patient weight gain was 0.777 kg per week and 81.9% of patients benefited from enteral nutrition.Conclusion: This specialized transdisciplinary unit where physician nutritionists and psychiatrists coordinate medical care together, allow a better understanding and management of extreme malnutrition associated with AN. Thanks to their expertise, care teams are less critical and less rejecting towards patients. Thus, therapeutic alliance could be optimized.

A 47-year-old woman came to our hospital with malnutrition and liver failure in August, 2011. 28 months earlier, when she had been assessed for a bari atric gastric band, medical history included morbid obesity (height 159 cm, weight 127 kg, BMI 45 kg/m2), arterial hypertension, and moderate restrictive respiratory insuffi ciency; oral food intake was high. The patient had laparoscopic adjustable gastric banding. She was subsequently lost to follow-up. 16 months after banding, she had acute vomiting, abdominal pain, dehydration, and acute renal failure, and was non-responsive to band loosening. On laparotomy, gastric necrosis necessitated subtotal gastrectomy and Roux-en-Y gastric bypass. She recovered with no surgical complications. At follow-up, low oral intake (900 kcal per day), chronic diarrhoea, weight loss, and vitamin defi ciencies were noted. Medications were proton pump inhibitors, oral vitamins, and dietary supplements. 12 months after gastric band removal, the patient had lost 80 kg since before banding (weight 47 kg, BMI 18·6 kg/m2) and came to our clinic with cachexia, liver encephalopathy, hypoglycaemia, sarco penia, oedema, ascites, and diarrhoea. There was no evidence of sepsis, bleeding, chronic hepatocellular insuffi ciency, or portal hypertension, and there were no risk factors for acute or chronic liver disease, except for previous obesity. Laboratory testing showed raised amino transferases, a prothrombin rate of 16% (indicating acute liver failure), hypoalbuminaemia, micronutrient defi ciency, and central pancytopenia (appendix). Ultra sound and CT scans showed a non-dysmorphic steatosic liver and ascites. All biological and morphological tests for infections, intoxi cations, or antitrypsin defi ciency, and gastro intestinal, cardiac, auto-immune, nephrological, haemo lytic, haemato logical, or overload diseases were negative. Trans jugular liver biopsy suggested normal hepatic venous pressure gradient and diff use acute fatty liver with pure microvesicular steatosis aff ecting all hepato cytes, without fi brosis or necrosis (fi gure). Specifi c digestive functions were assessed after parenteral nutri tion refeeding, under stable conditions and with high oral intake (2500 kcal per day) (appendix). Intestinal failure results from obstruction, dysmotility, surgical resection, congenital defect, or disease-associated loss of absorption, and is characterised by the inability to maintain protein-energy, fl uid, electrolyte, or micronutrient balance. Because the patient did not need any nutritional support before surgery, we thought that gastrojejunal bypass had profoundly altered absorptive function. This situation is similar to that seen in short bowel syndrome and is worsened by chronic bacterial overgrowth and pancreatic insuffi ciency (appendix). Intestinal failure contributed to severe malnutrition, microvesicular steatosis, and acute fatty liver failure. A multimodal intestinal failure programme was provided through a central venous line. Oral antidiarrhoeal treatment consisted of pancreatic enzymes, loperamide, and digestive decontamination. After 3 months of digestive and nutritional support, oral intake, nutritional status, liver function, and histology recovered (fi gure), although after 20 months the patient still needed parenteral nutrition. Post-bariatric intestinal failure is an emerging indication for parenteral nutrition or intestinal transplantation encountered in expert centres. Either early or delayed postsurgical chronic diarrhoea, especially combined with low oral intake, should be recognised as a strong indicator of intestinal failure. After optimising digestive functions and nutritional support (including enteral nutrition), some patients still need permanent parenteral nutrition, surgical re hab ilitation, and occasion ally intestinal transplantation.

We showed that glucose absorption is accelerated in the proximal intestine of morbidly obese humans, associated with increased expression of sodium dependent glucose co-transporter 1 (SGLT1), an altered incretin profile, hyperinsulinemia and hyperglycemia. This study aimed to examine the effects of energy restriction on glucose absorption, expression of intestinal glucose transporters and sweet taste receptors (STR), incretin hormone responses and glycemia in the morbidly obese. Methods: 10 non-diabetic, morbidly obese subjects (2M:8F; 45±3yrs, BMI: 46±3kg/m2) were studied before and after a 2-week VLCD (750kcal/day). On each occasion, endoscopic duodenal biopsies were collected before and after intraduodenal glucose infusion (30g glucose over 30 min, with 3g 3-O-methylglucose (3-OMG) to estimate glucose absorption). Blood glucose and plasma concentrations of 3-OMG, glucosedependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and insulin were measured over 240 min. Absolute expression of SGLT-1, GLUT2 and STR (T1R2) transcripts was quantified by PCR. Results After 2 weeks of VLCD, body weight (-5.6±0.5kg, P