Two years after BPD in morbidly obese patients, comorbidities are largely corrected and insulin resistance is fully reversed despite persistent obesity. Initial fat mass, but not residual intestinal length, is the strongest predictor of weight loss after BPD.

Hospital malnutrition is a detrimental prognostic factor regarding hospital mortality, complications, and length of stay. However, the role of hospitalization itself on nutritional status has not been fully elucidated. We report the results of a secondary analysis from the dataset of a recent cross-sectional study at Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Data from patients evaluated at admission and discharge were collected and compared. One hundred thirty-nine patients were evaluated. Mean length of stay was 13.6 (± 7.7) days. Patients at risk of malnutrition, according to NRS-2002, were 75 (53.9%), while 63 (45.3%) were malnourished according to ESPEN Criteria. Compared to admission, at discharge, patients reported a significant decrease in Mid-Upper Arm Circumference (MUAC)-from 26.5 cm (± 3.6) to 25.9 cm (± 3.7) (p = 0.016), a reduction in Phase angle (PhA)-from 4.25° (± 1.20) to 4.01° (± 1.15) (p = 0.005), fat-free mass (FFM)-from 47.5 kg (± 9.19) to 44.9 kg (± 9.4) (p = 0.03) and fat-free mass index (FFMI)-from 16.9 kg/m (± 2.3) to 15.8 kg/m (± 2.7) (p = 0.04). Laboratory data showed a reduction of albumin-from 29.2 (± 5.7) to 28.0 (± 5.9) (p = 0.01) and Onodera's PNI- from 29.1 (± 5.6) to 27.6 kg (± 5.6) (p = 0.039). At the multivariate linear regression analysis, the variables significantly associated with a worsening of PhA at discharge are the PhA value at admission and the diagnosis of malnutrition according to ESPEN Criteria. Hospitalization leads to significative changes in nutritional status. A clinical concern should be raised about the quality of hospital food and meal times and on the need for a clinical nutritionist on the ward.

Lipedema is a disabling disease characterized by symmetric enlargement of the lower and/or upper limbs due to deposits of subcutaneous fat, that is easily misdiagnosed. Lipedema can be primary or syndromic, and can be the main feature of phenotypically overlapping disorders. The aim of this study was to design a next-generation sequencing (NGS) panel to help in the diagnosis of lipedema by identifying genes specific for lipedema but also genes for overlapping diseases, and targets for tailored treatments. We developed an NGS gene panel consisting of 305 genes potentially associated with lipedema and putative overlapping diseases relevant to lipedema. The genomes of 162 Italian and American patients with lipedema were sequenced. Twenty-one deleterious variants, according to 3 out of 5 predictors, were detected in PLIN1, LIPE, ALDH18A1, PPARG, GHR, INSR, RYR1, NPC1, POMC, NR0B2, GCKR, PPARA in 17 patients. This extended NGS-based approach has identified a number of gene variants that may be important in the diagnosis of lipedema, that may affect the phenotypic presentation of lipedema or that may cause disorders that could be confused with lipedema. This tool may be important for the diagnosis and treatment of people with pathologic subcutaneous fat tissue accumulation.

No abstract