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Introduction: Introduction: starvation is usual in patients referred for endoscopic gastrostomy (PEG). A high risk of refeeding syndrome (RS) may contribute to poor prognosis. Objectives: this study aims to: a) evaluate serum phosphorus and magnesium when patients underwent PEG; b) determine the mortality rate during the first week and first month of enteral nutrition; and c) assess if hypophosphatemia or hypomagnesemia are associated with early mortality. Material and methods: retrospective study with patients followed in the Artificial Nutrition Clinic and died under PEG feeding. General nutritional assessment included NRS 2002, anthropometry and serum proteins. Serum phosphorus and magnesium were measured immediately before gastrostomy. Survival was recorded and compared to electrolyte and nutritional status. Results: one hundred and ninety-seven patients (137 men/60 women) aged 26-100 years. Most underwent PEG due to neurologic disorders (60.9%) and were malnourished according to body mass index (BMI) and serum proteins. Low phosphorus and magnesium were found in 6.6% and 4.6%, respectively. Hypophosphatemia was associated with malnutrition (p < 0.05). Mean survival was 13.7 ± 15.4 months. Mortality was 4.6% in the first week and 13.2% in the first month post-gastrostomy. Overall survival was shorter in malnourished patients but malnutrition did not directly influence early mortality (p > 0.05). Hypophosphatemia was associated with mortality during the first week (p = 0.02) and the first month of PEG feeding (p = 0.02). Conclusions: hypophosphatemia was uncommon but predicted early mortality after PEG. Although RS may be less frequent than expected, hypophosphatemia may be used as a RS marker and RS is the probable cause of increase early mortality in hypophosphatemic PEG-fed patients. [ABSTRACT FROM AUTHOR]

Competing Interests: The authors declare that they have no conflict of interest.

Competing Interests: The authors have no conflicts of interest to declare.

Competing Interests: The authors have no conflicts of interest to declare. Moreover, they are aware that the manuscript's copyright belongs to GE − Portuguese Journal of Gastroenterology.

Background: Hepatic glycogenosis (HG) is a complication of poorly controlled type 1 diabetes mellitus (T1DM), characterized by glycogen accumulation in hepatocytes. Mauriac syndrome (MS) is a glycogenic hepatopathy, initially described in 1930, characterized by growth failure, delayed puberty, cushingoid appearance, hepatomegaly with abnormal liver enzymes, and hypercholesterolemia. HG is a condition with good prognosis and fast resolution after adequate glycemic control (although it has potential for relapse), with no case of evolution to end-stage liver disease described., Case: We describe a 26-year-old female, with T1DM complicated by severe retinopathy. The patient maintained poor glycemic control since childhood, presenting glycated hemoglobin persistently higher than 10% and recurrent episodes of ketoacidosis. In adolescence, she developed hepatomegaly and fluctuating elevation of aminotransferases and triglycerides. A small, nonrepresentative hepatic biopsy suggested macrovacuolar steatosis and mild fibrosis. After 15 years of diabetes, the patient was referred for gastroenterology clinic due to chronic diarrhea and exuberant hepatomegaly. Laboratory showed persistent elevation of aminotransferases and triglycerides. Bilirubin, iron metabolism, and coagulation were normal; viral serologies and autoimmune study were negative. Upper endoscopy, ileocolonoscopy, and enteroscopy presented no lesions. Abdominal magnetic resonance imaging displayed massive hepatomegaly. Liver biopsy was repeated showing marked nuclear glycogenization, mild steatosis, and no fibrosis; electron microscopy revealed very large deposits of glycogen and pleomorphic mitochondria with an unusually dense matrix, described for the first time in this entity. The diagnosis of MS variant and diarrhea due to autonomic neuropathy were assumed., Conclusion: Currently, HG is a well-recognized disease that occurs at any age and can be present without the full spectrum of features initially described for MS. In the era of insulin therapy, this entity represents a rare complication, caused by low therapeutic compliance., Competing Interests: The authors have no conflicts of interest to declare.