Factors associated with intolerance after refeeding in mild acute pancreatitis.

OBJECTIVES: This study aimed to describe the mode of refeeding, frequency of intolerance, and related factors in mild acute pancreatitis (AP). METHODS: We included all cases of mild AP between January 2007 and December 2009 in an observational, descriptive, and retrospective study. We analyzed demographic and etiological data, admission variables, treatment, refeeding mode, intolerance frequency, and treatment. Intolerance-related variables were determined using a Cox regression. RESULTS: Two-hundred thirty-two patients were included (median age, 74.3 years, bedside index for severity in AP score, 1). Oral diet was reintroduced at 3 days (range, 0-11 days) in 90.9% of cases with a liquid diet. Intolerance to refeeding appeared in 28 patients (12.1%) at a median time of 1 day (range, 0-14 days). Oral diet was reduced or suspended in 71.4%; analgesic and antiemetic drugs were required in 64% and 35.7% of patients, respectively. The variables independently associated with intolerance to refeeding were choledocholithiasis (hazard ratio [HR], 12.35; 95% confidence interval [CI], 2.98-51.19; P = 0.001), fasting time (HR, 1.33; 95% CI, 1.09-1.63; P = 0.005), refeeding with complete diet (HR, 4.93; 95% CI, 1.66-14.66; P = 0.04), length of symptoms before admission (HR, 1.004; 95% CI, 1.001-1.006; P = 0.012), and metamizole dose (HR, 1.11; 95% CI, 1.02-1.21; P = 0.014). CONCLUSIONS: Intolerance to refeeding is an infrequent event. We have identified several factors independently associated with intolerance.

Fatty emaciation: a case report of suspected fat overload syndrome in oral refeeding.

Refeeding syndrome has been observed in patients receiving nutrition after a prolonged period of malnourishment and is characterized by multiple metabolic derangements. Besides hypophosphatemia and hypoglycemia, lipemia has been described in association with parenteral nutrition administration to the malnourished. The authors describe one anorexic patient who developed lipemia during oral refeeding, followed by a precipitous drop in hematocrit suggestive of fat overload syndrome.

Resveratrol improves insulin resistance of catch-up growth by increasing mitochondrial complexes and antioxidant function in skeletal muscle.

Caloric restriction followed by refeeding, a phenomenon known as catch-up growth (CUG), affects mitochondrial function and results in systemic insulin resistance (IR). We investigated the potential of resveratrol (RES) in CUG to prevent IR by increasing activity of the mitochondrial respiratory chain and antioxidant enzymes in skeletal muscle. Rats (8 weeks of age) were divided into 3 groups: normal chow, CUG, and CUG with RES intervention. Skeletal muscle and systemic IR were measured in each group after 4 and 8 weeks. Mitochondrial biogenesis and function, oxidative stress levels, and antioxidant enzyme activity in skeletal muscle were assessed. Catch-up growth-induced IR resulted in significant reductions in both average glucose infusion rate(60-120) at euglycemia and skeletal muscle glucose uptake. Mitochondrial citrate synthase activity was lower; and the activity of complexes I to IV in the intermyofibrillar and subsarcolemmal (SS) mitochondria were reduced by 20% to 40%, with the decrease being more pronounced in the SS fraction. Reactive oxygen species levels were significantly higher in intermyofibrillar and SS mitochondria, whereas activities of antioxidant enzymes were decreased. Oral administration of RES, however, increased silent information regulator 1 activity and improved mitochondrial number and insulin sensitivity. Resveratrol treatment decreased levels of reactive oxygen species and restored activities of antioxidant enzymes. This study demonstrates that RES protects insulin sensitivity of skeletal muscle by improving activities of mitochondrial complexes and antioxidant defense status in CUG rats. Thus, RES has therapeutic potential for preventing CUG-related metabolic disorders.

Thiamine supplementation in the critically ill.

PURPOSE OF REVIEW: To summarize the properties of thiamine and evaluate current evidence on thiamine status and supplementation, for different populations of critically ill patients. RECENT FINDINGS: Thiamine, in the form of thiamine pyrophosphate, is a critical co-factor in the glyocolysis and oxidative decarboxylation of carbohydrates for energy production. Different studies have shown that critical illness in adults and children is characterized by absolute or relative thiamine depletion, which is associated with an almost 50% increase in mortality. Thiamine deficiency should be suspected in different clinical scenarios such as severe sepsis, burns, unexplained heart failure or lactic acidosis, neurological disorder in patients with previous history of alcoholism, starvation, chronic malnutrition, long-term parenteral feeding, hyperemesis gravidarum, or bariatric surgery. Nonetheless, thiamine supplements are not routinely given to critically ill patients. Clinicians should be able to suspect and recognize risk factors for the occurrence of severe neurological disorders secondary to thiamine deficiency, as early treatment can prevent the appearance of permanent neurological damage. SUMMARY: Symptoms and signs associated with thiamine deficiency lack sensitivity and specificity in critically ill patients. Consequently, depletion is frequently unrecognized and underdiagnosed by clinicians. Potentially deleterious consequences of thiamine depletion should be avoided by early and appropriate supplementation.