The fat overload syndrome. Report of a case and literature review.

ABSTRACT A 10-month-old infant with hypoplasia of the intestinal mucosa had the fat overload syndrome develop while receiving intravenous fat emulsion at a dosage of 5 g/kg/day of fat for five weeks. This syndrome was characterized by fever, jaundice, easy bruisability, increased levels of serum transaminases, conjugated hyperbilirubinemia, and abnormal results of clotting studies. Management consisted of withdrawal of parenteral nutrition for 72 hours, followed by gradual reinstitution of protein and subsequent introduction of fat at a lower dosage.

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    ABSTRACT: A recent study attempts to add to the body of evidence that is emerging regarding the fish oil parenteral lipid product Omegaven™. The authors have shown from explant livers of children on chronic parenteral nutrition with Omegaven™ that biochemical improvement in cholestasis does not always reflect improvement in liver histology. These findings support 2 small case series that were previously published. Despite improvement and resolution of hyperbilirubinemia in all six infants, five of six infants had persistent or progressive hepatic fibrosis, while only one infant had regression of fibrosis. The study raises questions of whether there is a window of opportunity for efficacy of this preparation; also, an important question is if this omega-3 fatty acid-rich preparation is superior to newer "blended lipids" containing olive, coconut, soy, and fish oil.
    05/2015; 21(17):5115-8. DOI:10.3748/wjg.v21.i17.5115
  • Intensive Care Medicine 06/1994; 20(5):399-400. DOI:10.1007/BF01720919 · 5.54 Impact Factor
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    ABSTRACT: The authors describe a 21-year-old female with an isolated brain injury after a traffic accident. She developed multiple organ failure and hypertriglyceridemia, hemolysis, marked thrombocyto- and leukopenia and coagulation disorder. Bone marrow smear indicated hyperactivation and haemophagocytosis. TPN was started day 3. The administration of fat was proposed to be the trigger of the hyperactivation of the monocyte-macrophage system. However, there are other factors more likely to trigger this mechanism. Most critically ill patients tolerate fat emulsions better than other energy substrates. Creaming of fat emulsions as an in vitro agglutination occurring when the fat emulsion is added to sera from critically ill patients. The clinical significance of creaming is not known. Creaming occurs in most ICU patients (49 of 51) and in about 30% of ambulatory patients (62 of 200). The patients with creaming all had higher CRP levels than the 'non-creamers'. Creaming might occur also in patients with normal CRP but with increased concentrations of other acute phase proteins [1]. There is no correlation between the degree of creaming and the elimination rate of fat emulsion. Thus using CRP as a complementary tool for monitoring fat tolerance is not rational. The proposed pathogenesis for activation of phagocytosis by fat emulsion is based on the occurrence of in vivo creaming and a release of cytokines which will depress lipoprotein lipase. However, cytokine release is increased in most tranmatised patients and still these patients tolerate and utilise fat emulsions better or at least as good as the healthy man. TPN and its influence on immune function is frequently studied. Most studies are in vitro studies telling nothing about clinical effects. Palmblad made an extensive review of the potential influence of fat emulsions on the immune function in vivo [2]. The effect of fat emulsions on phagocytosis have been studied in four controlled studies in humans. The patients were severely ill due to cancer, sepsis or inflammatory bowel disease but no difference in phagocytic activity due to fat emulsions could be detected. The authors propose that the increase in intracranial pressure could be explained by administration of fat emulsion. In a study by Young et al. TPN was compared to enteral nutrition in 96 severely brain injured patients [3]. There were no differences between the groups in intracranial pressure. The clinical outcome was slightly better in the group treated with TPN. In patients with a heightened risk of increased intracranial pressure, substitution of lipid calories for glucose calories decreased the osmolal load. The conclusions drawn by the authors in the paper are too speculative. The ultimate influence of fat emulsions on phagocytosis or other variables of immune function in vivo is not known. The conclusion that creaming is one reason for impaired phagocytosis is not relevant since creaming as an in vitro phenomenon which is not proven to occur in vivo. Critically ill patients usually have a normal tolerance of fat emulsions. Patients with brain injury and in need of TPN benefit from a low osmolal load.
    Intensive Care Medicine 04/1994; 20(5):398-399. DOI:10.1007/BF01720918 · 5.54 Impact Factor