Pitfalls in anaphylaxis diagnosis and management at a university emergency department.

BACKGROUND: Some previous reports revealed suboptimal management of anaphylaxis (ANX) in the emergency department (ED). OBJECTIVE: To evaluate the recorded diagnosis and management of patients who presented with ANX at our university hospital ED and to assess how the management correlated with the severity of the case and the training level of the ED staff. METHODS: A descriptive study that involved reviewing the electronic medical records of patients who presented with ANX at the ED during a period of 4 years. RESULTS: When reviewing 1341 charts of potential cases, 60 met the criteria for ANX, but only 23% were correctly coded. Inaccurate coding was noted in 77%, mainly as an "allergic reaction." Systemic corticosteroids were administered in the ED to 85% of the patients and H1-antihistamines to 73%; only 20% received epinephrine. Ten patients required hospital admission, and, on discharge, only four patients (40%) were given epinephrine autoinjector prescriptions. Of the 50 who were discharged home, 48% were given epinephrine autoinjector prescriptions and 16% were given a referral for allergy evaluation. CONCLUSION: The observed low rates of appropriate diagnostic coding of ANX, of epinephrine administration, epinephrine autoinjector prescribing at discharge, and referral for allergy evaluation call for more education on these issues. Some of these pitfalls can be partly attributed to the setting in a university ED where health providers are usually busy in rendering urgent care.

Diet-induced obesity and hepatic steatosis in L-Fabp / mice is abrogated with SF, but not PUFA, feeding and attenuated after cholesterol supplementation.

Liver fatty acid (FA)-binding protein (L-Fabp), a cytoplasmic protein expressed in liver and small intestine, regulates FA trafficking in vitro and plays an important role in diet-induced obesity. We observed that L-Fabp(-/-) mice are protected against Western diet-induced obesity and hepatic steatosis. These findings are in conflict, however, with another report of exaggerated obesity and increased hepatic steatosis in female L-Fabp(-/-) mice fed a cholesterol-supplemented diet. To resolve this apparent paradox, we fed female L-Fabp(-/-) mice two different cholesterol-supplemented low-fat diets and discovered (on both diets) lower body weight in L-Fabp(-/-) mice than in congenic wild-type C57BL/6J controls and similar or reduced hepatic triglyceride content. We extended these comparisons to mice fed low-cholesterol, high-fat diets. Female L-Fabp(-/-) mice fed a high-saturated fat (SF) diet were dramatically protected against obesity and hepatic steatosis, whereas weight gain and hepatic lipid content were indistinguishable between mice fed a high-polyunsaturated FA (PUFA) diet and control mice. These findings demonstrate that L-Fabp functions as a metabolic sensor with a distinct hierarchy of FA sensitivity. We further conclude that cholesterol supplementation does not induce an obesity phenotype in L-Fabp(-/-) mice, nor does it play a significant role in the protection against Western diet-induced obesity in this background.