Variation in the management of pediatric diabetic ketoacidosis by specialty training.

OBJECTIVE: To compare management strategies for pediatric diabetic ketoacidosis (DKA) among physicians with different specialty training. METHODS: We conducted a mail survey of 1000 randomly selected physicians, including 200 pediatric endocrinologists, 200 general emergency physicians, 200 pediatric emergency physicians, 200 pediatric intensivists, and 200 pediatric chief residents. We posed questions regarding a hypothetical 10-year-old patient with new onset of diabetes mellitus who is approximately 10% dehydrated but alert, with venous pH of 7.1 and serum glucose concentration of 34.7 mmol/L (625 mg/dL). Questions involved the rate of rehydration, content of intravenous fluids, insulin therapy, potassium replacement, use of sodium bicarbonate, and adjustments in therapy for decreasing serum glucose concentration. We compared responses of physicians in each specialty and used multiple regression analysis to adjust for potential confounding variables, including number of years in practice, number of children with DKA seen per month, and practice setting. RESULTS: Five hundred eighty-one physicians (58.1%) completed the survey, with responses demonstrating significant, consistent differences between specialties. Extremes of responses included the following: (1) 59% of endocrinologists vs 11% of general emergency physicians would give an initial fluid bolus of less than 20 mL/kg (odds ratio [OR], 11.7; 95% confidence interval [CI], 5.0-27.7) (P < .001); (2) 83.5% of general emergency physicians vs 42.5% of pediatric intensivists would administer an initial insulin bolus (OR, 4.1; 95% CI, 2.0-8.7) (P < .001); (3) 58.2% of pediatric intensivists vs 9% of general emergency physicians would replace fluids over a period of greater than 24 hours (OR, 14.1; 95% CI, 5.5-37.5) (P < .001); and (4) 54.3% of general emergency physicians vs 7.3% of pediatric intensivists would use potassium chloride alone for potassium replacement (OR, 10.8; 95% CI, 5.0-23.8) (P < .001). All of these differences persisted after adjusting for the potential confounding variables. CONCLUSIONS: Substantial differences exist in the management of pediatric DKA among physicians of different specialties, presumably due to differences in specialty training. These differences obscure our ability to evaluate the treatment of DKA and highlight the necessity for further studies comparing the outcomes of different treatment strategies.

Differential recognition of microfilarial chitinase, a transmission-blocking vaccine candidate antigen, by sera from patients with Brugian and Bancroftian filariasis.

We examined the reactivity of human sera with recombinant microfilarial chitinase and with the antigenic determinant on the native parasite molecule identified by monoclonal antibody (MAb) MF1. In Brugian filariasis, the MF1 epitope is preferentially recognized by residents of endemic areas who remain amicrofilaremic and asymptomatic despite lifelong exposure to filarial worms. Reactivity with filarial chitinase and its MF1 epitope inversely correlates with microfilaremia levels in Bancroftian filariasis and is associated with a prolonged amicrofilaremic state following a single course of treatment with diethylcarbamazine. Chitinase does not appear to be a target of human antibodies that promote the adherence of cells to microfilariae, even though MAb MF1 itself promotes antibody-dependent, cell-mediated cytotoxic (ADCC) reactions that kill microfilariae in vitro. Such ADCC reactions are most often mediated by sera from amicrofilaremic patients with chronic elephantiasis that contain low or undetectable levels of IgG antibodies to chitinase. In contrast, antibodies to the MF1 epitope on this microfilarial stage-specific antigen are mostly present in amicrofilaremic donors without clinical lymphatic disease. These observations indicate that antibodies to the MF1 epitope of microfilarial chitinase reflect some degree of immune resistance to microfilaremia in a subgroup of patients with asymptomatic lymphatic filariasis. The amicrofilaremic state of individuals with chronic lymphatic disease appears to be mediated by reactivity to a different parasite antigen(s).