washed, the Vitros Signal Reagent was added to the well, and the luminescence was measured (ALOKA luminometer). The IgG fraction of serum samples from the patient and from five control individuals was purified with a MAbTrap TM Kit (Amersham Biosciences), and the IgG concentration was adjusted to 4.0 g/L. The purified IgG (0.08 mL) was incubated at 4°C for 24 h with 0.08 mL of PBS alone or with T 2 , T 3 , or T 4 (Sigma; at 4570, 42, and 768 nmol/L, respectively) dissolved in PBS. Each sample was mixed vigorously with 1.2 mL of polyethylene glycol (PEG; 125 g/L), centrifuged at 2800g for 30 min, aspirated, and washed with 1.2 mL of PEG (125 g/L). After the precipitates were dissolved in 0.001 mol/L hydrochloric acid (0.04 mL) and neutralized by equal amounts of 0.001 mol/L sodium hydroxide, T 2 and T 3 were measured by the FT 3 assay and T 4 by the FT 4 assay. The concentrations of T 2 were expressed as T 3 concentrations. Each sample was analyzed in duplicate. The ability of the purified IgG to bind T 2 , T 3 , or T 4 was defined as the difference between the FT 3 or FT 4 assay result and the respective blank value and is reported as the ␦T 2 , ␦T 3 , or ␦T 4 value.The ratios of FT 3 and FT 4 concentrations in PEG-treated samples (6 ) to those in untreated samples were significantly lower for the patient than for 37 other patients (Table 1 in the online Data Supplement); therefore, immunoglobulins in the patient's serum interfered with both the FT 3 and FT 4 assays. FT 3 and FT 4 values in the mixtures of serum with sheep IgG, bovine globulin, and gelatin did not differ significantly from those in the mixtures of serum and PBS only, suggesting that heterophilic antibodies and anti-gelatin antibodies did not cause the high FT 3 and FT 4 values.When we examined the patient's IgG binding with Vitros FT3II and FT 4 assay wells, the luminescence generated by the patient's serum was higher than that of the 5 control individuals (Table 1 in the online Data Supplement). This suggested that the patient's IgG bound to T 2 -and T 3 -gelatin.The FT 3 and FT 4 concentrations in purified IgG and in treated samples of purified IgG (6 ) were below the lower detection limits of the Elecsys assays, suggesting an absence of T 3 and T 4 contamination in the IgG fractions. The patient's ␦T 2 and ␦T 3 values were higher than those of the 5 control individuals, but the ␦T 4 value was within 2 SD of the values for the 5 controls (Table 1 in the online Data Supplement). This finding implies that the patient's IgG interacted with T 2 and T 3 but not with T 4 . The crossreactivity of the anti-T 3 antibody with T 2 in the Vitros FT3II assay was very low, whereas the patient's ␦T 2 value was evidently higher than that of 5 control individuals. We conclude that T 2 was bound to the patient's IgG.Because anti-gelatin antibodies in the patient's serum were not recognized, we suggest that the interfering substance were antibodies to T 2 and T 3 . As the interfering antibodies did not interfere with the Elecsys FT 3 assay, the interfering antib...

Introduction. One of the main factors involved in the pathogenesis of burn disease consists in the disturbance of microcirculation and haemostasis, caused by increased platelet aggregation. Mechanisms underlying the enhancement of platelet aggregation are poorly understood. Main results were obtained for adult patients at the onset of the burn disease, with no similar data on paediatric patients being available. There is evidence of a relationship between the size of platelets (MPV) and their functionality.Aim. To undertake a study of spontaneous and ADP-induced platelet aggregation and their size in children with burn disease.Materials and methods. We studied the aggregation and size of platelets in children aged 3–17 years, in whom burn areas covered 10–70 % of the body surface at the onset of the disease and before discharge. Spontaneous platelet aggregation was analysed under conditions of induced shear flow, whereas ADP-induced aggregation was studied employing a turbidimetric method. The study of platelet sizes was carried out using a conductometric method.Results. Spontaneous platelet aggregation increases significantly in children with burn disease. The integrated optical density of the formed aggregates, their area and perimeter were estimated for the first time. These indicators remained elevated even after burn wounds had been completely closed. In burn disease, changes in ADP-induced platelet aggregation were multidirectional in nature. Mean platelet volume (MPV) was increased during the acute period of burn disease, decreased during the period of toxaemia, and normalised by the time of patients’ discharge. Changes in MPV did not affect the aggregation properties of platelets. There was no correlation between the degree of aggregation and the severity of hyperfibrinogenemia. The blood of burn patients contained a large number of activated platelets, which was the reason for the increase in their spontaneous aggregation, not requiring the participation of exogenous inducers.Conclusion. An increase in spontaneous platelet aggregation was observed in children after a thermal injury, which remained elevated until the burn wounds were completely closed. A significant increase in the number of activated platelets constituted the reason for the increase in spontaneous platelet aggregation.Conflict of interest: the authors declare no confl ict of interest.Financial disclosure: the study had no sponsorship.