Summary: Fifty adults hospitalized with extensive burns formed the basis of the present study. Serum amyloid A protein, C-reactive protein, a r antichymotrypsm and a r acid glycoprotein were measured in serum samples taken on admission, and 3 and 7 days later. Fatal outcome was observed in 13 out of 14 (93%) patients with serum amyloid A protein over 100 mg/1 on admission and in only 2 of the remaining 36 (6%) patients with serum amyloid A protein below 100 mg/1. The median serum amyloid A protein concentration on admission in 15 patients with fatal outcome was 134 mg/1, and only 30 mg/1 in 35 patients who recovered (p < 0.00005). As a reference value, the level of 100mg serum amyloid A protein per litre on admission gave an evident predictive value (93%) and sensitivity (87%) for fatal outcome. The difference between serum amyloid A protein concentrations in patients with complications (median 642 mg/1) and those without complications (median 250 mg/1) was statistically very significant (p = 0.0003) three days after burn injury. The level of 400 mg/1 as a reference value 3 days after burn injury gave a reasonable predictive value (80%) and sensitivity (74%) for the development of postburn complications, but patients who died did not develop a hypermetabolic reaction and their serum amyloid A protein concentration remained below 400 mg/1, despite high serum amyloid A protein concentrations observed on admission (above 100 mg/1). No statistical significance was observed for the other 3 acute phase proteins investigated in this study.

Apolipoprotein H (apoH) is considered to be a necessary cofactor for the binding of certain antiphospholipid antibodies to anionic phospholipids. Some apoH-dependent antiphospholipid antibodies also exert lupus anticoagulant (LA) activity, which seems to depend on antiphospholipid antibody epitope specificity. The aim of this study was to evaluate whether the presence of less frequent apoH alleles may induce structural or conformational changes in these "LA-dependent" regions that may initiate more frequent autoimmune responses in subjects. We selected patients with confirmed LA activity and none or low titers of anticardiolipin antibodies that had been sent to the laboratory for routine antiphospholipid antibody determination. Many of them had some clinical manifestation of antiphospholipid syndrome. Antibodies to apoH were determined with a commercially available anticardiolipin/apoH ELISA kit. ApoH protein polymorphism (apoH phenotype) was demonstrated by isoelectric focusing and immunoblotting. Our results showed that 47/74 (63.5%) of our selected LA-positive patients also had elevated apoH-dependent antiphospholipid antibody titers. These results point to two subgroups of patients according to the LA potency of apoH-dependent antibodies. A strong positive correlation (non-linear or linear) for apoH-dependent antibody titers and LA activity was observed in both subgroups of patients. In this study, we did not find significant differences in the distribution of apoH phenotypes among control subjects and patients with apoH-dependent/LA-positive auto- antibodies.

No abstract

No abstract