Clinical application of a new latex photometric immunoassay reagent, LPIA-GENESIS D-dimer, and its performance in patient-derived plasma samples.

INTRODUCTION: We previously reported an antibody MIF-220 that recognizes a specific structure induced on the surface of thrombin-activated E-domain of one fibrin molecule bound with the D-domains of other fibrinogen/fibrin molecules. Utilizing MIF-220, we produced a test kit for cross-linked fibrin degradation products (XDP), LPIA-GENESIS D-dimer (LG-DD), and evaluated basic performance characteristics for clinical application. We then attempted to apply LG-DD to see its eligibility in clinical plasma samples. METHOD: The characteristic performances requested for clinical use were studied including limit of quantitation, within-run imprecision, day-to-day imprecision, antigen excess, interference study, and method comparison with LPIAACE-Ddimer (ACE-DD) available on the market. RESULTS: The performance characteristics were all satisfactory. Extraordinarily high concentrations of XDP are occasionally obtained by ACE-DD in samples with collection problems, but not by LG-DD, indicating that a certain XDP species present in the former was not measured by LG-DD. Structural studies suggested that the "B-b" set of polymerization sites must be involved as well in the maintenance of cross-linked fibrin in vivo. CONCLUSION: LG-DD was able to measure a wide range of XDP, that is, 0.20-35.0 µg FEU/mL that covers the levels of XDP in most of the clinical samples. LG-DD was found to almost avoid false-positive results noticed in samples as mentioned above, and this feature seems to be preferable to established kits for the measurement of XDP.

[Spontaneous remission of acquired factor XIII inhibitor concurrent to development of IgA-λ type multiple myeloma].

Coagulation factor XIII is a fibrin-stabilizing factor that leads to the crosslinking of fibrin when activated by thrombin. Acquired factor XIII inhibitor is caused when antibodies are generated against factor XIII, reducing its activity. Here we report a case of acquired factor XIII inhibitor. Although prednisolone was administered, factor XIII activity was not recovered. Interestingly, the activity normalized following the onset of multiple myeloma. The presence of inhibitors was evaluated in the patient's plasma by absorption tests and enzyme-linked immunosorbent assay. Immunoglobulin G inhibitors of factor XIII were present at admission, but later decreased with the onset of the IgA-λ-type myeloma. Thus, it is possible that the level of factor XIII inhibitors and polyclonal immunoglobulins could have been suppressed by the progression of myeloma, resulting in the normalization of factor XIII activity.