Browsing by Subject "Electrophoresis"

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    Characterization of Casirivimab Plus Imdevimab, Sotrovimab, and Bamlanivimab Plus Etesevimab-Derived Interference in Serum Protein Electrophoresis and Immunofixation Electrophoresis.
    (The journal of applied laboratory medicine, 2022-10) Scholl, Ashley Rose; Korentzelos, Dimitrios; Forns, Taylor E; Brenneman, Ethan K; Kelm, Matthew; Datto, Michael; Wheeler, Sarah E; Carlsen, Eric D

    Background

    Therapeutic monoclonal antibodies can be a source of assay interference in clinical serum protein electrophoresis (SPEP) and immunofixation electrophoresis (IFE), producing monoclonal bands that can be misinterpreted as a monoclonal gammopathy related to a B-cell or plasma cell neoplasm. The extent to which new anti-COVID-19 monoclonal antibodies produce this interference is unknown.

    Methods

    Casirivimab plus imdevimab, sotrovimab, and bamlanivimab plus etesevimab were spiked into patient serum samples to evaluate for SPEP/IFE interference, to characterize the position of therapy-derived bands relative to a reference band (either combined beta band or beta 1 band, depending on instrument platform), and to confirm heavy and light chain utilization of each medication. Serum samples from patients who had recently received casirivimab plus imdevimab or sotrovimab were also evaluated for comparison.

    Results

    When spiked into serum samples, all tested anti-COVID-19 monoclonal antibodies generated interference in SPEP/IFE. Importantly, the patterns of interference differed between spiked serum samples and serum from patients who had recently received casirivimab plus imdevimab or sotrovimab.

    Conclusions

    Imdevimab can be added to the growing list of therapeutic monoclonal antibodies that produce sustained interference in SPEP/IFE. Although casirivimab and sotrovimab also produce assay interference in vitro, these antibodies are not reliably detected in serum from recently infused patients. The value of relative band position in recognizing bands that may represent therapeutic monoclonal antibodies is also emphasized. Clinicians and laboratorians should consider therapeutic monoclonal antibody interference in diagnostic SPEP/IFE and review a patient's medication list when new or transient monoclonal bands are identified.
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    Transfer of human chromosomes via human minisegregant cells into mouse cells and the quantitation of the expression of hypoxanthine phosphoribosyltransferase in the hybrids.
    (J Cell Sci, 1978-04) Tourian, A; Johnson, RT; Burg, K; Nicolson, SW; Sperling, K
    The behaviour of human cells arrested in mitosis can be severely perturbed so as to generate numerous small minisegregants containing very few chromosomes. These cells can be separated according to size and DNA content and fused with intact cells. In this paper we describe the production and some properties of proliferating cell hybrids generated by fusion of human minisegregant cells derived from a HeLa strain with mouse A9 cells deficient in hypoxanthine phosphoribosyltransferase (HPRT, EC 2.4.2.8). The hybrids were shown to contain up to 10 human chromosomes including a single X. Independently derived hybrid clones were quantitatively characterized and compared with the parental phenotypes with respect to HPRT. Human isozymes of each of the 3 enzymes HPRT, glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and phosphoglycerate kinase (EC 2,7.2.3) were found. Tests to evaluate both structure and function of HPRT were utilized. The specific activity of HPRT of more than 10 hybrids tested was approximately 10% that of the HeLa parent. Structural characterization of HPRT from hybrid cells as evidenced by heat inactivation and electrophoretic mobility results in a 'human-like' phenotype. Functional characterization of parental HPRT results in kinetic constants for cofactor and substrate which do not permit distinction of human and of human and mouse enzymes; HPRT from the minisegregant hybrids had normal kinetic constants. The reduced specific activity of HPRT in the hybrids is discussed in terms of the inability of the mouse environment to regulate the full expression of the human structural gene.