Treatment of antibody-mediated accelerated rejection using plasmapheresis.

Accelerated antibody-mediated rejection is believed to be due to an anamnestic response of an allograft recipient to donor antigens. Few reports have demonstrated successful reversal of this type of rejection, and no consensus exists for either diagnosis or treatment. Accelerated antibody-mediated rejection was suspected on the basis of clinical findings and confirmed by cytotoxic and flow crossmatches, and leukocyte antibody screens. Serial crossmatches and antibody screens were performed through post-transplant day 112. Plasmapheresis was performed on post-transplant days 1, 2, 4, 6, 12, 14, 20, and 28. The duration of treatment was determined by the cytotoxic crossmatch results. We present a case of successfully treated accelerated antibody-mediated rejection using plasmapheresis and aggressive immunosuppression. Serial crossmatch and leukocyte antibody screen results are presented that confirm the production of anti-donor antibody and demonstrate the effectiveness of the treatment protocol in eliminating detectable levels of the anti-donor antibody. At 6 months post-transplant, the patient has a serum creatinine of 1.1 and has not had any additional rejection episodes or infectious complications. The protocol suggested in this paper allows for rapid diagnosis, institution of treatment, and monitoring the efficacy of treatment, providing the basis for follow-up clinical trials.

Concurrence of anaphylaxis and acute heparin-induced thrombocytopenia in a patient with heparin-induced antibodies.

We report the occurrence of acute heparin-induced thrombocytopenia in a patient with anaphylaxis that began immediately after an intravenous bolus dose of unfractionated heparin. This case report is the first to document the concurrence of these 2 reactions to heparin. An abrupt fall in platelet count was documented immediately after the anaphylactic response. Study results for antibodies characteristic of heparin-induced thrombocytopenia were positive in 2 assays: serotonin release assay and heparin platelet factor 4 enzyme-linked immunosorbent assay. The patient's antibody was exclusively immunoglobulin G. Any explanation for the relationship between the antibody response observed and the histamine release remains speculative.

der(1)t(1;19)(p12;p11): a new nonrandom chromosomal abnormality in myelodysplastic syndrome.

The der(1)t(1;19)(p12;p11) has not been previously reported in myelodysplastic syndrome (MDS). Fluorescence in situ hybridization (FISH) using chromosome 1- and chromosome 19-specific probes, performed on the bone marrow (BM) cells of this patient confirmed the initial karyotype, i.e., 47,XY,+der(1)t(1;19)(p12;p11).

Immunoglobulin and T-cell receptor gene rearrangement.

Gene rearrangement involves a complex process of DNA splicing and deletion that produces a unique genetic code in each B or T lymphocyte. These novel DNA sequences encode immunoglobulin or T-cell receptor proteins that function in recognition of foreign antigens. Recent advances in DNA technology permit laboratory detection of clonal gene rearrangements in lymphoid malignancies including lymphocytic leukemia, lymphoma, and myeloma. Practical applications of gene rearrangement testing include distinguishing reactive from malignant lymphoid proliferations, and assignment of B- or T-cell lineage to a neoplastic process. Active investigation is underway to devise practical strategies for detecting minimal residual disease based on tumor-specific gene rearrangements.