Blue nails and acquired immunodeficiency syndrome: not always associated with azidothymidine use.

Nail dyschromia in patients infected with human immunodeficiency virus (HIV) was first described in 1987 by Furth and Kazakis. It has since been reported in many patients with the acquired immunodeficiency syndrome (AIDS), predominantly in those taking azidothymidine. There have been only three reports of nail pigmentation in HIV-infected patients who had not received azidothymidine. We describe such a case.

Red cell fragmentation syndrome with the use of subclavian hemodialysis catheters.

The red cell fragmentation syndrome can occur due to abnormalities of the heart or the blood vessels or vascular malformations. We describe three patients who developed symptomatic hemolytic anemia due to red cell fragmentation with the use of single-lumen subclavian hemodialysis catheters. Retrospective analysis of 75 other patients who had undergone dialysis through this catheter disclosed five additional cases. Red cell fragmentation appears to be associated with partial catheter occlusion by thrombus or development of a clot at the catheter tip or both. The fragmentation resolved in all cases on withdrawal of the catheter. All patients with this catheter should be closely monitored for the red cell fragmentation syndrome, and the catheter should be withdrawn if it develops. White cell fragmentation was also seen in one patient.

Murine monoclonal anti-T cell antibodies for treatment of steroid-resistant acute graft-versus-host disease.

Four different murine monoclonal anti-T cell antibodies were administered to 15 patients with severe steroid resistant graft versus host disease (GVHD) in a phase I clinical trial in order to evaluate feasibility and toxicity. Antibodies 9.6 (IgG2a) and 35.1 (IgG2a) bind to separate epitopes on the E receptor (Tp50); antibody 10.2 (IgG2a) binds to the murine Lyt-1 homolog (Tp67); and antibody 12.1 (IgG2a) binds to a cell surface antigen with a molecular weight of approximately 100,000 daltons (Tp100). A total of 151 infusions were given, ranging in dose from one to 20 mg, each administered over a one to four hour period. One patient received a total of 259 mg of antibody over a period of 45 days. Six infusions (4%) in two patients were associated with fever or fever and chills. By decreasing the infusion rate, subsequent infusions to these two patients were accomplished without additional reactions. Although most of the patients treated with monoclonal antibodies required platelet support, the number of platelet units given was not significantly different from similar patients not receiving monoclonal antibodies. Six of ten patients receiving intermediate to high doses (5-20 mg) antibody therapy had evidence of at least partial improvement in GVHD in at least one involved organ system. None of the patients became immunized to mouse immunoglobulin. Our results suggest that therapy of GVHD with murine monoclonal anti-T cell antibodies is feasible and that these antibodies apparently can be administered to marrow transplant patients without significant toxicity. Further studies are required to determine which antibodies or combinations of antibodies have optimal anti-GVHD effect.

Fatal graft-versus-host disease in a patient with lymphoblastic leukemia following normal granulocyte transfusion.

A woman with lymphoblastic lymphoma was treated with combination chemotherapy. She subsequently became febrile while granulocytopenic and was given unirradiated granulocyte transfusions from normal, unrelated donors. She recovered, but 12 days later noted the onset of progressive skin rash, hepatic dysfunction, diarrhea and pancytopenia and, 22 days after her last granulocyte transfusion, died of gram negative septicemia. Histologic examination of multiple tissues including the skin, liver, and intestinal tract showed changes characteristic of acute graft-versus-hose disease (GVHD). Y-chromatin analysis of the patient's peripheral blood just before death indicated the presence of male cells. HLA typing of lymphocytes and skin fibroblasts from the patient and lymphocytes from the family and granulocyte donors was also consistent with engraftment of cells from one of the male granulocyte donors. This donor most likely was homozygous for one of the patient's halotypes, perhaps facilitating engraftment of his cells and subsequent development of transfusion-induced acute GVHD. Until more precise guidelines can be established, we recommend that all cellular blood products given to patients receiving intensive chemotherapy be irradiated with 1500 rad.