The nuances of lymphocytopenia.

We have discussed the causes of lymphocytopenia and attempted to categorize them according to pathogenesis. This effort may be tenuous at best, because so much is still unknown about lymphocyte function and kinetics. In describing pathogenesis we have reported what has been published and not speculated on mechanisms when they were not stated. Many of these reports were decades apart, and the technical resources available to the investigators were varied. We suspect, for example, that many of the lymphocyte changes secondary to inflammation and infection will have a common pathogenesis (for example, cytokines and endotoxins). Undoubtedly, the picture will become much clearer in the years ahead.

The platelet volume-number relationship in patients infected with the human immunodeficiency virus.

The pathophysiology of thrombocytopenia in the acquired immune deficiency syndrome has not been elucidated completely. Many findings in these patients are identical to those with immune thrombocytopenic purpura. However, recent findings in acquired immune deficiency syndrome patients including the effect of zidovudine on platelet count and the demonstration of ultrastructural changes and viral RNA in megakaryocytes, have suggested that the human immunodeficiency virus may directly infect megakaryocytes, and play a role in acquired immune deficiency syndrome-related thrombocytopenia. To investigate further the mechanism of decreased platelet counts in human immunodeficiency virus-infected patients, the platelet volume-number relationship and corresponding bone marrow findings in 34 patients infected with human immunodeficiency virus were studied. Parameters evaluated included platelet count and mean platelet volume; bone marrow cellularity, megakaryocyte number, and number and percentage of denuded megakaryocyte nuclei. Two thirds of the platelet counts were low, and of these 92% had an inappropriately low mean platelet volume. These individuals had a platelet-volume number relationship that is very similar to that seen in myelosuppressive disorders. In addition, more than 90% of the bone marrows from thrombocytopenic patients had either normal or decreased numbers of megakaryocytes. These observations provide additional evidence to support the hypothesis that the pathophysiology of human immunodeficiency virus-associated thrombocytopenia may be due, at least in part, to a direct effect on the megakaryocytes.

Hematology analyzers.

An overview of current hospital hematology analyzers has been presented. The technology involved is extraordinarily sophisticated and has provided us with interesting new and potentially useful parameters. Even the instrument evaluation process is becoming increasingly complex, but new standards are being developed that provide guidance for users. As the forces of technology and cost-containment converge, pressures arise to alter our thinking about traditional laboratory testing. Recent interest has been particularly focused on the differential count. The hematology laboratory is vastly changed from that of 25 years ago, and it's almost impossible to speculate on what it will be like a quarter century from now.

Ultrastructural diagnosis of histologically atypical idiopathic thrombocytopenic purpura.

The histological and electron microscopic findings in the spleen of a 61-year-old white man with corticosteroid-unresponsive idiopathic thrombocytopenic purpura (ITP) are described. Light microscopically, the spleen lacked features characteristic of ITP, such as germinal centers and foamy histiocytes. Ultrastructurally, however, platelet phagocytosis, which is diagnostic of this entity, was readily demonstrable in splenic cord macrophages.

Evaluation of an automated blood smear analyzer.

The performance of a diff3 System prototype instrument that does automated leukocyte differential counts, erythrocytic morphology determinations, and leukocyte count and platelet count estimates, was compared with performance by laboratory personnel for a five-week period in an active general hospital. Using experienced supervisors as the referee method, this instrument performed as well as the routine laboratory staff in all aspects of leukocyte differential counting. With respect to erythrocytic morphology, estimates of hypochromia were inferior to those of the routine laboratory staff; comparisons of estimates of macrocytosis and polychromasia were not significantly different. Leukocyte and platelet numerical estimate performance by the diff3 System was not as good as that of automated cell-counting instruments, but categorization of platelet concentration as normal or abnormal did compare favorably with estimation by laboratory personnel. The flagging of abnormal slides by the instrument was comparable in sensitivity to that by the routine laboratory staff; however, specificity was less, with a significantly greater number of false positives obtained by use of the instrument.