CD7 and CD56-positive primary effusion lymphoma in a human immunodeficiency virus-negative host.

Primary effusion lymphoma is an entity with distinctive features. The majority of cases are diagnosed in patients infected with human immunodeficiency virus. We report a case of pleural-based primary effusion lymphoma in an elderly patient negative for human immunodeficiency virus. By flow cytometry, lymphoma cells expressed CD7, CD38, CD45, CD56, HLA-DR, and kappa surface light chains. A monoclonal rearrangement of the immunoglobulin heavy chain and the presence of human herpesvirus 8 genome were detected. Our case lacked CD30 or CD138 with expression of surface light chains. There was strong expression of CD7 and CD56. These findings are unusual or unique in primary effusion lymphoma. Our report suggests that aberrant expression of T cell and natural killer cell markers can be seen in primary effusion lymphoma.

Modulation of in vitro erythropoiesis. Studies with euthyroid and hypothyroid dogs.

The interactions of adrenergic agonists and thyroid hormones on the growth of erythroid colony-forming units were studied in cultures of dog marrow before and after the establishment of hypothyroidism. Erythroid colony growth in cultures form euthyroid dogs was enhanced by isoproterenol and other adrenergic agonists having beta 2-receptor specificity. With hypothyroidism, however, this responsiveness was lost, and sensitivity to alpha-agonists, such as phenylephrine and norepinephrine, was acquired. This alteration in receptor specificity appeared to be dependent upon thyroid hormone and was rapidly reversible. Preincubation of marrow cells from hypothyroid animals with thyroid hormone resulted in the reappearance of responsiveness to beta-adrenergic agonists and the loss of sensitivity to alpha-agonists. These findings are in agreement with previous suggestions that beta-adrenergic receptor activity is modulated by thyroid hormone levels and demonstrate that the specificity of adrenergic modulations of erythropoiesis in culture may accurately reflect the thyroid status of the intact animal.

Erythropoietin assay: present status of methods, pitfalls, and results in polycythemic disorders.

Mammalian erythropoiesis is regulated primarily by the hormone erythropoietin (ESP). Studies of ESF have provided information about its biochemistry and its role in regulating hemoglobin synthesis. Such studies rely on assays for erythropoietic activity in biological fluid. The assay which has proven most valuable and is used most widely is based upon the incorporation of radioactive iron into newly-formed red cells of polycythemic mice. While this assay has gained wide acceptance, it is expensive, cumbersome, imprecise, and insensitive, capable of reliably detecting no less than 50 milliunits of erythropoietin. Improvements in assay techniques will require new methodology relying primarily on immunologic recognition for the determination of hormone activity. Currently under development and in experimental use are radioimmunoassays and a hemagglutination inhibition assay. While work has progressed in these areas, these assays are not of proven value at present and meaningful physiological correlations have not emerged from their use. Alternatively, assays for hormone activity using suspensions of hematopoietic cells and the measurement of incorporation of radioactive isotopes into hemoglobin have provided both improvement in sensitivity and precision. The disadvantage of these types of assays is that they are sensitive to factors other than ESF and may give misleading information, depending on whether the factors present stimulate or inhibit cellular proliferation and hemoglobin synthesis. While such techniques may provide a temporary solution to some problems associated with assaying ESF for purification or physiological studies, they are not the best answer to the overall problem of hormone detection and characterization. The most important contribution to this field will be the availability of large amounts of highly purified and well-characterized ESF.

The influence of thyroid hormones on in vitro erythropoiesis. Mediation by a receptor with beta adrenergic properties.

The erythropoietic effect of various thyroid hormones has been studied using erythroid colony formation by canine marrow cells. Although erythropoietin was required for colony growth, physiologic levels of thyroid hormones significantly enhanced colony numbers. The order of potency of the thyroid compounds in their in vitro erythropoietic effect parallels their known calorigenic potency in vivo, suggesting that the in vitro effect is physiologically relevant. A series of studies linked the mechanism of thyroid action to adrenergic receptors on responsive cells. Propranolol, a global beta-blocker, inhibited thyroid hormone-responsive erythroid colonies. When adrenergic antagonists having different blocking characteristics were added to culture, the thyroid hormone effect was blocked by those compounds having beta(2)-subspecificity. Velocity sedimentation analysis showed that the peak of colony-forming cells which respond to thyroid hormone and the adrenergic agonist, isoproterenol, sedimented at an identical rate (7.54 mm/h), which is slower than the major peak of colony-forming cells responding to erythropoietin alone (8.62 mm/h). These results demonstrate thyroid hormonal enhancement of in vitro erythroid colony growth which appears mediated by a receptor with beta(2)-adrenergic properties. The data suggest that changes in hormone-target cell interaction may occur during states of abnormal thyroid function.