摘要:

AbstractLithium carbonate ameliorates neutropenia associated with cancer chemotherapy. The effect of lithium on platelet suppression has not, however, been well established. In the present study, five patients with ovarian carcinoma received daily lithium during alternate cycles of treatment with hexamethylmelamine, cyclophosphamide, adriamycin, and cis‐platinum. Analysis of myelosuppression was performed on 24 paired consecutive cycles given at identical doses, one with and one without lithium. During lithium cycles, nadir leukocyte, neutrophil, and platelet counts were significantly higher (P<0.01,<0.01,<0.05 respectively) and the interval between treatments was shorter (P<0.01). One patient who has received 11 cycles of chemotherapy continues to receive 100% doses owing to the beneficial effect of lithium on chemotherapy‐induced thrombocytopenia. Lithium was poorly tolerated by some patients because of either tremor or nausea and vomiting, in spite of nontoxic serum lithium levels. The amelioration of drug‐induced platelet suppression as well as neutrophil suppression noted in this study suggests that lithium's effect on hematopoiesis is not limited to stimulation of neutrophil production. The ability of lithium to decrease chemotherapyinduced myelosuppression suggests that lithium administration may facilitate escalation of chemotherapy doses in selected pat

ISSN:0361-8609    

DOI:10.1002/ajh.2830160402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractThis study was undertaken to test the effects of certain arachidonate derivatives, PGF2α, PGI2and TxB2on in vitro bone marrow granulocyte colony growth (CFU‐C) in leukemia patients receiving maintenance chemotherapy and in normal controls. The addition of PGF2α did not result in increased numbers of colonies, but it did cause a shift in the size of the colonies so that there was a significant increase in larger colonies (P<0.001) and significantly fewer small colonies (P<0.05) as compared to untreated samples. Of the prostenoids tested in a Tris‐buffered system, PGI2affected the greatest increase in CFU‐C (P<0.01) followed by PGF2α (P<0.05) whereas 6‐keto‐PGF1α (the stable hydrate of PGI2) did not affect colony growth. Time‐response curves revealed a linear growth pattern for PGF2α with a peak at 10 days, whereas there was a 6‐day growth lag with PGI2followed by linear growth with a peak at 13 days. TxB2added to cultures significantly reduced the number of bone marrow CFU‐C at all doses tested.The prostanoid effects on CFU‐C derived from leukemic patients on maintenance chemotherapy and from normal individuals were iden

ISSN:0361-8609    

DOI:10.1002/ajh.2830160403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractSynergistic effects between agonists on platelet aggregation have long been appreciated. Recently epinephrine was reported to induce maximal aggregation of aspirin‐treated platelets when combined with ADP or thrombin, and to increase fibrinogen binding of nonaspirin‐treated platelets stimulated with low doses of ADP. The present study extends these observations to correlate fibrinogen binding in response to various combinations of ADP, epinephrine, and thrombin with platelet aggregation and14C‐serotonin release using aspirin‐treated platelets as well as platelets from stored concentrates. When fresh platelets were stimulated with epinephrine (5 μM) together with either ADP (10 μM) or thrombin (150 mU/ml), fibrinogen binding increased by 180% compared to binding observed in response to ADP or thrombin alone. This was accompanied by enhanced platelet aggregation, but no increase in14C‐serotonin release. While both ADP and epinephrine potentiated the aggregation and fibrinogen binding of stored platelets in response to high doses of thrombin (150 mU/ml), maximal aggregation was achieved only with thrombin (150 mU/ml) and epinephrine (5μM) in combination. The data thus suggest that 1) epinephrine induces maximal aggregation of aspirin‐treated platelets stimulated with thrombin or ADP by significantly enhancing fibrinogen receptor exposure independently of the cyclooxygenase‐mediated release reaction; 2) epinephrine stimulates platelets by a mechanism different from that of thrombin or ADP; and 3) as demonstrated by others, the ability of platelets from stored concentrates to aggregate and to bind fibrinogen in response to ADP can be enhanced by epinephrine, and, in addition, these platelets can aggregate and bind fibrinogen maximally when stimulated with combinations of epinephr

ISSN:0361-8609    

DOI:10.1002/ajh.2830160404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractTransferrin‐iron uptake by peripheral blood monocytes was studied in vitro to test the hypothesis that the relative paucity of mononuclear phagocyte iron loading in hereditary hemochromatosis results from a defect in uptake of iron from transferrin. Monocytes from nine control subjects and 17 patients with hemochromatosis were cultured in the presence of59Fe‐labelled human transferrin. There was no difference in59Fe uptake between monocytes from control subjects and monocytes from patients with hemochromatosis who had been treated by phlebotomy and who had normal body iron stores. However,59Fe uptake by monocytes from iron‐loaded patients with hemochromatosis was significantly reduced compared with either control subjects or treated hemochromatosis patients. It is likely that this was a secondary effect of iron loading since iron uptake by monocytes from treated hemochromatosis patients was normal. Assuming that monocytes in culture reflect mononuclear phagocyte iron metabolism in vivo, this study suggests that the relative paucity of mononuclear phagocyte iron loading in hemochromatosis is not related to an abnormality in transferrin‐iron uptake by thes

ISSN:0361-8609    

DOI:10.1002/ajh.2830160405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractFollowing brief exposure to acetylphenylhydrazine, the potassium permeability of the human erythrocyte membrane is selectively augmented. While a similar increase in potassium permeability results from the intracellular accumulation of calcium (the Gardos phenomenon), we have found a number of features that allow these two pathways to be distinguished from one another. The acetylphenylhydrazine pathway does not require calcium for its activation, and can be seen even in the presence of a molar excess of the calcium chelator EGTA. The transmembrane potassium movement via this channel has a specific requirement for the anion chloride, and it can be inhibited by furosemide. The potassium that moves through the Gardos pathway, on the other hand, can be accompanied by any permeant anion, and is inhibitable by quinidine or cetiedil. Thus, acetylphenylhydrazine exposure seems to promote K + Cl cotransport, whereas the Gardos pathway represents a potassium conductive channel.While full demonstration of both these pathways requires harsh in vitro manipulation, the large electrochemical potassium gradient favoring the movement of this cation out from the erythrocyte suggests that even a partial activation of either pathway could cause intracellular dehydration and thus contribute importantly to the pathophysiology of in vivo red cell destruction.

ISSN:0361-8609    

DOI:10.1002/ajh.2830160406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractAn investigation of relatives of 652 patients entered on studies of the Polycythemia Vera Study Group yielded five documented cases of the disease among the parents of patients. When compared with expected values based on the Connecticut Tumor Registry and other population studies a significant increase was found in the lifetime incidence of polycythemia vera in parents of these patients.

ISSN:0361-8609    

DOI:10.1002/ajh.2830160407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractGlycosylated hemoglobin (glyco Hb) was determined by affinity chromatography and Hb S1and Hb F by Bio‐Rex 70 chromatography in patients with sickle cell anemia, SC disease, Sβ+‐thalassemia, and Sββ‐thalassemia. SC and Sβ‐thalassemia patients had normal levels of glyco Hb whereas SS patients had significantly lower levels. Within each group of patients a direct correlation existed between Hb F and glyco Hb or Hb S1levels. A similar relationship was noticed when glyco Hb and Hb F levels were compared in red cell populations of various densities (ages). Hb F seems to influence glycosylation through its effect on red ce

ISSN:0361-8609    

DOI:10.1002/ajh.2830160408

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractWe investigated whether the rosetting of B‐lymphoblastoid cell lines (B‐LCL) by peripheral blood lymphocytes (PBLs) reflected possible interactions between lymphoid cells and immature cells of the hematopoietic system. Rosette formation could be blocked by the addition of soluble antigen extracted from B‐LCL or blasts obtained from patients with acute myelogenous leukemia (AML). This inhibition was specific for AML blasts (similarly extracted material from melanoma lines had no inhibitory effect) and for the B‐LCL receptor (leukemic extracts had no effect on surface receptors for sheep red blood cells (E) or antibody‐sensitized red blood cells (EA)). The B‐LCL receptor is present on leukemic Sezary T‐cells as well as normal T‐cells and its sensitivity to various enzymatic treatments is markedly different from that of E and EA receptors. In addition, B‐LCLs derived from in vitro EB‐viral infection of a normal donor's B lymphocytes were significantly rosetted by that donor's autologous PBLs. These data suggest the B‐LCL receptor, present on mature T‐cells, can recognize self determinants on myeloblasts and B‐LCL. Further investigation will determine whether this interaction can affect the function

ISSN:0361-8609    

DOI:10.1002/ajh.2830160409

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractInformation regarding infectious complications was obtained on 127 patients with hairy cell leukemia who were diagnosed between March 1974 and April 1982. Forty‐seven patients (37%) had 111 documented infections (cultures positive), and 40 patients (31.5%) had 113 nondocumented infections (no culture results available, or cultures negative). The remaining 40 patients (31.5%) had no significant infections during the course of their disease. Patients without infection lived significantly longer than did patients who developed an infection (92%v49% were alive at 4 years;P= .0012). Thirty‐three of the 47 patients with documented infection have died; 29 of an infectious problem and four of a noninfectious problem. There was also a statistically significant difference in actuarial survivals between the documented‐infection and nondocumented infection groups (P= .007). The two most common types of infection were bacteremia (30 episodes) and pneumonia (27 episodes). In the culture‐documented group with bacteremia, E coli and P aeruginosa caused ten and eight infections, respectively, and three infections were due to S aureus. There were eight systemic infections of nonbacterial origin; in five, the organism cultured was M kansasii, and three were fungal infections. Blood counts at the time of diagnosis were not correlated with subsequent development of infection. Patients with hairy cell leukemia have a significant susceptibility to infections that can affect morbidity and mortality. Many of the infectious complications encountered are those common in patients whose immune system is compromised; however, the occurrence of disseminated atypical mycobacterial disease requires a heightened aw

ISSN:0361-8609    

DOI:10.1002/ajh.2830160410

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractThree patients with idiopathic pancytopenia and hypercellular bone marrow who developed carcinoma of the lung within two years of diagnosis are reported. All three patients had macrocytic anemia associated with a megaloblastic marrow in the presence of normal serum vitamin B12 and folic acid levels. Neutropenia with monocytosis, elevated serum muramidase and LAP scores, and increased fetal hemoglobin levels were also found. In all cases Ham's tests were negative with a normal bone marrow karyotype. In all three patients, pancytopenia due to myelodysplasia, a probable preleukemic state, was diagnosed initially prior to the appearance of carcinoma of the lung.One of the patients showed improved leukocyte and platelet counts during chemotherapy, while the other two died before chemotherapy could be administered. In the light of the above findings we suggest that carcinoma of the lung may be the cause of a paraneoplastic syndrome with pancytopenia, particularly in patients with a hypercellular marrow with a normal karyotype.

ISSN:0361-8609    

DOI:10.1002/ajh.2830160411

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY