ISSN:0953-7104    

DOI:10.3109/09537109109005507

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.Immune thrombocytopenia is a relatively common problem associated with the clinical usage of drugs. Drugs frequently implicated include quinine, quinidine, heparin, penicillins, cephalosporins, co-trimoxazole, gold and D-penicillamine. Bleeding including bruising and purpura is the usual clinical manifestation except in immune heparin-induced thrombocytopenia in which thrombosis occurs more frequently than bleeding. Cessation of the offending drug is the important step in the treatment but other measures may also be required such as platelet transfusion and steroid therapy for patients with clinical bleeding or antithrombotic therapy with warfarin and dextran or low molecular weight heparin/heparinoid for patients with heparin-induced thrombocytopenia and thrombosis. Idiosyncratic drug-induced thrombocytopenia is mediated by an antibody which binds to platelets only in the presence of the drug resulting in the clearance of sensitised platelets by the reticuloendothelial system. In quinine/quinidine-induced thrombocytopenia, the antibodies recognise drug-dependent epitopes on platelet membrane glycoproteins Ib-IX and/or glycoproteins IIb-IIIa. In immune heparin-induced thrombocytopenia the current data suggest a mechanism which probably involves the binding of heparin-antibody complexes to the platelet Fc receptors but the precise mechanism is yet to be fully characterised. The associated thrombosis in this condition is likely to be due to platelet activation and possibly endothelial cell damage induced by the heparin-related antibody.

ISSN:0953-7104    

DOI:10.3109/09537109109005508

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109109005509

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.Platelet aggregation responses to adenosine diphosphate, adrenaline, collagen, arachidonic acid and ristocetin were measured in healthy subjects, predominantly blood donors residing in Riyadh, the capital city of Saudi Arabia. They were divided according to ethnic origin into Saudi Arabs n = 517, Westerners (Europeans and Americans) n = 93, South East Asians (Koreans and Filipinos) n = 154, and West Africans n = 77. Significant differences in the aggregation responses were found between the four ethnic groups. Saudi Arabs and Westerners showed better aggregation responses to ADP than Asians and Africans. Aggregability in response to collagen was greater in Saudis and Africans than in Westerners and Asians. There was remarkable inhibition of adrenaline induced-aggregation in Asians while other populations produced comparable results. Inhibited responses to arachidonic acid were most prevalent among Westerners and to a lesser extent in Asians than in Saudis and Africans. Ristocetin-induced aggregation was significantly inhibited in Africans and less so in Asians and Arabs and most pronounced in Westerners. These variations in platelet aggregability, which could not be related to blood group distribution, smoking habits, income, physical parameters of height and weight may be due to genetic and dietary factors. These ethnic differences should be taken into account when assessing aggregation responses in patients.

ISSN:0953-7104    

DOI:10.3109/09537109109005510

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.Using a platelet counting technique, spontaneous platelet aggregation (SPA) was determined in citrated whole blood (WB) and platelet-rich plasma (PRP) obtained from 27 patients with insulin-dependent diabetes mellitus and from 32 healthy controls. SPA in WB, but not in PRP, was significantly enhanced in the patients compared with the controls. In the patient group, SPA in WB correlated positively with poor metabolic control as measured by glycosylated haemoglobin (Hb A1). Furthermore, the increased SPA in WB from diabetics was found to be associated with an increased mechanical fragility of red blood cells (RBC) measured as liberation of haemoglobin into the plasma in stirred samples of WB. Pentoxifylline, which is believed to increase the deformability of RBC, reduced the extent of SPA in WB from the patients but was without effect on SPA in PRP from the patients or in WB from the controls.

ISSN:0953-7104    

DOI:10.3109/09537109109005511

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.Blood platelets exposed to hypotonic medium are known to undergo a regulatory volume decrease (RVD), mediated by increased conductive permeability of K+and Cl-. It is presently shown that RVD in platelets is controlled by a lipoxygenase product, apparently by a selective regulation of K+permeability. This conclusion is supported by the following observations: (a) lipoxygenase inhibitors, nordihydroguaiaretic acid (NDGA), N-(3-phenoxycinnamyl)-acetohydroxamic acid (BW A4C), methyl 2-[(3,4-dihydro-3,4-dioxo-naphthalenyl)amino]-benzoate (CGS 8515), and 5,8,11,14-eicosatetraynoic acid, inhibit RVD with IC50values of 3,6,10, and 5μM, respectively. In contrast, aspirin and indomethacin, known cycloxygenase inhibitors, are innocuous; (b) an eluate from platelets undergoing RVD restores RVD in NDGA-treated platelets; (c) the eluate is unstable (t1/2= 8 s and 2 min in the presence and absence of platelets, respectively); furthermore, albumin promotes platelet RVD; (d) known lipoxygenase products, 12-hydroperoxyeicosatetraenoic acid, 12-hydroxyeicosatetraenoic acid and leukotriene D4, restore RVD in NDGA-treated platelets at 0.1–1.0μM; (e) the extended hypotonic swelling of gramicidin-treated platelets, expressing Cl-permeability, is insensitive to NDGA.It is hypothesized that the lipoxygenase product selectively opens K+channels in platelets, in analogy with the effect of lipoxygenase products in cardiac atrial cells andAplysiasensory neurons.

ISSN:0953-7104    

DOI:10.3109/09537109109005512

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.The role of intracellular histamine in the activation of human platelets was explored using the novel histamine antagonist N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine (DPPE). DPPE inhibited aggregation, [32P]-phosphatidic acid production (an index of phospholipase C activity) and the increase in cytosolic calcium ([Ca2+]i) in response to collagen. In contrast, while at higher concentrations DPPE inhibited aggregation in response to ADP and the thromboxane mimetic EP171, it failed to inhibit EP171-induced [32P]-phosphatidic acid production or increases in [Ca2+]i elicted by either ADP or EP171. Collagen but neither ADP nor EP171 caused the significant formation of intracellular histamine. The biochemical changes induced by collagen have been shown previously to be, at least partly, secondary to thromboxane generation. Collagen-induced arachidonic acid release was therefore assessed. DPPE inhibited the release of arachidonic acid in response to collagen but had no effect on its subsequent conversion to thromboxane. The findings imply that intracellular histamine acts at an early stage in collagen-induced platelet activation, most likely prior to arachidonic acid release, and further that DPPE inhibits ADP and EP171-induced activation by a non-histamine related effect.

ISSN:0953-7104    

DOI:10.3109/09537109109005513

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

SUMMARY.Platelet Immunology: Fundamental and Clinical Aspects. Immunologie plaquettaire: aspects fondamentaux et cliniques. Proceedings of the first European Symposium on platelet immunology held in Paris, March, 1990. Colloque INSERM Vol. 206

ISSN:0953-7104    

DOI:10.3109/09537109109005514

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor