The purpose of this review has been to draw the attention of clinicians towards the possibility that some of the patients they are treating for thrombosis may have an underlying immune disturbance. This could involve functional abnormalities of the complement system (as in acquired angioneurotic oedema or in paroxysmal nocturnal haemoglobinuria), or cell-mediated immunological damage to the vessel wall (as in Behcet's syndrome or Buerger's disease), or the presence of circulating antibodies (the lupus anticoagulant or antibodies to heparin). While obviously our knowledge on most aspects is still very incomplete, the awareness of the association of thrombosis with certain immune disorders should encourage further detailed studies of mechanisms and enhance our understanding of the role of blood constituents and the vessel wall in thrombogenesis.
{"title":"Thrombosis and immune disorders.","authors":"J Vermylen, D Blockmans, B Spitz, H Deckmyn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The purpose of this review has been to draw the attention of clinicians towards the possibility that some of the patients they are treating for thrombosis may have an underlying immune disturbance. This could involve functional abnormalities of the complement system (as in acquired angioneurotic oedema or in paroxysmal nocturnal haemoglobinuria), or cell-mediated immunological damage to the vessel wall (as in Behcet's syndrome or Buerger's disease), or the presence of circulating antibodies (the lupus anticoagulant or antibodies to heparin). While obviously our knowledge on most aspects is still very incomplete, the awareness of the association of thrombosis with certain immune disorders should encourage further detailed studies of mechanisms and enhance our understanding of the role of blood constituents and the vessel wall in thrombogenesis.</p>","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"393-412"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14221358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-05-01DOI: 10.1016/S0308-2261(18)30018-3
S. Moncada, E.A. Higgs
{"title":"1 Arachidonate Metabolism in Blood Cells and the Vessel Wall","authors":"S. Moncada, E.A. Higgs","doi":"10.1016/S0308-2261(18)30018-3","DOIUrl":"https://doi.org/10.1016/S0308-2261(18)30018-3","url":null,"abstract":"","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"Pages 273-292"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138183865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Many human atherosclerotic lesions, showing no evidence of fissure or ulceration, contain a large amount of fibrin which may be in the form of mural thrombus on the intact surface of the plaque, in layers within the fibrous cap, in the lipid-rich centre, or diffusely distributed throughout the plaque. Small mural thrombi are invaded by SMCs and collagen is deposited in patterns closely resembling the early proliferative gelatinous lesions. In experimental animals, thrombi are converted into lesions with all the characteristics of fibrous plaques, and in saphenous-vein bypass grafts, fibrin deposition is the main cause of wall thickening and occlusion. There seems little doubt that fibrin deposition can both initiate atherogenesis and contribute to the growth of plaques. Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease. Fibrin may stimulate cell proliferation by providing a scaffold along which cells migrate, and by binding fibronectin, which stimulates cell migration and adhesion. Fibrin degradation products, which are present in the intima, may stimulate mitogenesis and collagen synthesis, attract leukocytes, and alter endothelial permeability and vascular tone. In the advanced plaque fibrin may be involved in the tight binding of LDL and accumulation of lipid. Thus there is extensive evidence that enhanced blood coagulation is a risk factor not only for thrombotic occlusion, but also for atherogenesis. Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.
{"title":"Fibrinogen, fibrin and fibrin degradation products in relation to atherosclerosis.","authors":"E B Smith","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Many human atherosclerotic lesions, showing no evidence of fissure or ulceration, contain a large amount of fibrin which may be in the form of mural thrombus on the intact surface of the plaque, in layers within the fibrous cap, in the lipid-rich centre, or diffusely distributed throughout the plaque. Small mural thrombi are invaded by SMCs and collagen is deposited in patterns closely resembling the early proliferative gelatinous lesions. In experimental animals, thrombi are converted into lesions with all the characteristics of fibrous plaques, and in saphenous-vein bypass grafts, fibrin deposition is the main cause of wall thickening and occlusion. There seems little doubt that fibrin deposition can both initiate atherogenesis and contribute to the growth of plaques. Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease. Fibrin may stimulate cell proliferation by providing a scaffold along which cells migrate, and by binding fibronectin, which stimulates cell migration and adhesion. Fibrin degradation products, which are present in the intima, may stimulate mitogenesis and collagen synthesis, attract leukocytes, and alter endothelial permeability and vascular tone. In the advanced plaque fibrin may be involved in the tight binding of LDL and accumulation of lipid. Thus there is extensive evidence that enhanced blood coagulation is a risk factor not only for thrombotic occlusion, but also for atherogenesis. Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.</p>","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"355-70"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14647681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diabetes mellitus, vascular disease and thrombosis.","authors":"J D Banga, J J Sixma","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"465-92"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14647683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thrombosis and the vessel wall.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"273-565"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14850313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
On the basis of in vitro studies, biochemistry and cell biology the interactions between platelets, other circulating blood cells and the vessel wall are complex and wide-ranging. In essence, the effects of platelets adhering to injured luminal surface might include: Aggregation and adherence of further platelets; Activation of coagulation and fibrin formation; Displacement of AT-III from endothelial surface; Recruitment and activation of potentially injurious polymorphonuclear leukocytes and monocytes; Recruitment and proliferation of smooth muscles cells from the vessel media to the intima; Vasoconstriction; Initiation of feedback mechanisms such as PGI2 release to limit the process. These effects are capable of contributing to the initial lesions and the progression of the atherosclerosis. As the lesions become more complex, and particularly as the normal endothelium is lost, there is morphological evidence that there is deposition of thrombus (for discussion see Chapter 4) and 111In-labelled platelet imaging experiments in patients document platelet uptake onto atherosclerotic plaques (Davis et al, 1978).
在体外研究、生物化学和细胞生物学的基础上,血小板和其他循环血细胞与血管壁之间的相互作用是复杂而广泛的。从本质上讲,血小板粘附在损伤的管腔表面的作用可能包括:进一步的血小板聚集和粘附;凝血和纤维蛋白形成的激活;AT-III在内皮表面的位移;潜在有害的多形核白细胞和单核细胞的募集和激活;平滑肌细胞从血管介质向内膜的募集和增殖;血管收缩;启动反馈机制,如PGI2发布,以限制流程。这些作用能够促进初始病变和动脉粥样硬化的进展。随着病变变得更加复杂,特别是正常内皮的丧失,形态学证据表明存在血栓沉积(详见第4章),111in标记的患者血小板成像实验记录血小板摄取到动脉粥样硬化斑块上(Davis et al, 1978)。
{"title":"Platelet and vessel wall interaction and the genesis of atherosclerosis.","authors":"C N Chesterman, M C Berndt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>On the basis of in vitro studies, biochemistry and cell biology the interactions between platelets, other circulating blood cells and the vessel wall are complex and wide-ranging. In essence, the effects of platelets adhering to injured luminal surface might include: Aggregation and adherence of further platelets; Activation of coagulation and fibrin formation; Displacement of AT-III from endothelial surface; Recruitment and activation of potentially injurious polymorphonuclear leukocytes and monocytes; Recruitment and proliferation of smooth muscles cells from the vessel media to the intima; Vasoconstriction; Initiation of feedback mechanisms such as PGI2 release to limit the process. These effects are capable of contributing to the initial lesions and the progression of the atherosclerosis. As the lesions become more complex, and particularly as the normal endothelium is lost, there is morphological evidence that there is deposition of thrombus (for discussion see Chapter 4) and 111In-labelled platelet imaging experiments in patients document platelet uptake onto atherosclerotic plaques (Davis et al, 1978).</p>","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 2","pages":"323-53"},"PeriodicalIF":0.0,"publicationDate":"1986-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14077313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-02-01DOI: 10.1016/S0308-2261(86)80007-8
Karel A. Dicke, Gary Spitzer
The role of autologous marrow transplantation has been reviewed in this chapter. The transplantation results in first remission are difficult to interpret due to the prognostically heterogeneous patient population transplanted and the ever-changing natural history of first complete remission due to more aggressive conventional-dose chemotherapy regimen. The biological role of marrow purging, i.e. elimination of leukaemic cells from the graft, is yet unclear. It is the opinion of the authors that studies in second and subsequent remission can resolve burning issues such as the efficacy of various high-dose conditioning regimens and of different methods of elimination of leukaemic cells such as procedures based on immunological methods, monoclonal antibodies and on differences in sensitivity of stem cells and leukaemic cells to in vitro chemotherapy. It may well be that a large number of patients is needed and, therefore, a multi-centre study is indicated.
{"title":"Clinical studies of autografting in acute lymphocytic leukaemia","authors":"Karel A. Dicke, Gary Spitzer","doi":"10.1016/S0308-2261(86)80007-8","DOIUrl":"10.1016/S0308-2261(86)80007-8","url":null,"abstract":"<div><p>The role of autologous marrow transplantation has been reviewed in this chapter. The transplantation results in first remission are difficult to interpret due to the prognostically heterogeneous patient population transplanted and the ever-changing natural history of first complete remission due to more aggressive conventional-dose chemotherapy regimen. The biological role of marrow purging, i.e. elimination of leukaemic cells from the graft, is yet unclear. It is the opinion of the authors that studies in second and subsequent remission can resolve burning issues such as the efficacy of various high-dose conditioning regimens and of different methods of elimination of leukaemic cells such as procedures based on immunological methods, monoclonal antibodies and on differences in sensitivity of stem cells and leukaemic cells to in vitro chemotherapy. It may well be that a large number of patients is needed and, therefore, a multi-centre study is indicated.</p></div>","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 1","pages":"Pages 85-103"},"PeriodicalIF":0.0,"publicationDate":"1986-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14075119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-02-01DOI: 10.1016/S0308-2261(86)80008-X
C.R.J. Singer, A.H. Goldstone
{"title":"Clinical studies of ABMT in non-Hodgkin's lymphoma","authors":"C.R.J. Singer, A.H. Goldstone","doi":"10.1016/S0308-2261(86)80008-X","DOIUrl":"10.1016/S0308-2261(86)80008-X","url":null,"abstract":"","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 1","pages":"Pages 105-150"},"PeriodicalIF":0.0,"publicationDate":"1986-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14638919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-02-01DOI: 10.1016/S0308-2261(86)80015-7
Elizabeth A. Macintyre
{"title":"The use of monoclonal antibodies for purging autologous bone marrow in the lymphoid malignancies","authors":"Elizabeth A. Macintyre","doi":"10.1016/S0308-2261(86)80015-7","DOIUrl":"10.1016/S0308-2261(86)80015-7","url":null,"abstract":"","PeriodicalId":75718,"journal":{"name":"Clinics in haematology","volume":"15 1","pages":"Pages 249-267"},"PeriodicalIF":0.0,"publicationDate":"1986-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14639646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}