Is change of the vessel wall a risk factor for venous thrombosis?

ABO blood group and improvement of preoperative fragment prothrombin 1,2 in orthopaedic surgery Sir—F R Rosendaal (April 3, p 1167)1 designates high concentration of factor VIII (>1500 IU/L) as the most frequent risk factor for venous thrombosis. He relates the genes that code for ABO blood group to the amount of this clotting factor in plasma. In 79 patients having hip or knee arthroplasties,2 which are associated with high risk of venous thromboembolic disease (VTED), 41 patients with blood groups other than O had presurgical concentrations of fragment prothrombin 1,2 (F1,2) higher than those with group O (p=0·004), whereas the remaining hypercoagulable markers we measured—D-dimer (D-D) and thrombin-antithrombin complex (TAT)—showed no such difference. Since F1,2 is a marker of generation of thrombin, a preoperative rise could be due to an increase in factor VIII in patients with groups A, B, and AB. In these blood groups clinical episodes of VTED are usually associated with triggering agents; thus, hip 3 or knee arthroplasty can be included among the risk factors, in interaction with genetic factors, as Rosendaal proposes in the multicausal model for thrombosis. Our findings are relevant because we have described the existence of a hypercoagulable state before hip or knee arthroplasty;4 here, plasma concentrations of activation coagulation markers in the patient groups were higher than those in the healthy individuals of similar age. The contribution of ABO antigenic system to hypercoagulability and consequent disclosure of thrombotic event, will demand much additional investigation in such surgery.

system and allogeneic transfusion. Transfus Sci 1999; 2 0 : 17–20. 4 Iturbe T, Cornudella R, De Miguel R, Olave MT, Moreno JA, Gutiérrez M. Existence of a hypercoagulability state prior to prosthetic hip or knee surgery. Haematologica 1999; 84: 87–88.

Is change of the vessel wall a risk factor for venous thrombosis? Sir—In his report on the causes of venous thrombosis, F R Rosendaal (April 3, p 1167)1 states that the known risk factors for this disorder fall into two groups: stasis of the blood and changes in the composition of the blood, excluding the third group of changes in the vessel wall which would be a risk factor only for arterial thrombosis. However, if the changes in the venous wall are difficult to assess everywhere in the body, the eye and retina is ideal for their observation. Fundus observation, fluorescein angiography, and histopathological studies show that most retinal venous thromboses occur at arteriovenous crossings or at the level of the lamina c r i b o s a .2,3 This thrombosis results from a change in the venous wall due to compression of an artery on the vein at the site of an arteriovenous crossing2,4 or to the compression of the lamina cribosa on the central retinal vein. These compressions cause a narrowing of the vein (Gunn sign) and may induce the transformation of the laminar venous blood flow into a turbulent flow at the level of the vessel narrowing. The turbulent flow can

*Haematology and Traumatology Departments, Zaragoza University Hospital, 50009 Zaragoza, Spain 1

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Claire Verougstraete University Hospital Brugmann and St Pierre, Université Libre de Bruxelles, 1020 Brussels, Belgium 1

Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999; 3 5 3 : 1167–73. 2 Frangieh GT, Green WR, Barraquer-Somers E, Finkelstein D. Histopathologic study of nine branch retinal vein occlusions. Arch Ophthalmol 1982; 100: 1132–40. 3 Green WR, Chan CC, Hutchins GM, Terry JM. Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases. Tr Am Ophthalmol Soc 1981; 79: 373–422. 4 Weinberg D, Dodwell DG, Fern SA. Anatomy of arteriovenous crossings in branch retinal vein occlusion. Am J Ophthalmol 1990; 109: 298–302. 5 Clemett RS. Retinal branch vein occlusion: changes at the site of obstruction. Br J Ophthalmol 1974; 5 8 : 548–54.

Platelet counts and prognosis of pancreatic cancer

*Teodoro Iturbe, Rosa Cornudella, Roberto De Miguel, María José Varo, Martín Gutiérrez

Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999; 3 5 3 : 1167–73. 2 Salvati EA, Lachiewicz P. Thromboembolism following total hipreplacement arthroplasty. The efficacy of dextran-warfarin in prophylaxis. J Bone Joint Surg 1976; 58A: 921–25. 3 Iturbe T, Cornudella R, De Miguel R, et al. Hypercoagulability state in hip and knee surgery: influence of ABO antigenic

damage the venous endothelium, which in turn, can initiate the coagulation process. The damage of the venous wall may sometimes be shown by fluorescein angiography: 5 in normal retinal blood vessels, there is no leakage or staining of the vascular wall, while staining and leakage caused by endothelial incompetence have been shown at pathological arteriovenous crossings, or at the site where the central retinal vein crosses the lamina cribosa. Parietal abnormalities may not have been identified in internal medicine as a general cause of venous thrombosis, but play a major part in the eye where they are easy to detect. I suggest that changes in the venous wall may be one of the risk factors that can interact with the acquired and genetic risk factors described by Rosendaal.

Endothelial damage with venous wall staining at level of arteriovenous crossing where venous thrombosis occurred

Sir—In their report on vascular endothelial growth factor, platelet counts, and prognosis in renal cancer, Kenneth O’Byrne and colleagues (May 1, p 1494)1 provide evidence for a harmful effect on survival in patients with platelet counts greater than Hernandez and 3 3 8⫻1 09/L. colleagues2 reported an association between raised platelet counts and inferior survival in patients with cervical cancer, and there have been similar observations in patients with endometrial, ovarian, and lung cancer. The potential mechanisms, apart from the expected morbidity due to increased thrombogenicity, especially

THE LANCET • Vol 353 • June 19, 1999