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microcytosis, hypochromia, thrombocytopenia, and neutropenia, whereas the official petrol-pump attendants did not differ from the controls. None of the subjects had leukaemia, but we concluded that they were at higher than usual risk. If similar studies were to be done, chronic benzene toxicity would probably prove a major health hazard in many countries of the developing world, causing serious blood dyscrasias, some of which progress to aplastic anaemia and leukaemia. Governments should promote research into the extent of the danger, to educate the public about the hazards of petroleum. They should also introduce and enforce legislation to reduce benzene in petrol to below 1 %, ensure the sale of petrol only through electrically or hand-driven pumps conforming with established criteria for safety, and improve the safety and work conditions of young motor-mechanics in small workshops.

40% in the TIMI 0/1group vs 42% in the TIMI 2group. As expected, the proportion of MI patients with Lp(a) values greater than 20 mg/dl was much higher than that in controls (24-4%). Raised LP(a) values therefore do not seem to be clinically detrimental to thrombolytic therapy with pro-urokinase. However, Lp(a) may still constitute a physiological risk factor for thrombosis since the pharmacological doses of pro-urokinase that were used for thrombolysis might simply overwhelm any inhibitory action of Lp(a). It should also be noted that Lp(a) does not inhibit plasminogen activation in the fluid phase.7 Although pro-urokinase is believed to have a low lytic state potential there may still be sufficient activation of plasma plasminogen to provide effective thrombolysis even in the presence of high Lp(a) concentrations.

Department of Haematology, South African Institute for Medical Research and the University of the Witwatersrand,

Departments of Clinical Chemistry and Cardiology, University Hospital. D-3400 Gottingen, Germany

Baragwanath Hospital, PO Bertsham, Soweto 2013, South Africa

ALAN F. FLEMING

1 Niazi GA, Fleming AF. Blood dyscrasia m unofficial vendors of petrol and heavy oil and motor mechanics m Nigeria. Trop Doct 1989; 19: 55-58.

Lack of association between raised serum Lp(a) concentration and unsuccessful thrombolysis after acute myocardial infarction SIR,- There is now substantial evidence that lipoprotein Lp(a) is a major risk factor for atherosclerosis, coronary heart disease, and thrombosis.1,2 The

of apolipoprotein(a) is closely homologous to plasminogen3,4 and the possible involvement of Lp(a) in fibrinolysis has been investigated. Several in vitro studies have demonstrated that Lp(a) can compete for plasminogen binding sites on molecules and cells.’ We therefore investigated whether raised Lp(a) concentrations might also impair

1. Uterman G. The mysteries of lipoprotein(a). Science 1989; 246: 904-10. 2. Scanu AM, Gless GM. Lipoprotein(a): heterogeneity and biological relevance. J Clin Invest 1990; 85: 1709-15. 3. Mclean JW, Tomlinson JE, Kuang W, et al. cDNA sequence of human apolipoprotein (a) is homologous to plasminogen. Nature 1987; 330: 132-37. 4. Kratzin H, Armstrong VW, Niehaus M, Hilschman N, Seidel D. Structural relationship of an apolipoprotein(a) phenotype (570 kDa) to plasminogen: homologous knngle domains are linked by carbohydrate-nch regions. Biol Chem Hoppe-Seyler 1987; 368: 1533-44. 5. Miles LA, Plow EF. Lp(a): an interloper into the fibrinolytic system. Thromb Haemostas 1990; 63: 331-35. 6. TIMI Chesebro JM, Knatterud G, Roberts R, et al. Thrombolysis in myocardial infarction trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Circulation 1987; 76: 142-54. 7. Hajjar KA, Gavish D, Breslow JL, Nachman RL. Lipoprotein(a) modulation of endothelial cell surface fibrinolysis and its potential role in atherosclerosis. Nature

1989; 339: 303-05.

structure

thrombolytic therapy for acute myocardial infarction (MI). Patients with acute MI received a 20 mg bolus of pro-urokinase (saruplase) within six hours of the event, followed by an infusion of 60 mg over 60 min. The efficacy of the thrombolytic therapy was assessed by coronary angiography 6-12 h after the initial bolus and the patency of the infarct-related artery was graded on the TIMI scalePatients were assigned to two groups: those with a successful reperfusion (TIMI 2) and those in whom reperfusion was unsuccessful (TIMI 0 or 1). The ejection fraction size was significantly higher and the peak areas of creatine kinase (CK) and CK-MB after infarction were significantly lower in patients with successful reperfusion (table), presumably reflecting the limitation of infarct size in this group. The distribution of LP(a) concentrations, however, did not differ between the groups (table). Median values of the two groups were similar - 12 mg/dl in the TIMI 0/1group vs 13-4 mg/dl in TIMI ≥22 group-as were the proportions of patients with Lp(a) values of 20 mg/dl or greaterDETAILS OF MI PATIENTS WITH

0/1)

V. W. ARMSTRONG C. NEUBAUER E. SCHÜTZ U. TEBBE

AND WITHOUT (TIMI SUCCESSFUL REPERFUSION AFTER THROMBOLYTIC THERAPY WITH PRO-UROKINASE

(TIMI 2)

Fatal effect of re-exposure to

heparin after previous heparin-associated thrombocytopenia and thrombosis

patients with a history of heparin-associated thrombocytopenia and thrombosis (HATT), the wisdom of re-exposure to heparin after a thromboembolic event has been questioned. We report such a patient. In 1984, a 65-year-old woman had a massive pulmonary embolism and a thrombosis of the left iliofemoral venous axis on day 16 of subcutaneous (sc) unfractionated heparin treatment for ankle sprain. Platelet count was 85 x 109/1, with fibrinogen 0-43 g/l, factor V 50%, fibrin degradation products 40 µg/1 (normal < 10). The diagnosis of HATT was confirmed by positive platelet aggregation tests.2 Thus, heparin was discontinued and the patient was treated with intravenous urokinase followed by oral anticoagulants and antiplatelet agents. The platelet count returned to normal on day 19 (186 x 109/1) and there were no coagulation abnormalities. On day 25 the pulmonary angiogram had returned to normal and the patient was discharged on coumarin therapy. 3 months later platelet aggregation tests were negative and she had no further thromboembolic complication. In 1990 the patient presented with a SIR,-In

severe venous thromboembolism. She was treated with sc unfractionated heparin 30 000 IU daily and alteplase intravenously. The initial platelet count was 296 x 109/1 and fibrinogen was 2-54 g/1. She improved clinically, but had thrombocytopenia (platelets 73 x 109/1) and a low fibrinogen (0-94 g/1) on day 15 of heparin therapy. On day 17, she had signs of severe recurrent pulmonary embolism. Alteplase was given in combination with intravenous unfractionated heparin. On day 19, she had acute ischaemia of the left leg. Angiography showed complete obstruction of the common iliac artery with several thrombi in the abdominal aorta; the platelet count was 34 x 109/1. Heparin was discontinued and several white clots were surgically extracted from the left iliac artery, but after a recurrence of arterial thrombosis the patient died =

on

Mean (SD) shown *Serial enzyme measurements done every 2 h for the first 16 h and then every 4 h for the next 28 h after bolus injection of pro-urokmase, and area under the peak calculated. Mann Whitney test tp