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A lower erythrocyte deformability, which causes impairment of the microcirculation, is postulated to contribute to diabetic organ complications. Erythrocyte deformability was measured in four groups of type 1 (insulin-dependent) diabetic subjects and 30 controls by filtration and ektacytometry. Twenty-five patients without organ complications, 21 with microalbuminuria, 13 with overt nephropathy and 12 with leg ulceration were studied. No decreased erythrocyte deformability was found in any of the diabetic groups with either technique, and neither did the total group of 71 diabetic subjects have a lower erythrocyte deformability when compared with the controls. In order to imitate local conditions in the kidney, erythrocyte deformability was also measured in hyperosmolar solutions. Again no differences were found between the diabetic groups separately or as a whole and the controls. Furthermore no correlation was found between erythrocyte deformability and the plasma glucose or glycosylated haemoglobin level.

Three patients are described with severe systemic atherosclerosis, including aortic occlusion, in the presence of a spectrum of risk factors, including hypercholesterolaemia, hypertension, a positive family history of cardiovascular problems, and hyperhomocysteinaemia. In all three patients high levels of anticardiolipin antibodies were found. The possible pathogenic role of antiphospholipid antibodies in atherosclerosis in the context of hyperhomocysteinaemia in these patients is discussed. (Ann Rheum Dis 2001;60:699-701) We describe three patients with severe systemic atherosclerosis including one with aortic occlusion. High levels of antiphospholipid antibodies (aPLs) and hyperhomocysteinaemia were present in all three patients, who were also heavy smokers. To our knowledge, this is the first report in which the relation between severe atherosclerosis, aPLs, and hyperhomocysteinaemia is discussed. There has been much debate about the possible pathophysiological role of aPLs in atherosclerosis. The presence of these autoantibodies and other known atherogenic factors in our patients is discussed. Case reportsPATIENT 1 A 41 year old man was seen at our outclinic because of hypertension. He smoked 10 cigarettes a day with a history of 25 pack years. His father also had had hypertension and angina pectoris. Apart from the hypertension (blood pressure 220/110 mm Hg), a physical examination was unremarkable. In particular, no bruits were heard over the renal arteries. The patient was taking amlodipine 5 mg/day and atenolol 100 mg/day. Ultrasound examination of his abdomen showed a smaller left kidney (12.7 cm right side; 9.2 cm left side), which had shrunk since a similar investigation one year previously (12.3 cm). As renal artery stenosis was suspected, angiography was performed.Injection of contrast into the descending thoracic aorta showed that the aorta was occluded. Huge intercostal arteries feeding collaterals over the abdominal wall to the pelvic and leg arteries were found. Severe atheromatous plaques, an occluded left renal artery, a partially (70%) occluded right renal artery, an occluded coeliac trunk, and partially (50%) occluded superior mesenteric artery were found (fig 1).In view of these findings, additional laboratory tests were carried out (table 1). Homocysteine levels were very high, and folate levels were slightly decreased. After folate treatment (5 mg once a day), homocysteine levels normalised (although still in the higher range) as measured by the methionine loading test. Anticardiolipin antibodies of both IgM and IgG class were present at high levels (repeated testing), whereas lupus anticoagulant and Venereal Disease Research Laboratory results were negative. High density lipoprotein (HDL) cholesterol concentration was decreased and triglycerides were increased. Treatment with coumarins was started.The risk of complications during or after extensive vascular surgery were explained to the patient. He declined the oVer of surgical intervention. So far (one year later), he is doin...

Background/Aims: Usually, the appropriate dosage of low-molecular-weight heparin during haemodialysis is empirically based on the clinical effect. We studied the pharmacokinetics of dalteparin during standard haemodialysis in different groups of patients to assess the added value of measuring the anti-Xa activity for dose monitoring and adjustments. Methods: The pharmacokinetics of intravenously administered dalteparin during haemodialysis was studied in 9 patients during 27 haemodialysis sessions. Six patients received a single bolus dose of dalteparin (group 1), and 3 patients received a higher initial bolus dose of dalteparin followed by a second bolus dose after 2 h (group 2). The clinical effect was evaluated by visual inspection for clot formation in the extracorporeal circuit. Results: The pharmacokinetic curve suggests a zero-order process of elimination. The mean decrease in anti-Xa activity (slope) was comparable in all patients. The mean anti-Xa activity at the end of haemodialysis (C_last) was 0.15 IU/ml in group 1 and 0.60 IU/ml in group 2. Conclusion: We conclude that measuring anti-Xa activity can be used to monitor the elimination of dalteparin during haemodialysis and is highly reproducible.

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