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We read with interest the letter from Prandoni et al. (1) reporting the high risk of thromboembolic recurrence after interruption of oral anticoagulants in patients with antiphospholipid antibodies suffering a first episode of venous thrombosis. The authors obtained these results in patients with lupus anticoagulant alone, and in patients with both lupus anticoagulant and anticardiolipin antibodies. We have found similar results in patients with anticardiolipin antibodies alone suffering an episode of venous thromboembolism. From 1991 to 1994, 204 consecutive patients were hospitalized in our department for deep venous thrombosis (proved by echoDoppler or phlebography) or pulmonary embolism (proved by lung scan or pulmonary angiography). Lupus anticoagulant (LA) and anticardiolipin antibodies (ACLA) were tested for 153 patients. Of these, 6 (3.9%) had LA alone, 3 (1.9%) had both LA and ACLA (one also had factor V Leiden) and 18 (1 1%) had ACLA alone (ELISA assay above 7 UGPL, normal values below 7 UGPL). One of these 18 patients had also factor V Leiden. None of these patients had systemic lupus erythematosus. After exclusion of one patient with isolated LA and one patient with both LA and ACLA because of a history of cancer, the remaining 151 patients were followed prospectively for 1 to 4years (mean 27 months). All patients were treated with heparin followed by fluindione for three to six months (targeted IN : 2-3). Three patients in the ACLA group, 2 in the group with both LA and ACLA, 1 in the LA group and 19 in the control group had long-term oral anticoagulation for recurrent deep venous thrombosis or atrial fibrillation. Six patients

Background-Neuropathological data are very scarce in systemic sclerosis and fail to demonstrate primary changes in the brains of such patients. Case Descriptions-A 41-year-old woman with CREST syndrome developed signs of dementia after an episode of severe dehydration and died two months later of septic shock. A 63-year-old woman with CREST syndrome and a history of two unexplained transient ischemic attacks had had balance disorders since age 62. She died of severe pulmonary hypertension. In both cases, the autopsy showed extensive wall calcification of small arteries and arterioles in the brain, primarily in the basal ganglia, and also in the frontal lobes and the cerebellar area in the second case. No known cause of cerebrovascular calcification was found in either patient. Conclusion-The neuropathological findings in these two patients suggest that systemic sclerosis may induce primary vascular changes in the brain, of which calcification may be a marker. (Stroke. 1998;29:719-721.)

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