No abstract

The Hemostasis and Thrombosis Laboratory at the Oregon Health Sciences University identified 80 patients with significantly elevated anticardiolipin antibody (ACLA) levels. We reviewed all of their available medical records and found that 25 of these patients had associated neurological symptoms or disorders. These symptoms and disorders could be grouped into four distinct clinical patterns comprising encephalopathy, multiple cerebral infarctions, migraine-like headaches, and visual abnormalities including amaurosis fugax and ischemic optic neuropathy. Cerebral ischemia best explained these neurological dysfunctions. There was no correlation between the presence or absence of neurological disease and ACLA levels, but ACLA levels were higher in patients with encephalopathy than in others with neurological involvement (p less than 0.05). How neurological dysfunction and the presence of these antiphospholipid antibodies are related remains to be clarified. Nevertheless, in patients with unexplained cerebral ischemia, establishing the presence of ACLA may have prognostic and therapeutic importance. In particular, acute immunosuppressive therapy and plasmapheresis may be useful in patients with acute ischemic encephalopathy.

The rarity of atherosclerotic vascular disease and a mild bruising tendency in Greenland Eskimos has been linked to their ingestion of omega 3 fatty acids contained in foods obtained from the sea. Previous studies have shown that feeding salmon oil to normal volunteers resulted in reductions of plasma cholesterol and triglycerides. We wished to learn whether salmon oil feeding would result in the incorporation of omega 3 fatty acids into platelets and whether platelet function or platelet-vessel interaction would be altered. Diets containing salmon oils led to the incorporation of eicosapentaenoic acid (C20:5 omega 3) into platelets (6.1%) with a reduction in arachidonic acid (C20:4 omega 6). The ratio of C20:5/C20:4 increased from 0.0045 on the control diet to 0.3 on the salmon diet. Bleeding times were prolonged (from 6.75 to 10 min, p less than 0.005), platelet retention on glass beads was mildly reduced (from 89% to 78%, p less than 0.0005), and platelet aggregation in response to dilute concentrations of ADP was inhibited in the subjects ingesting the salmon oil. We conclude that in normal subjects dietary omega 2 fatty acids derived from salmon oil are incorporated into platelet phospholipids and that these changes are accompanied by alterations in bleeding time and platelet function.

Invasive lines are used frequently in patients with hemostatic defects, often without any attempt to correct the abnormalities. Nevertheless, rates of hemorrhage are low and appear to be closely related to the level of experience of the physician rather than to defects in hemostasis. These findings suggest that the use of blood components for preprocedure correction of hemostatic defects is not necessary, except in those patients who have the most severe hemostatic abnormalities.

No abstract

We describe 2 patients with marked elevations of anticardiolipin antibodies who developed multipleorgan disease characterized by a noninflammatory vasculopathy. Their cases were remarkable for the fulminant nature of their thrombotic diathesis, which was heralded by a prominent livedo reticularis of the extremities. Both patients had a serologic profile and salivary gland biopsy findings that were consistent with a diagnosis of primary Sjogren's syndrome.The lupus anticoagulant (LAC) is an immunoglobulin with antiphospholipid activity that is associated with a thrombotic diathesis (1). It reacts with cardiolipin, a phospholipid found in the VDRL reagent, and a correlation between the presence of the LAC, anticardiolipin antibodies (ACLA), and the occurrence of thrombosis has been observed. Patients with the LAC and elevated ACLA can develop a broad range of manifestations in addition to the thrombosis. A variety of therapies has been used for this "anticardiolipin syndrome. " Two patients with the syndrome were referred to us; both were treated successfully with plasmapheresis and with immunosuppression and anticoagulation therapy.

Antithrombin III (Human) (AT III) was administered to 18 patients with documented hereditary AT III deficiency. In eight patients with no ongoing clinical symptoms of thrombosis, the percent increase per unit AT III infused per kilogram of body weight ranged from 1.56% to 2.74%, and the half-life from 43.3 to 77.0 hours. No significant difference was noted between patients receiving and those not receiving coumarin therapy. In clinically ill patients, the in vivo recovery was significantly lower and ranged from 0.64% to 1.90% increase per unit AT III infused/kg. Efficacy of AT III was evaluated in 13 patients for the prevention or treatment of thrombosis. AT III was efficacious as assessed by the absence of thrombotic complications after surgery and/or parturition, and the nonextension and nonrecurrence of thrombosis in patients exhibiting an acute thrombotic episode. No side effects were noted. Follow-up studies indicated no hepatitis B seroconversion and no alanine aminotransferase elevations in patients who were not transfused with other blood products.

Fifty patients who underwent aortocoronary saphenous-vein bypass-graft surgery were randomly assigned to one of three groups to determine the effects of antiplatelet or anticoagulant therapy on graft patency. Twenty-four patients served as controls; 13 patients received aspirin (325 mg three times a day) and dipyridamole (75 mg three times a day); and 13 patients received closely regulated warfarin therapy. Medications were begun on the third post-operative day. Six months after surgery, all patients underwent coronary angiography to assess graft patency. There were no statistically significant differences between groups in various clinical, hemodynamic and angios, 27 of 33 grafts (82 per cent) with aspirin and dipyridamole and 29 of 37 grafts (78 per cent) with warfarin (P less than 0.5), all patients had at least one patent graft. Postoperative treatment either with aspirin and dipyridamole or with warfarin failed to improve the patency of the grafts.