Transient anticardiolipin antibodies, functional protein S deficiency, and deep vein thrombosis

Abstract

A 30-year-old man presented with an episode of deep vein thrombosis. He was found to have primary antiphospholipid syndrome with anticardiolipin antibodies and protein S deficiency. All other investigations were negative. Three months later, anticardiolipin antibodies were negative and protein S levels were normal. The transient presence of anticardiolipin antibodies and functional protein S deficiency in this patient suggests a new mechanism for the association between anticardiolipin antibodies and venous thrombosis.

Clinical trials for the antiphospholipid syndrome

“…Reports of a transient and reversible acquired protein-S deficiency at the time of thrombosis in patients with antiphospholipid antibodies [43][44][45][46][47][48][49] are particularly interesting given the fact that these autoantibodies can be detected with relatively high frequency in these patients. In several studies, acquired free protein-S deficiency was associated with both antiphospholipid antibodies and procoagulant laboratory measures in patients with SLE and the APS [21,46,50,51].…”

Cerebral and vein thrombosis, transient protein S deficiency, and anticardiolipin antibodies

“…aPL have been found to be associated with recurrent spontaneous abortions and systemic arterial and venous thrombosis, as well as thrombosis of the cerebral vessels [1,2]. Recently, cases of deep vein thrombosis or severe diffuse thromboembolic disease associated with the transient presence of anticardiolipin antibodies (aCL) and functional protein S deficiency have been reported [ 3 ] , suggesting a new, possibly autoimmune mechanism [4] for the thrombosis in the primary aPL syndrome. Low levels of free protein S in patients with aPL may be a factor contributing to the thrombotic diathesis associated with the aPL syndrome.…”

“…We, among others [2], have encountered difficulty with automated white cell counting of neonatal blood using the Coulter STKS due to incomplete lysis of red cells. In addition to neonatal blood, problems with incomplete lysis of red cells have been seen in post-splenectomy states, megaloblastic anemia, hemoglobinopathies, and liver disease [1,3]. We would like to extend this list to include the myelodysplastic syndromes (MDS).…”

“…Osmotic fragility of red cells is related to the ratio of mean surface area (MSA) to mean cell volume [3]. Neonatal and post-splenectomy red cells have a higher content of membrane phospholipids and cholesterol, leading to an increased MSA and increased red cell resistance of hypotonic lysis [ 3 ] .…”

“…Neonatal and post-splenectomy red cells have a higher content of membrane phospholipids and cholesterol, leading to an increased MSA and increased red cell resistance of hypotonic lysis [ 3 ] . Red cell membrane abnormalities are virtually unstudied in MDS.…”