Search

Anti-phospholipid syndrome (APS) recapitulates the link between autoimmunity and pregnancy failure: Acquired anti-phospholipid antibodies (aPL) play a pathogenic role in pregnancy complications. The diagnosis of obstetric APS can easily be pursued when women present with laboratory and clinical features fulfilling the international classification criteria. Standard therapeutic approach to obstetric APS consists in the association of anti-platelet agents and anticoagulants. Most patients achieve a live birth thanks to conventional treatment; however, approximately 20% fail to respond and are managed with additional therapeutic tools added on the top of conventional treatment. Surely, a refinement of risk stratification tools would allow early identification of high-risk pregnancies that warrant tailored treatment. In real life, obstetricians and rheumatologists face complex diagnostic scenarios including women with pregnancy morbidities other than those mentioned in classification criteria such as one or two early losses and premature birth after 34 weeks due to preeclampsia or placental insufficiency, women with low-titer aPL not fulfilling criteria laboratory requirements, women with positive non-criteria aPL, asymptomatic aPL carriers, and infertile women found to be aPL-positive. This review focuses on some of the several unanswered questions related to diagnostic, prognostic, and therapeutic aspects in obstetric APS.

SUMMARY Acute myocardial infarction is relatively uncommon in patients under the age of 40 years. Unlike the older patients where rupture of coronary artery atherosclerotic plaque is the main underlying pathology, the pathogenesis in younger patients can be varied and may require different diagnostic and therapeutic approaches. Hypercoagulable state associated with nephrotic syndrome and antiphospholipid syndrome can lead to the development of occlusive coronary artery thrombus in absence of atherosclerotic coronary artery disease. Acute myocardial infarction in such a setting can sometimes be the first manifestation of an underlying disease. We describe a case of myocardial infarction in a young man with both nephrotic and antiphospho-lipid syndromes and present a brief literature review.

Acute cytomegalovirus (CMV) infection is associated with thromboembolism. However, cerebrovascular ischemic events have not been reported in relation to acute CMV infection. A patient with a transient ischemic attack and acute CMV infection is described. Transient appearance of anti-phospholipid antibodies suggests a causal relationship between the two. Physicians should be alert to symptoms and signs of acute CMV infection in patients with idiopathic cerebrovascular ischemic events. J. Med. Virol. 84:487–489, 2012. 2012 Wiley Periodicals, Inc.

We report on 2 cases of chronic relapsing thrombotic thrombocytopenic purpura, in which anti-phospholipid antibodies were also found. The first patient was felt to have the anti-phospholipid antibody syndrome, while the second patient had anti-phospholipid antibodies without clinical manifestations of the anti-phospholipid antibody syndrome. We discuss chronic relapsing thrombotic thrombocytopenic purpura and the anti-phospholipid antibody syndrome. Furthermore, we introduce the possibility of an association between chronic relapsing thrombotic thrombocytopenic purpura and the presence of anti-phospholipid antibodies.

The clinical course and laboratory findings of a patient with autoimmune haemolytic anaemia due to anti-phospholipid antibodies and secondary to a systemic lupus erythematosus-like syndrome are described. IgG and IgM with anti-phospholipid activity coexisted in both sera and acid eluates prepared from the patient's red cells, as demonstrated by ELISA using a panel of anionic and neutral phospholipids. The anti-erythrocyte binding activity of eluted autoantibodies, determined by a radioactive antiglobulin technique, was totally inhibited by absorption with phospholipid micelles. The patient's serum also contained an IgM warm haemolysin detectable with enzyme-treated cells only, as well as anti-C, -E and -S alloantibodies.