Recurrent cerebral infarction and the antiphospholipid syndrome: effect of intravenous gammaglobulin in a patient with systemic lupus erythematosus

Article Abstract:

Some people with systemic lupus erythematosus (SLE) or certain other autoimmune disorders (in which the body makes antibodies against its own tissues) develop high levels of antiphospholipid antibodies directed against certain fatty compounds that form the membranes around cells. This can result in antibodies clustered around, and blocking the function of, cells such as platelets, which are important for clotting. People with this antiphospholipid syndrome (APLS) typically develop cerebral infarction (stroke) and aseptic (nonbacterial) endocarditis (inflammation of the heart lining). A case is reported of a 23-year-old woman with severe APLS who was successfully treated with gamma globulin injections. The patient had developed transient neurological dysfunction and poor clotting at age 16. She subsequently developed kidney disease with high blood pressure, low levels of platelets and white blood cells, a clotting disorder, and cerebral infarction. She had been treated with steroids and aspirin, antihypertensive drugs, and a cytotoxic drug to suppress immune function, but her condition worsened in later years. The patient suffered a stroke in the presence of low platelets and normal blood pressure, and did not respond to various drug regimens. An initial treatment with gamma globulin slightly improved platelet levels, but septic (infectious) arthritis and a clot in the leg developed. Two further gamma globulin treatments resulted in improved platelet levels but similar levels of antiphospholipid antibodies, and allowed modification of anticoagulants and other drug treatments. The report suggests that gamma globulin therapy is effective and should be considered in the treatment of patients with severe APLS. Septic infection is a possible complication, and the therapy is expensive and must be given intravenously. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Stroke (Disease), Stroke, Antiphospholipid antibodies, Gamma globulins

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A novel assay for neutrophil clustering activity of human sera: relation to disease activity and neutropenia in systemic lupus erythematosus

Article Abstract:

A method was devised to measure activity in the blood serum which causes clustering of neutrophils, a type of white blood cell. The method is simple and reproducible; it entails microscopic examination for clustering of neutrophils after addition of serum. Aggregation of neutrophils causes injury to blood vessels and is seen in a number of disease states of the lung and central nervous system and in rheumatic disorders. High clustering activity was found in 19 out of 30 patients with active systemic lupus erythematosus (SLE) and was also found in a higher proportion, 14 out of 20 patients, when the disease flared. High clustering activity was particularly common in patients with SLE who had kidney involvement and in certain patients with central nervous system disorders. Neutrophil clustering was not seen in any of the 10 patients with SLE that was not active. Only 2 out of 20 patients with rheumatoid arthritis, another rheumatic disease, had high clustering activity. If patients with SLE had neutropenia (low numbers of neutrophils in their blood), they were found to have high levels of clustering activity. Glucocorticoids and non-steroidal anti-inflammatory drugs which are given as treatment for SLE had little direct effect on neutrophil clustering activity. There was a slight correlation between clustering activity and the levels of immune complexes that contained C1q, a component of the complement system which causes lysis of cells that contain foreign molecules, such as microorganisms. The clustering of neutrophils may be caused by binding of immune complexes to the neutrophils, which causes aggregation of the cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Granulocytes, Neutrophils, Immune complexes, Lupus erythematosus, Neutropenia

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Transplantation with allogenic bone marrow from a donor with systemic lupus erythematosus (SLE): successful outcome in the recipient and induction of an SLE flare in the donor

Article Abstract:

A bone marrow transfer from one brother with systemic lupus erythematosus (SLE) to another brother with cancer who had the identical antigenic profile does not appear to have transmitted SLE. This was considered a potential possibility because bone marrow cells mediate SLE autoantibody production. The transplant recipient developed mild graft versus host disease, which responded to treatment, and had a temporarily elevated level of anti-C1q antibodies. The donor developed severe pulmonary alveolitis six months later. This flare-up of his disease may have been an effect of the bone marrow tap.

Care and treatment, Acute leukemia, Promyelocytic, Acute myelocytic leukemia, Homografts

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