Screening for lupus anticoagulant and anticardiolipin antibodies in women with fetal loss

Article Abstract:

It is estimated that 15 percent of all pregnancies result in spontaneous fetal death in the first or second trimester of pregnancy. If a woman has three or more miscarriages (recurrent fetal loss), it is unlikely that future pregnancies will have a successful outcome. The most common abnormalities associated with fetal death include those affecting uterine and cervical function, infections in the uterus, and hormone abnormalities. Recent studies have focused on the role of lupus anticoagulants (proteins, also called antiphospholipid antibodies, that are present in the blood) in fetal death. The association between lupus anticoagulants and recurrent fetal loss was first identified in women with systemic lupus erythematosus (SLE, a connective tissue disease). In some cases, elevated blood levels of lupus anticoagulants and anticardiolipin antibodies (antibodies that attack a cell membrane protein called cardiolipin) have been associated with fetal death. In order to investigate further the relationship between lupus anticoagulants, anticardiolipin antibodies and fetal death, blood samples from 77 women whose pregnancies ended in first or second trimester fetal death were tested. Seventeen of the women had lupus anticoagulants or anticardiolipin antibodies. Thirty-five of the women had more than two episodes of fetal death, and seven of these women had lupus anticoagulants, six had elevated blood levels of anticardiolipin antibodies, and two had both. Eleven women with lupus anticoagulants or anticardiolipin antibody had a total of 54 pregnancies that resulted in seven live births. Of the remaining 31 women, who had only one or two episodes of fetal death, one had lupus anticoagulants and none had anticardiolipin antibodies. It is concluded that lupus anticoagulants and anticardiolipin antibodies are associated with recurrent fetal death, and that women who experience recurrent fetal death should be tested for lupus anticoagulants and anticardiolipin antibodies. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Miscarriage, Anticardiolipin antibodies, Blood chemical analysis, Fetal death, blood

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Familial antithrombin III deficiency and Mycoplasma pneumoniae pneumonia

Article Abstract:

Thrombosis (the development of blood clots) occurred in the vein of the thigh of a 10-year-old girl who had pneumonia caused by the bacteria Mycoplasma pneumoniae. With further examination the girl was diagnosed to have type I familial antithrombin III deficiency. Antithrombin III is a molecule that inhibits some of the molecules involved in the clotting of blood. Without the inhibitor, blood clots readily form. Type I familial antithrombin III deficiency is a disorder that is inherited in a manner that occurs more frequently than would occur by chance alone. The prevalence of antithrombin III deficiency is one case in 2,000 to 5,000 individuals. Two to three percent of the blood clots that occur in young people are thought to be the result of antithrombin III deficiency. It is not certain what causes the development of the blood clots. In general, situations that have been associated with the development of blood clots are immobility, trauma, surgery, pregnancy and the use of oral contraceptives. In this case the thrombosis was associated with Mycoplasma pneumoniae pneumonia. It is felt that individuals with familial antithrombin III deficiency who have an infection should be treated prophylactically with drugs to prevent the development of blood clots. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Complications and side effects, Pediatric diseases, Thrombosis, Mycoplasma pneumonia, Deficiency diseases, Thrombosis in children

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Bone marrow aplasia in B cell chronic lymphocytic leukaemia: successful treatment with antithymocyte globulin

Article Abstract:

Patients with chronic lymphocytic leukemia (CLL) can develop anemia (decreased levels of hemoglobin in the blood, which carries oxygen to other cells in the body). Some patients, in the end stages of disease, have low levels of cells in their blood. Approximately 6 percent of CLL patients have red cell aplasia (failure to generate red blood cells). A certain subtype of T lymphocytes, T-gamma cells, contain receptors for immunoglobulin G molecules. These cells may inhibit the growth of precursor red blood cells in the bone marrow. Treatment with cyclosporin-A, an immune-suppressing agent, and antibody molecules which react specifically with T-gamma cells can stop the inhibition of the growth of red blood cells. A case study is reported on a patient with B-cell CLL whose numbers of blood cells were reduced because of the lack of all types of precursor cells in the bone marrow. This is the first time depletion of all precursor cells has been reported in patients with CLL. The patient was treated with corticosteroids and immunoglobulin with no success. However, when given antibodies to thymocytes, the levels of blood cells returned to normal. This indicates that T lymphocytes were responsible for the suppression of the growth of the cells in the bone marrow. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Care and treatment, Physiological aspects, Antibodies, Chronic lymphocytic leukemia, Pure red cell aplasia

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