Haemostatic factors associated with vascular thrombosis in patients with systemic lupus erythematosus and the lupus anticoagulant

Article Abstract:

Patients with systemic lupus erythematosus may have prolonged bleeding, as measured by the APTT laboratory test (activated partial thromboplastin time). This is caused by lupus anticoagulant, a circulating autoantibody that reacts with a lipid, or fat, involved in the activation of the clotting process. (An autoantibody is an antibody produced by the immune system against the body's tissues.) Patients with lupus anticoagulant do not have a tendency toward increased bleeding, but reports suggest that they have an increase in thrombosis (clot formation) in arteries and veins, perhaps due to inhibition of prostacyclin or other factors that regulate blood clotting. Prostacyclin is a locally-produced, locally-acting hormone found in many tissues. Factors of coagulation and fibrinolysis (clot breakdown) were studied in 106 patients (100 female, 46 male) with systemic lupus erythematosus. Seventeen patients had the lupus anticoagulant, and significantly more of these patients had a history of thrombosis associated with cerebral infarction (death of brain tissue), low levels of platelets (blood cells needed for clotting), and miscarriages. Levels of two fibrinopeptides (clot-related proteins) were significantly higher in the subjects with lupus anticoagulant. One protein, fibrinopeptide A, reflects activation of coagulation, while fibrinopeptide B (beta 15-42) is related to fibrinolysis. The A peptide was elevated only in patients with a recent thrombosis and may be useful for predicting thrombosis. The B peptide was slightly elevated in patients with and without recent thrombosis, and is thus less specific, or useful, in predicting lupus anticoagulant-associated thrombosis. In addition, thromboxane B2 (a hormone related to prostacyclin) was elevated in two patients with cerebral infarction and thus may also be a marker for thrombosis. A marker for prostacyclin was reduced in only some patients with lupus anticoagulant, and so there may be possible to identify subgroups of lupus patients who have lupus anticoagulant. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cases, Symptomatology, Signs and symptoms

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Avascular necrosis of bone in systemic lupus erythematosus: possible role of haemostatic abnormalities

Article Abstract:

Systemic lupus erythematosus (SLE), a chronic inflammatory disease of the connective tissues, causes abnormalities of the joints, kidneys, skin, nervous system, and mucous membranes. SLE has been associated with avascular necrosis of the bone (ANB), the destruction of bone tissue due to an inadequate blood supply. The factors that may contribute to the development of ANB include the use of corticosteroids, inflammation of the blood vessels, fatty clots, and blood vessel constriction associated with Raynaud's disease. Also, blood abnormalities may interfere with the blood supply to the bone thereby resulting in ANB. The predisposing factors for ANB associated with SLE were assessed in 24 patients with SLE and ANB and 87 SLE patients without ANB. The average ages of patients with and without ANB at time of SLE diagnosis were 24 and 31 years, respectively. The average maximal daily dose of the corticosteroid drug, prednisolone, was 50.8 milligrams (mg) in patients with ANB and 41.8 mg in patients without ANB. The features of SLE that were unrelated to ANB were Raynaud's phenomenon, increased blood lipids, kidney disorders, high blood pressure and disease activity. A greater proportion of SLE patients with ANB had lupus anticoagulant, a factor that inhibits blood coagulation, and shorter activated partial thromboplastin time, an index of blood clotting. The findings suggest that several factors including blood abnormalities, young age, and corticosteroid use may be involved in the pathogenesis of avascular necrosis of the bone in systemic lupus erythematosus. (Consumer Summary produced by Reliance Medical Information, Inc.)

Bones, Abnormalities, Blood, Osteonecrosis, Necrosis

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High incidence of herpes zoster in patients with systemic lupus erythematosus: an immunological analysis

Article Abstract:

Systemic lupus erythematosus (SLE) is an autoimmune disease, meaning that the immune system attacks the body's own tissues as if they were foreign. Patients with SLE are frequently treated with immunosuppressive agents and corticosteroids, which further reduce their resistance to infection. Herpes zoster, also known as shingles, is a form of recurrent infection with the varicella zoster virus (VZV), the same virus responsible for chickenpox. Although chickenpox primarily affects children, herpes zoster affects elderly or immunocompromised patients through reactivation of the virus. Investigators in Japan found a 43 percent incidence of herpes zoster in patients with SLE. This figure is quite high compared with the 3.2 to 21 percent incidence in Western countries and the estimated 0.5 percent incidence in the general population. Japanese patients with SLE seem to be much more susceptible to this virus than Caucasians. The high incidence of herpes zoster among patients with SLE is believed to arise because of defects in cellular immunity caused by the underlying disease and corticosteroid treatment. (Consumer Summary produced by Reliance Medical Information, Inc.)

Japan, Physiological aspects, Varicella-zoster virus, Shingles (Disease), Herpes zoster

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