Anti-platelet antibodies: a prognostic marker in pregnancies associated with lupus nephritis

Article Abstract:

Thrombocytopenia is a condition that occurs when there is an abnormal decrease in the number of blood cells called platelets (cells required for normal blood clot formation). The most likely cause of the thrombocytopenia is the production of specific proteins called antiplatelet antibodies that destroy blood platelets. This can cause a serious problem during pregnancy because the antibodies can be passed from the mother to the fetus, which can result in thrombocytopenia in the fetus. Delivery by cesarean section is recommended to reduce the risk of internal bleeding in the head of the fetus that can occur during delivery. Although rare, this condition can occur in pregnant women who have systemic lupus erythematosus (SLE), a connective tissue disease. SLE is also considered to be an autoimmune disease, in which the body makes proteins called autoantibodies that attack and destroy the body's own tissues. Lupus anticoagulant and anticardiolipin antibodies are found in the blood of pregnant women with SLE, and these antibodies are associated with spontaneous abortion or miscarriage. This article describes the case reports of two pregnant women with SLE. Both women had previous pregnancies that resulted in miscarriage, neonatal death, and live birth. The women were being treated with prednisone and azathioprine for their SLE. They developed high blood pressure, proteinuria (protein in the urine), and thrombocytopenia at weeks 23 and 26 of pregnancy. Both women had low levels of platelets and had antiplatelet antibodies in their blood. One woman experienced stillbirth at week 25 of pregnancy. The other woman had a cesarean delivery at week 28, but the baby died four days later. The results of these case studies indicate that antiplatelet antibodies in pregnancy are associated with a poor fetal outcome. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Systemic lupus erythematosus, Connective tissue diseases

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Theca-lutein ovarian cysts associated with placental chorioangioma

Article Abstract:

Chorioangioma is a tumor that develops in the placenta. Most of these tumors are very small and are diagnosed after delivery when the placenta can be examined. When the tumors are large enough, they can be identified by ultrasound scanning. The most common complications of this type of tumor are an increased amount of amniotic fluid surrounding the fetus (hydramnios), growth retardation, fetal heart failure, and destruction of fetal red blood cells (hemolytic anemia). This article describes the case report of a 30-year-old women who was in her 26th week of pregnancy when she developed hydramnios. Ultrasound scanning showed a normal fetus with a large excess of amniotic fluid. Two weeks later, the internal membranes containing the amniotic fluid ruptured and a cesarean section was performed to delivery the fetus. The female infant weighed three pounds and was in poor condition. Both of the woman's ovaries were larger than normal and contained several cysts (theca-lutein cysts). The placenta contained a tumor that weighed half a pound. The woman recovered and left the hospital eight days after delivery. Six weeks later, an ultrasound was performed and showed that the ovaries had returned to their normal size. The infant remained in the neonatal care unit for 59 days and then was well enough to go home. In most cases, theca-lutein cysts on the ovaries are benign and need not be removed by surgery. Cases of the unnecessary surgical removal of these cysts that resulted in sterility have been reported. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cases, Ovarian tumors, Placental diseases, Placenta diseases, Angioma

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Nicotine induced gastric injury: a quantitative macroscopic and microscopic analysis of the protective effects of sucralfate and feeding

Article Abstract:

There is extensive evidence linking cigarette smoking to peptic (gastric and duodenal) ulcer disease, but the exact mechanisms underlying this association remain unknown. Nicotine, an important component of cigarette smoke, has been shown to potentiate (increase) the gastric damage resulting from ethanol (alcohol) ingestion, but does not appear to cause ulceration in and of itself. The effect of nicotine on the microscopic structure of the gastric mucosa is not known; subthreshold damage may require the actions of an additional irritant, such as ethanol, for the pathology to become apparent. To evaluate the effects of nicotine on gastrointestinal microscopic anatomy, and to investigate the effects of sucralfate (a protective agent) and feeding on nicotine-induced changes in gastric morphology, an animal study was carried out with anesthetized male rats who had been either food-deprived for 24 hours or fed as they desired prior to the experiment. The stomach was exposed to nicotine, sucralfate, ethanol, or a combination of these drugs, and the rat stomachs were removed and subjected to microscopic analysis. Both nicotine and ethanol induced microscopically detectable injury, and the two drugs acted synergistically to produce a greater degree of damage than the sum of each individually. Sucralfate pretreatment reduced the amount of damage done by both nicotine and ethanol. By the same token, prior feeding reduced the amount of injury induced by both nicotine and ethanol. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Nicotine, Alcohol, Alcohol poisoning, Peptic ulcer, Sucralfate, Gastric mucosa

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