Biomedical subjects
Publications and source records attributed to W J Sweeney.
Our case demonstrates that nonimmune hydrops and hydrocephalus may be associated by the common pathway of intracranial hemorrhage and the development of anemia. The anemia apparently resulted in cardiomegaly with pericardial effusion and ascites as well as marked extramedullary hematopoiesis.
BACKGROUND: Pheochromocytoma recurs commonly. The treatment for pheochromocytoma is adrenalectomy, and successful pregnancy has been achieved after bilateral adrenalectomy. Recurrent pheochromocytoma in pregnancy carries a high risk for mother and fetus. CASE: A primigravid woman with prior bilateral adrenalectomy for pheochromocytoma was followed during her pregnancy with careful attention to the possibility of tumor recurrence. Maternal tachycardia, elevated urinary catecholamines, and rising hematocrit levels indicated recurrence of the pheochromocytoma at 18 weeks' gestation. Medical therapy and antenatal testing were instituted. Labor was induced at 36 weeks' gestation because of decreasing amniotic fluid volume, and a healthy 2649-g infant was delivered vaginally. No maternal complications occurred in the postpartum period. CONCLUSION: One of the signs of recurrent pheochromocytoma is hemoconcentration which, in combination with increased catecholamines, may lead to uteroplacental insufficiency. With intense surveillance, good outcomes may be achieved.
BACKGROUND: Nevus sebaceous is a congenital hamartomatous skin lesion that is commonly associated with other abnormalities and is most frequently located on the face and head. To our knowledge, there are no previous reports of the ultrasonographic appearance of nevus sebaceous or of an association with cystic adenomatoid malformation of the lung. CASE: A patient was referred at 25 weeks' gestation with multiple fetal anomalies, including echogenic soft-tissue structures external to the cranium and face, a large right-side intrathoracic mass, and abdominal ascites. After a preterm delivery, nevus sebaceous and a congenital cystic adenomatoid malformation of the lung were diagnosed. Neonatal death occurred secondary to pulmonary hypoplasia. CONCLUSION: Nevus sebaceous should be considered in the differential diagnosis when echogenic soft-tissue structures are seen on prenatal ultrasound. A detailed ultrasound examination is warranted to rule out other associated abnormalities.
The effectiveness of contingency contracting to improve the on-task behavior of 3 primary-age students was evaluated using an ABABA single-subject replication design. The contract was developed by the teacher and the consequences were selected by the students. Increases in on-task behavior were observed each time that the contingency contracts were in effect. This study has important implications for the use of contracting with primary school children.
We studied an 18-year-old woman with progressive hirsutism, secondary amenorrhea, and polycystic ovarian disease. Excess androstenedione was secreted by the ovaries, most likely because of a genetic deficiency of ovarian 17-ketosteroid reductase, the enzyme that converts androstenedione to testosterone. Markedly elevated basal plasma levels of androstenedione, estrone, and testosterone were regulated by gonadotropin but not by ACTH. The rate of androstenedione production in the patient's blood at base line and after administration of dexamethasone was very high (10.0 to 11.6 mg per day; value in control women with hirsutism, less than 4.1 mg per day), whereas her blood production of testosterone was 0.64 to 0.7 mg per day, similar to or higher than that in control women with hirsutism. The fractional blood conversion ratio of androstenedione to testosterone was normal (5.6 percent). Thus, 88 to 93 percent of the testosterone in the blood was derived from the peripheral conversion of androstenedione, and very little testosterone was secreted by the ovaries. These in vivo biochemical data suggest that the patient had a deficiency of ovarian 17-ketosteroid reductase activity but normal pubertal activity. The patient's two younger sisters with peripubertal symptoms of androgen excess also had elevated serum levels of androstenedione. We propose that the increased secretion of androstenedione in the three siblings in this family was probably due to a genetic deficiency of ovarian 17-ketosteroid reductase.
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