Glycogen levels in human term placental disks, umbilical cords, and membranes

Glycogen in the placenta and its appendages is important for fetal well-being. The precise location of the glycogen stores, however, is unknown. This study was initiated to quantitate glycogen levels at well-defined sampling sites in more than 641 samples from 10 uncomplicated pregnancies and to correlate these glycogen levels with clinical and morphological variables. By biochemical assay, glycogen levels were greatest in the midumbilical cord section (29.08 +/- 1.18 mg/g dry wt) and lowest in the amnionic membrane (2.31 +/- 0.08 mg/g dry wt). Within the placental disk, parenchymal glycogen levels were greatest near the cord insertion (9.31 +/- 2.68 mg/g dry wt) and lowest at the periphery (5.71 +/- 1.14 mg/g dry wt). The midumbilical cord glycogen level showed strong direct correlations (P < .001) with birth weight, umbilical cord weight, and total calculated umbilical cord glycogen and somewhat lower but significant (P < .037) direct correlations with the calculated mean umbilical cord glycogen level, total calculated placental glycogen content, and placental weight. The glycogen level in the middisk parenchymal section from the fetal surface correlated directly with gestational age. Periodic acid-Schiff stains showed that magenta glycogen granules were most abundant in the cytoplasm of the vascular smooth muscle cells. These data show significant variations in glycogen levels among sampling sites. Definition of the precise sampling site is important for clinicopathologic studies of placental glycogen and for interstudy correlations.     

Diskitis caused by Actinobacillus actinomycetemcomitans

A 32-year-old man with acquired immunodeficiency syndrome (AIDS) admitted to the hospital for treatment of visceral leishmaniasis was inadvertently given 10 times the prescribed first dose of sodium stibogluconate ([Sb] 6.5 g instead of 0.65 g). He experienced no immediate major toxicity during the first 48 hours, but a significant rise of pancreatic enzyme activities was observed (amylase at 10 times the upper limit of normal, lipase at 50 times the upper limit of normal) without clinical signs or indications on computed tomography (CT) of pancreatitis. The third day after the overdose, he developed appendicitis, which appeared coincidental; he recovered uneventfully from surgery. Most of the overdose of Sb was eliminated within the first few hours. Pharmacokinetics remained linear; the rapid, long elimination half-lives (2.7 hours and 54 hours, respectively) were similar to those in previously published results. The administration of a chelating agent, dimercaptosuccinic acid (DMSA), 72 hours after the Sb overdose did not modify the pharmacokinetics of the medication.