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Three patients were seen with acute mesenteric venous thrombosis. With a transhepatic access, percutaneous pharmacologic thrombolysis was performed in one patient with extensive thrombosis of the portal and mesenteric veins, resulting in complete thrombolysis of the portal vein and partial thrombolysis of the superior mesenteric vein. In two patients with focal thrombosis, the use of mechanical devices achieved complete thrombolysis. Percutaneous thrombolysis of portal and mesenteric veins with a transhepatic approach, followed by coil embolization, is a promising endovascular technique for treatment of symptomatic acute mesenteric venous thrombosis.

Twenty-two patients with malignant biliary obstruction and 21 patients with suspected obstruction of biliary-enteric anastomoses were evaluated over a 12-month period with magnetic resonance (MR) cholangiography and cross-sectional MR imaging. In patients with malignant obstruction, MR cholangiography helped accurately determine the status of the biliary ductal system by identifying the exact location and extent of the obstruction and the severity of duct dilatation. In so doing, MR cholangiography helped determine whether percutaneous transhepatic cholangiography with antegrade stent placement or retrograde cholangiography with stent placement constituted the more suitable treatment. Cross-sectional MR imaging was necessary to identify the organ of tumor origin, define the tumor margins, and determine the stage of disease. This information helped evaluate the appropriateness of curative surgical therapy versus palliative drainage procedures. In patients with biliary-enteric anastomoses, MR cholangiography clearly depicted the site of the anastomosis and demonstrated the status of the intrahepatic ducts, thereby helping determine which patients would benefit from undergoing antegrade duct cannulation with a drainage procedure or perhaps balloon dilation. In some of these patients, MR cholangiography was sufficient to help plan therapeutic intervention. MR cholangiography also demonstrates the presence and size of biliary stones and associated findings such as intraductal tumor growth. In addition, MR cholangiography may obviate retrograde cholangiography, which can be technically difficult to perform.

Antiphospholipid syndrome is characterized by recurrent fetal loss, arterial and venous thromboses, thrombocytopenia and circulating antiphospholipid antibodies. Few patients have a rapidly progressive, fatal outcome. We report two young patients with systemic lupus erythematosus and antiphospholipid antibodies who died after a short course of disease. Although clinical and laboratory findings differed in both patients--small vessel thromboses and microangiopathic hemolytic anemia mimicking thrombotic thrombocytopenic purpura predominated in one of the patients while small and medium size vessel thromboses without hemolysis were present in the other case--autopsy revealed widespread visceral thromboses in both of them, features consistent with a diagnosis of catastrophic antiphospholipid syndrome. This syndrome has not been reported to occur in association with Pneumocistis carinii pneumonia as we describe in one of our patients.

Dehydroepiandrosterone (DHEA) decreases the activity of hepatic tyrosine aminotransferase (TAT), a glucocorticoid-inducible enzyme, in the obese, hypercorticosteronemic Zucker rat. To investigate the mechanism of this antiglucocorticoid action, the effect of exogenous DHEA on hepatic glucocorticoid receptor (GC) number and affinity was quantitated. Food supplementation with DHEA (0.6% w/w) for 1 or 7 days had no effect on either receptor number or affinity in obese Zucker rats. After 28 days, however, DHEA treatment resulted in a nearly 40% decrease in cytosolic hepatic receptor content (Bmax; fmol/mg cytosolic protein) without any change in affinity (Kd) in both lean and obese rats. DHEA treatment for 28 days also resulted in an increased liver size and cytosolic protein content. When the hepatic GC receptor content was normalized based on the change in liver size and protein content, the apparent number of GC binding sites per liver was not affected by DHEA treatment. This observation suggests that DHEA's effect on GC receptor content may not be a specific action and that downregulation of the GC receptor is not the mechanism of DHEA action on GC induced TAT activity. This is supported by the effect of DHEA on obese rat TAT activity in the same experiment where the greatest inhibition occurred after only 1 day of treatment. From these experiments it is concluded that although long-term DHEA treatment may decrease the relative concentration of GC receptors in rat liver, this change is not the mechanism through which DHEA mediates its acute antiglucocorticoid action.

The obese Zucker rat is a model of youth-onset obesity associated with hyperphagia. In this study, dehydroepiandrosterone's effect at decreasing food intake and body weight in the obese Zucker rat was investigated. Rats were treated with a dehydroepiandrosterone-supplemented diet (0.0, 0.06, 0.15, 0.3, or 0.6%) for 7 days. The 0.3 and 0.6% treatment groups showed a dramatic decrease in daily food intake, which was evident the 1st day. In addition to the reduction in food intake, body weight changes also were affected significantly in the high-dose treatment groups. The possibility that these dehydroepiandrosterone-induced changes were correlated to perturbations in central neurotransmitter levels associated with appetite control was investigated. The hypothalamus, frontal cortex, striatum, and hippocampus of dehydroepiandrosterone-treated animals were assayed for neurotransmitters known to have inhibitory or stimulatory effects on feeding behavior (serotonin, dopamine, norepinephrine, and epinephrine). Significant differences from steroid-free controls were noted only in the levels of hypothalamic serotonin in animals treated with dehydroepiandrosterone. Serotonin in the hypothalamus has been shown to decrease feeding behavior. The magnitude of dehydroepiandrosterone's effect on hypothalamic serotonin correlated with its effect on feeding behavior. Thus, dehydroepiandrosterone may reduce hyperphagia by altering hypothalamic levels of serotonin.

The uterine atony are the most common cause of postpartum hemorrhage. Manual compression and pharmacologic methods are usually used with a successful result. When pharmacologic methods fail to control hemorrhage from atony, surgical measures should be undertaken to arrest the bleeding before it becomes life-threatening. We presents the utilization of electrical uterine defibrillation in two cases with acute hemorrhage confirming the effectivity of the proceeding.