The efficiency of Gd‐EOB‐DTPA‐enhanced magnetic resonance cholangiography in living donor liver transplantation: a preliminary study

The aim of this study was to evaluate utility of gadoxetic acid disodium (Gd‐EOB‐DTPA)‐enhanced magnetic resonance cholangiography (MRC) for the detection of biliary complications after living donor liver transplantation (LDLT). A total of 18 patients with suspected biliary complications underwent MRC. T2‐weighted MRC and contrast‐enhanced MRC (CE‐MRC) were used to identify the biliary complications. MRC included routine breath‐hold T2‐weighted MRC using half‐Fourier acquisition single‐shot turbo spin‐echo (HASTE) sequences and Gd‐EOB‐DTPA‐enhanced MRC T1‐weighted volumetric interpolated breath‐hold examination (VIBE) sequences. Before confirming the biliary complications, one observer reviewed the MRC images and the CE‐MRC images separately. The verification procedures and MRC findings were compared, and the sensitivity, specificity, and accuracy of both techniques were calculated for the identification of biliary complications. The observer found six of seven biliary complications using CE‐MRC. The sensitivity was 85.7% and the accuracy was 94.4%. Using MRC alone, sensitivity was 57.1% and accuracy was 55.5%. The accuracy of Gd‐EOB‐DTPA‐enhanced MRC was superior to MRC in locating biliary leaks (p < 0.05). The usage of Gd‐EOB‐DTPA‐enhanced MRC yields information that complements the MRC findings that improve the identification of biliary complications. We recommend the use of MRC in addition to Gd‐EOB‐DTPA‐enhanced MRC to increase the preoperative accuracy when assessing the biliary complications after LDLT.     

Spontaneous external jugular vein pseudoaneurysm treated by thrombin injection: Case report and literature review

Although external jugular vein (EJV) aneurysms are infrequent, regardless of etiology, spontaneous pseudoaneurysms (PAs) are extremely rare and generally require surgery. We describe a case of spontaneous PA of the EJV, which was successfully treated by percutaneous thrombin injection.     

Hormone Replacement Therapy Shortens QT Dispersion in Healthy Postmenopausal Women

Background: The aim of the study was to investigate the effects of hormone replacement therapy (HRT) on myocardial repolarization characteristics in postmenopausal women without coronary artery disease. Methods: Fifty‐one consecutive healthy postmenopausal women (age 48 ±; 5) with negative exercise stress testing were prospectively enrolled into the study. Standard 12‐lead electrocardiograms were obtained to evaluate the effects of 6 months of HRT on QT intervals, corrected QT intervals (QTcmax and QTcmin), QT dispersion (QTd), and corrected QTd (QTcd). Hormone regimens were continuous 0.625 mg/day conjugated equine estrogen (CEE) plus 2.5 mg/day medroxyprogesterone acetate (MPA) or 0.625 mg/day CEE alone depending on the hysterectomy status. Results: Although not statistically significant, CEE alone or in combination with MPA increased QTmax and QTmin values. However, the increase in QTmin was greater than the increase in QTmax, which resulted in statistically significant shortening of QTd (P = 0.007 in CEE and P < 0.001 in CEE + MPA groups). There was a significant prolongation of QTcmin values after 6 months in patients assigned to the CEE group (P = 0.001). The QTcd values were significantly shortened by HRT with both regimens (for CEE group 49 ±; 13 ms vs 38 ±; 13 ms, P = 0.01; for CEE + MPA group 49 ±; 14 ms vs 36 ±; 13, P < 0.001). Conclusion: HRT significantly decreased the QTd and QTcd in postmenopausal women without coronary artery disease, independent of the addition of MPA to the regimen. This improvement in myocardial repolarization may be one of the mechanisms of the favorable effects of HRT on cardiovascular system. However, the clinical implications of the shortening of QTd in postmenopausal women with HRT must be clarified. A.N.E. 2001; 6(3):193–197     

Rescue of defective G protein–coupled receptor function in vivo by intermolecular cooperation

G protein–coupled receptors (GPCRs) are ubiquitous mediators of signaling of hormones, neurotransmitters, and sensing. The old dogma is that a one ligand/one receptor complex constitutes the functional unit of GPCR signaling. However, there is mounting evidence that some GPCRs form dimers or oligomers during their biosynthesis, activation, inactivation, and/or internalization. This evidence has been obtained exclusively from cell culture experiments, and proof for the physiological significance of GPCR di/oligomerization in vivo is still missing. Using the mouse luteinizing hormone receptor (LHR) as a model GPCR, we demonstrate that transgenic mice coexpressing binding-deficient and signaling-deficient forms of LHR can reestablish normal LH actions through intermolecular functional complementation of the mutant receptors in the absence of functional wild-type receptors. These results provide compelling in vivo evidence for the physiological relevance of intermolecular cooperation in GPCR signaling.