Median arcuate ligament syndrome: Predictor of ischemic complications?

Median arcuate ligament syndrome (MALS) is a pathologic entity that can affect the celiac axis. Due to the extensive collateral network of mesenteric circulation, stenosis of one mesenteric artery does not lead to significant symptoms. The purpose of this study was to describe multidetector computed tomography (MDCT) angiography findings of celiac artery entrapment by the median arcuate ligament and determine those patients with high risks of ischemic complications. From January 2012 to March 2016, 103 patients with celiac artery (CA) compression by median arcuate ligament were detected. In 23 patients collateral circulation was developed. In order to investigate the problem, we managed to estimate the correlation between range of stenosis of CA and presence of collateral circulation between the celiac artery (CA) and superior mesenteric artery (SMA). A statistically significant correlation was found between range of CA stenosis and collateral circulation presence (Spearman's correlation coefficient 0.339, P < 0.0001). In conclusions, based on our observations, we hypothesize that ischemia as a result of mesenteric vessel narrowing by the median arcuate ligament may occur more often than indicated by clinical symptoms and described in literature. Clin. Anat. 29:1025–1030, 2016. © 2016 Wiley Periodicals, Inc.     

Complex percutaneous extraction of a 15-year-old atrial lead dislodged into the subclavian vein

We present a case of a 50-year-old patient with DDD pacing failure who underwent atrial lead extraction. The lead was implanted 15 years ago, and 4 months ago it dislodged into the subclavian vein following a fracture. The lead was removed via the femoral vein approach using a Cook Medical device (Byrd Femoral Workstation, Dotter basket) and pigtail catheter.     

From the Cover: Loss of phosphatidylinositol 4-kinase 2α activity causes late onset degeneration of spinal cord axons

Phosphoinositide (PI) lipids are intracellular membrane signaling intermediates and effectors produced by localized PI kinase and phosphatase activities. Although many signaling roles of PI kinases have been identified in cultured cell lines, transgenic animal studies have produced unexpected insight into the in vivo functions of specific PI 3- and 5-kinases, but no mammalian PI 4-kinase (PI4K) knockout has previously been reported. Prior studies using cultured cells implicated the PI4K2α isozyme in diverse functions, including receptor signaling, ion channel regulation, endosomal trafficking, and regulated secretion. We now show that despite these important functions, mice lacking PI4K2α kinase activity initially appear normal. However, adult Pi4k2a^GT/GT animals develop a progressive neurological disease characterized by tremor, limb weakness, urinary incontinence, and premature mortality. Histological analysis of aged Pi4k2a^GT/GT animals revealed lipofuscin-like deposition and gliosis in the cerebellum, and loss of Purkinje cells. Peripheral nerves are essentially normal, but massive axonal degeneration was found in the spinal cord in both ascending and descending tracts. These results reveal a previously undescribed role for aberrant PI signaling in neurological disease that resembles autosomal recessive hereditary spastic paraplegia.     

Hepatocyte steatosis in HCV patients promotes fibrosis by enhancing TGF-beta liver expression.

Aim: The objective of this study was to examine the relationship between TGF-beta expression in steatotic liver and the stage and yearly progression rate of fibrosis in chronic hepatitis C (CHC) patients. Methods: We examined 44 CHC fatty liver patients, using 76 non-steatotic CHC patients as controls. The stage of hepatic fibrosis was assessed on a score scale. TGF-beta expression was determined with the use of monoclonal serum and the ABC three-step method. Results: We demonstrated a positive correlation of steatosis with the stage of fibrosis (P < 0.05). No relationship of thiskind was found with the yearly progression rate of fibrosis (P > 0.09). In steatotic biopsies, TGF-beta expression index in portal spaces and lobules was found to be higher as compared to TGF-beta expression in biopsies without steatosis (P < 0.05). Conclusion: In CHC patients steatosis induces the development of fibrosis by elevating the hepatic expression of TGF-beta.