VA Collaborative Study of Liver Disease in Drug Addicts: Preliminary Report

2015 ◽  
pp. 167-169
Author(s):  
L. B. Seeff ◽  
H. J. Zimmerman ◽  
E. C. Wright ◽  
E. R. Schiff ◽  
C. H. Tamburro ◽  
...  
2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22183-e22183
Author(s):  
F. Perazzo ◽  
V. Denninghoff ◽  
G. Pasccon ◽  
M. G. Pallotta ◽  
M. Tatangelo ◽  
...  

e22183 Background: Several studies have suggested that KRAS somatic mutations predict resistance to Cetuximab treatment in colorectal cancers. The aim of this report is to present the mutational status of KRAS, BRAF and epidemiological data of an Argentinean population of CR tumors which may have future clinical practice implications. Methods: Patients were prospectively selected from the databases of 8 Argentinean public and private hospitals with colorectal cancer between January and December 2008. We analyzed the presence of KRAS point mutations in codons 12 and 13, and the BRAF-V600E from formalin fixed sections with Polymerase Chain Reaction (PCR) amplification-sequencing. Results: A total of 146 patients, 41.8% (61) F and 57.2% (85) M, with a median age of 58.1 years (range, 17–88), 45.2% (66) were current smokers, 50% (73) never smoke. 41.4% (60) have family history of cancer and 9.6% (14) have personal history of a previous tumor. 63.2% were European Caucasian, 30.3% American Caucasian and 0.7% of Asian origin. The media BMI was 25.9 (range, 16- 47). The primary tumor site was 21.9% (32) right colon, 5.5% (8) transverse colon, 45.2% (66) left colon and 27.4%(40) rectal cancer. Adenocarcinoma was the unique histotype and mucinous differentiation was observed in 14.7% (21). The Pathological Stage at diagnosis was Stage I 3.42% (5), II 24% (35), III 33.6% (49) and IV 39% (57). 60.3% (88) where found to be wild type, while the other 39.7% (58) showed the KRAS mutation in the following amino acids: GLY12ALA 5.2% (3), GLY12ASP 25.9% (15), GLY12CYS 3.4% (2), GLY12SER 1.7% (1), GLY12VAL 62.1 % (36), GLY13ARG 1.7% (1). We analyzed in 49 patients the mutational status of BRAF-V600E, only 2 patients showed the presence of both mutations, 23 presented BRAF and KRAS wild type, 20 had a KRAS mutation while the BRAF was wild type, only 4 patients reveled a mutation of BRAF in the presence of a KRAS wild type. Conclusions: This is the first Argentinean collaborative study of the mutational status of KRAS and BRAF. Our preliminary report based in 146 patients, revealed similar mutational KRAS results in codon 12 and 13 than the reports of Europe. This is probably due to the ethnic origin of Argentinean population. No significant financial relationships to disclose.


2018 ◽  
Vol 37 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Roger F. Butterworth ◽  
Ali Canbay

Background: Non-alcoholic fatty liver disease (NAFLD) is the leading chronic hepatic condition worldwide and new approaches to management and treatment are limited. Summary: L-ornithine L-aspartate (LOLA) has hepatoprotective properties in patients with fatty liver of diverse etiology and results of a multicenter randomized clinical trial reveal that 12 weeks treatment with oral LOLA (6–9 g/d) results in a dose-related reduction in activities of liver enzymes and triglycerides together with significant improvements of liver/spleen CT ratios. A preliminary report described improvements of hepatic microcirculation in patients with non-alcoholic steatohepatitis (NASH) following treatment with LOLA. Mechanisms responsible for the beneficial effects of LOLA in NAFLD/NASH involve, in addition to its established ammonia-lowering effect, metabolic transformations of the LOLA-constituent amino acids L-ornithine and L-aspartate into L-glutamine, L-arginine, and glutathione. These metabolites have well-established actions implicated in the prevention of lipid peroxidation, improvement of hepatic microcirculation in addition to anti-inflammatory, and anti-oxidant properties. Key Messages: (1) LOLA is effective for the treatment of key indices in NAFLD/NASH. (2) Mechanisms other than LOLA’s ammonia-lowering action have been postulated. (3) Further assessments in the clinical setting are now required.


1997 ◽  
Vol 25 (3) ◽  
pp. 301-306 ◽  
Author(s):  
James E. Heubi ◽  
James V. Higgins ◽  
Eric A. Argao ◽  
Rosa I. Sierra ◽  
Bonny L. Specker

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