Background:
Dexlansoprazole has been shown to be efficacious for the treatment of gastroesophageal reflux disease. However, there is a paucity of data about its efficacy for Helicobacter pylori ...eradication. The aim of this study was to evaluate the efficacy of dexlansoprazole for H. pylori eradication as triple therapy in real-world practice.
Methods:
Adult patients with endoscopically proven H. pylori related peptic ulcer diseases or gastritis were recruited for this study. The eradication status was assessed based on the results of the 13C-urea breath test performed 4 weeks after treatment. According to the different treatment regimens, the patients were allocated to group A: Esomeprazole 40 mg b.i.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d. for 7 days; group B: Esomeprazole 40 mg q.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d. for 7 days, or group C: Dexlansoprazole 60 mg q.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d. for 7 days.
Results:
A total of 215 patients (49% males) were enrolled in this study, with a mean age of 55 years. The eradication rates in group A, B, and C were 94.7% (71/75), 89.6% (69/77), and 93.7% (59/63) (p = 0.457), respectively. The adverse events were similar between the three groups (p = 0.068).
Conclusions:
This study suggests that dexlansoprazole-based triple therapy has an acceptable eradication rate for H. pylori infection.
OBJECTIVES:Because administration of 17β-estradiol following trauma-hemorrhage improves cardiovascular responses, we investigated whether the salutary effects of 17β-estradiol on cardiac function are ...mediated via Akt-dependent heme oxygenase-1 up-regulation under those conditions.
DESIGN:Experimental animal study.
SETTING:University laboratory.
SUBJECTS:Male Sprague-Dawley rats.
INTERVENTIONS:Rats underwent trauma-hemorrhage (mean blood pressure ∼40 mm Hg for 90 mins) followed by fluid resuscitation. Before resuscitation, rats received either vehicle, 17β-estradiol (1 mg/kg), or 17β-estradiol plus the phosphoinositide 3-kinase inhibitor wortmannin (1 mg/kg). At 2 hrs after trauma-hemorrhage or sham operation, the rats were killed.
MEASUREMENTS AND MAIN RESULTS:Cardiac function, heart tissue myeloperoxidase activity, cardiac and circulatory cytokine levels, cardiac intercellular adhesion molecule-1, and chemokine levels were measured. Cardiac Akt and heme oxygenase-1 were also determined. We found that 17β-estradiol prevented the trauma-hemorrhage-induced impairment in cardiac function and increase in cardiac myeloperoxidase activity. Cardiac and systemic interleukin-6 and tumor necrosis factor-α levels as well as cardiac intercellular adhesion molecule-1, cytokine-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 contents were increased following trauma-hemorrhage, which were normalized by 17β-estradiol. Administration of 17β-estradiol following trauma-hemorrhage restored cardiac Akt phosphorylation and further increased heme oxygenase-1 expression. Coadministration of wortmannin following trauma-hemorrhage abolished the previous effects by 17β-estradiol.
CONCLUSIONS:These results suggest that the 17β-estradiol-meditated improvement in cardiac function following trauma-hemorrhage occurs via Akt-dependent heme oxygenase-1 up-regulation.
Background: Concurrent acute cholecystitis and acute cholangitis is a unique clinical situation. We tried to investigate the optimal timing of cholecystectomy after adequate biliary drainage under ...this condition. Methods: From January 2012 to November 2017, we retrospectively screened all in-hospitalized patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) and then identified patients with concurrent acute cholecystitis and acute cholangitis from the cohort. The selected patients were stratified into two groups: one-stage intervention (OSI) group (intended laparoscopic cholecystectomy at the same hospitalization) vs. two-stage intervention (TSI) group (interval intended laparoscopic cholecystectomy). Interrogated outcomes included recurrent biliary events, length of hospitalization, and surgical outcomes. Results: There were 147 patients ultimately enrolled for analysis (OSI vs. TSI, 96 vs. 51). Regarding surgical outcomes, there was no significant difference between the OSI group and TSI group, including intraoperative blood transfusion (1.0% vs. 2.0%, p = 1.000), conversion to open procedure (3.1% vs. 7.8%, p = 0.236), postoperative complication (6.3% vs. 11.8%, p = 0.342), operation time (118.0 min vs. 125.8 min, p = 0.869), and postoperative days until discharge (3.37 days vs. 4.02 days, p = 0.643). In the RBE analysis, the OSI group presented a significantly lower incidence of overall RBE (5.2% vs. 41.2%, p < 0.001) than the TSI group. Conclusions: Patients with an initial diagnosis of concurrent acute cholecystitis and cholangitis undergoing cholecystectomy after ERCP drainage during the same hospitalization period may receive some benefit in terms of clinical outcomes.
Cytomegalovirus (CMV) colitis typically presents in immunocompromised and inflammatory bowel disease (IBD) patients. Several studies have been conducted on the endoscopic characteristics of CMV ...colitis in IBD patients.
The endoscopic findings of CMV colitis in non-IBD patients and their relationship with inhospital mortality are unclear. We aimed to describe the endoscopic presentation in these patients and to determine the endoscopic predictors of inhospital mortality.
Patients with CMV colitis diagnosed using histology between April 2002 and December 2016 at the Linkou Chang Gung Memorial Hospital, Taiwan, were retrospectively enrolled. Patients diagnosed with IBD during follow-up were excluded. Patient data, including underlying diseases, endoscopic presentation, laboratory data, clinical course, complications, and clinical outcomes, were collected. The independent risk factors for inhospital mortality were analyzed with logistic regression. The difference of overall survival was compared using Kaplan-Meier survival curve and log rank test. All statistical calculations were performed using SPSS software, version 21.
Sixty-nine patients were enrolled, and 8 IBD patients were excluded. Within the 61 non-IBD patients, 31 were diagnosed by colonoscopy and others by sigmoidoscopy. Ulceration (77%) was the most common endoscopic finding, followed by a cobblestone appearance (19.7%), colitis with/without erosions (9.8%), pseudomembrane (9.8%), and tumor/polyp-like lesions (8.2%). Among the patients who underwent full-length colonoscopy, 35.3% presented with right-sided colitis, 23.5% with left-sided colitis, and 32.4% with pancolitis. Pancolitis was identified as a negative predictor of inhospital mortality (odds ratio, 6.8; 95% confidence interval, 1.233-37.497;
=0.028) and overall survival (log rank
=0.018).
Colonoscopy is recommended for precise CMV colitis diagnosis and outcome prediction in non-IBD patients.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Cholangiocarcinoma (CCA) is a devastating disease without effective treatments. 1α,25(OH)2D3, the active form of Vitamin D, has emerged as a new anti-cancer regimen. However, the side effect of ...hypercalcemia impedes its systemic administration. 25(OH)D is biologically inert and needs hydroxylation by CYP27B1 to form 1α,25(OH)2D3, which is originally believed to only take place in kidneys. Recently, the extra-renal expression of CYP27B1 has been identified and in vitro conversion of 25(OH)D to 1α,25(OH)2D3 has been found in some cancer cells with CYP27B1 expression. In this study, CYP27B1 expression was demonstrated in CCA cells and human CCA specimens. 25(OH)D effectively represses SNU308 cells growth, which was strengthened or attenuated as CYP27B1 overexpression or knockdown. Lipocalcin-2 (LCN2) was also found to be repressed by 25(OH)D. After treatment with 800 ng/mL 25(OH)D, the intracellular 1α,25(OH)2D3 concentration was higher in SNU308 cells with CYP27B1 overexpression than wild type SNU308 cells. In a xenograft animal experiment, 25(OH)D, at a dose of 6 μg/kg or 20 μg/kg, significantly inhibited SNU308 cells’ growth without inducing obvious side effects. Collectively, our results indicated that SNU308 cells were able to convert 25(OH)D to 1α,25(OH)2D3 and 25(OH)D CYP27B1 gene therapy could be deemed as a promising therapeutic direction for CCA.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
1 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama; and 2 Department of Sugery, Chang Gung Memorial Hospital, Chang Gung University ...College of Medicine, Taoyuan, Taiwan
Submitted 4 April 2008
; accepted in final form 14 July 2008
Although trauma-hemorrhage produces tissue hypoxia, systemic inflammatory response and organ dysfunction, the mechanisms responsible for these alterations are not clear. Using a potent selective inducible nitric oxide (NO) synthase inhibitor, N -3-(aminomethyl) benzylacetamidine (1400W), and a nonselective NO synthase inhibitor, N G -nitro- L -arginine methyl ester ( L -NAME), we investigated whether inducible NO synthase plays any role in producing hepatic injury, inflammation, and changes of protein expression following trauma-hemorrhage. To investigate this, male Sprague-Dawley rats were subjected to midline laparotomy and hemorrhagic shock (mean blood pressure 35–40 mmHg for 90 min) followed by fluid resuscitation. Animals were treated with either vehicle (DMSO) or 1400W (10 mg/kg body wt ip), or L -NAME (30 mg/kg iv), 30 min before resuscitation and killed 2 h after resuscitation. Trauma-hemorrhage/resuscitation induced a marked hypotension and increase in markers of hepatic injury (i.e., plasma -glutathione S -transferase, tissue myeloperoxidase activity, and nitrotyrosine formation). Hepatic expression of iNOS, hypoxia-inducible factor-1 , ICAM-1, IL-6, TNF- , and neutrophil chemoattractant (cytokine-induced neutrophil chemoattractant-1 and macrophage inflammatory protein-2) protein levels were also markedly increased following trauma-hemorrhage/resuscitation. Administration of the iNOS inhibitor 1400W significantly attenuated hypotension and expression of these mediators of hepatic injury induced by trauma-hemorrhage/resuscitation. However, administration of L -NAME could not attenuate hepatic dysfunction and tissue injury mediated by trauma-hemorrhage, although it improved mean blood pressure as did 1400W. These results indicate that increased expression of iNOS following trauma-hemorrhage plays an important role in the induction of hepatic damage under such conditions.
hypoxia-inducible factor-1 ; myeloperoxidase activity; cytokine; chemokine
Address for reprint requests and other correspondence: I. H. Chaudry, Center for Surgical Research, Univ. of Alabama at Birmingham, 1670 Univ. Blvd., G094 Volker Hall, Birmingham, AL 35294-0019 (e-mail: Irshad.Chaudry{at}ccc.uab.edu )
Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama
Submitted 14 February 2008
; accepted in final form 16 April 2008
p38 MAPK has been ...reported to regulate the inflammatory response in various cell types via extracellular stimuli. p38 MAPK activation also results in the induction of heme oxygenase (HO)-1, which exerts potent anti-inflammatory effects. Although studies have shown that 17β-estradiol (E 2 ) prevented organ dysfunction following trauma-hemorrhage, it remains unknown whether p38 MAPK/HO-1 plays any role in E 2 -mediated attenuation of intestinal injury under those conditions. To study this, male rats underwent trauma-hemorrhage (mean blood pressure 40 mmHg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, E 2 (1 mg/kg body wt), the p38 MAPK inhibitor SB-203580 (2 mg/kg body wt) or E 2 plus SB-203580. Two hours thereafter, intestinal myeloperoxidase (MPO) activity and lactate, TNF- , IL-6, ICAM-1, cytokine-induced neutrophil chemoattractant (CINC)-1, and macrophage inflammatory protein (MIP)-2 levels were measured. Intestinal p38 MAPK and HO-1 protein levels were also determined. Trauma-hemorrhage led to an increase in intestinal MPO activity and lactate, TNF- , IL-6, ICAM-1, CINC-1, and MIP-2 levels. This was accompanied with a decrease in intestinal p38 MAPK activity and increase in HO-1 expression. Administration of E 2 normalized all the above parameters except HO-1, which was further increased following trauma-hemorrhage. Administration of SB-203580 with E 2 abolished the E 2 -mediated restoration of the above parameters as well as the increase in intestinal HO-1 expression following trauma-hemorrhage. These results suggest that the p38 MAPK/HO-1 pathway plays a critical role in mediating the salutary effects of E 2 on shock-induced intestinal injury.
p38 MAPK inhibitor; CINC-1; MIP-2; MPO
Address for reprint requests and other correspondence: I. H. Chaudry, Center for Surgical Research, Univ. of Alabama at Birmingham, G094 Volker Hall, 1670 Univ. Blvd., Birmingham, AL 35294-0019 (e-mail: irshad.chaudry{at}ccc.uab.edu )
AIM:To establish the prognosis and feasibility of en-bloc vascular resection of stage pancreatic adenocarcinoma of the head and uncinate process.METHODS:We retrospectively analyzed 87 patients with ...stage pancreatic adenocarcinoma,who were subjected to pancreaticoduodenectomy (PD) and pylo-rus-preserving PD (PPPD) between 1996 and 2006 in Chang Gung Memorial Hospital,Taiwan. Twelve and 75 patients underwent PD/PPPD with and without resection of portal vein/superior mesenteric vein (PV/SMV),respectively.RESUL...
Cancer treatment in female adolescent and young adult (AYA) cancer survivors (i.e., those diagnosed between 15 and 39 years of age) may adversely affect multiple bodily functions, including the ...reproductive system.
We initially assembled a retrospective, nationwide population-based cohort study by linking data from two nationwide Taiwanese data sets. We subsequently identified first pregnancies and singleton births to AYA cancer survivors (2004-2018) and select AYA without a previous cancer diagnosis matched to AYA cancer survivors for maternal age and infant birth year.
The study cohort consisted of 5151 and 51,503 births to AYA cancer survivors and matched AYA without a previous cancer diagnosis, respectively. The odds for overall pregnancy complications (odds ratio OR, 1.09; 95% confidence interval CI, 1.01-1.18) and overall adverse obstetric outcomes (OR, 1.07; 95% CI, 1.01-1.13) were significantly increased in survivors compared with matched AYA without a previous cancer diagnosis. Specifically, cancer survivorship was associated with an increased risk of preterm labour, labour induction, and threatened abortion or threatened labour requiring hospitalisation.
AYA cancer survivors are at increased risk for pregnancy complications and adverse obstetric outcomes. Efforts to integrate individualised care into clinical guidelines for preconception and prenatal care should be thoroughly explored.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Abstract Background Despite advances in intensive care medicines, hemorrhagic shock leading to multiple organ failure remains the major causes of death in the injured host. Although studies have ...shown that 17β-estradiol (E2) prevents trauma-hemorrhage-induced lung damage, it remains unknown whether protein kinase B (Akt)/heme oxygenase (HO)-1 plays any role in E2-mediated lung protection after trauma-hemorrhage. Materials and methods After a 5-cm midline laparotomy, male rats underwent hemorrhagic shock (mean blood pressure ∼40 mm Hg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, E2 (1 kg/mg), E2 plus phosphoinositide 3-kinase inhibitor LY294002 (5 mg/kg), or LY294002. At 2 h after trauma-hemorrhage or sham operation, lung tissue myeloperoxidase activity, wet-to-dry-weight ratio, inflammatory mediators, and apoptosis were measured. Lung Akt, HO-1, and cleaved caspase-3 protein levels were also determined. Results E2 attenuated the trauma-hemorrhage-induced increase in lung myeloperoxidase activity, edema formation, inflammatory mediator levels, and apoptosis, which was blocked by co-administration of LY294002. Administration of E2 normalized lung Akt phosphorylation and further increased HO-1 expression and decreased cleaved caspase-3 levels after trauma-hemorrhage. Co-administration of LY294002 prevented the E2-mediated attenuation of shock-induced lung injury. Conclusions Our results collectively suggest that Akt-dependent HO-1 upregulation may play a critical role in E2-meditated lung protection after trauma-hemorrhage.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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