Luis Rodrigo

Prof. Luis Rodrigo

Hospital Universitario Central de Asturias, Gastroenterology, Oviedo. SPAIN
+2
orcid

Research Focus & Metrics

Academic Career Length

51Years (1976-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 August 2005 in Gastroenterology
Verified
Journal Article
Closed access
RARaul J. Andrade
Raul J. Andrade
Mª Isabel LucenaMª Isabel Lucena
Mª Isabel Lucena
MFM Carmen Fernández
M Carmen Fernández
GPGloria Pelaez
Gloria Pelaez
KPKetevan Pachkoria
Ketevan Pachkoria
SDSpanish Group for the Study of Drug-Induced Liver Disease
Spanish Group for the Study of Drug-Induced Liver Disease

1 January 1997 in Journal of Hepatology
Verified
Journal Article
Closed access
BSBasilio Soto
Basilio Soto
ASArmandó Sánchez-Quijano
Armandó Sánchez-Quijano
Luis RodrigoLuis Rodrigo
Luis Rodrigo
JOJuan Angel del Olmo
Juan Angel del Olmo
MGManuel García-Bengoechea
Manuel García-Bengoechea
ELEduardo Lissen
Eduardo Lissen

5 May 2009 in American Journal of Gastroenterology
Verified
Journal Article
Closed access
ALAngel Lanas
Angel Lanas
LGLuis A García-Rodríguez
Luis A García-Rodríguez
MPMónica Polo-Tomás
Mónica Polo-Tomás
MPMarta Ponce
Marta Ponce
IAInmaculada Alonso-Abreu
Inmaculada Alonso-Abreu
SGSantiago Garcia
Santiago Garcia
The American Journal of Gastroenterology is published by Nature Publishing Group (NPG) on behalf of the American College of Gastroenterology (ACG). Ranked the #1 clinical journal covering gastroenterology and hepatology*, The American Journal of Gastroenterology (AJG) provides practical and professional support for clinicians dealing with the gastroenterological disorders seen most often in patients. Published with practicing clinicians in mind, the journal aims to be easily accessible, organizing its content by topic, both online and in print. www.amjgastro.com, *2007 Journal Citation Report (Thomson Reuters, 2008)

10 May 2006 in Gut
Verified
Journal Article
Closed access
ALAngel Lanas
Angel Lanas
LGL A García-Rodríguez
L A García-Rodríguez
MAM T Arroyo
M T Arroyo
FGF Gomollón
F Gomollón
FFF Feu
F Feu
JPJ M Piqué
J M Piqué
Background: The risks and benefits of coxibs, non-steroidal anti-inflammatory drugs (NSAIDs), and aspirin treatment are under intense debate. Objective: To determine the risk of peptic ulcer upper gastrointestinal bleeding (UGIB) associated with the use of coxibs, traditional NSAIDs, aspirin or combinations of these drugs in clinical practice. Methods: A hospital-based, case–control study in the general community of patients from the National Health System in Spain. The study included 2777 consecutive patients with endoscopy-proved major UGIB because of the peptic lesions and 5532 controls matched by age, hospital and month of admission. Adjusted relative risk (adj RR) of UGIB determined by conditional logistic regression analysis is provided. Results: Use of non-aspirin-NSAIDs increased the risk of UGIB (adj RR 5.3; 95% confidence interval (CI) 4.5 to 6.2). Among non-aspirin-NSAIDs, aceclofenac (adj RR 3.1; 95% CI 2.3 to 4.2) had the lowest RR, whereas ketorolac (adj RR 14.4; 95% CI 5.2 to 39.9) had the highest. Rofecoxib treatment increased the risk of UGIB (adj RR 2.1; 95% CI 1.1 to 4.0), whereas celecoxib, paracetamol or concomitant use of a proton pump inhibitor with an NSAID presented no increased risk. Non-aspirin antiplatelet treatment (clopidogrel/ticlopidine) had a similar risk of UGIB (adj RR 2.8; 95% CI 1.9 to 4.2) to cardioprotective aspirin at a dose of 100 mg/day (adj RR 2.7; 95% CI 2.0 to 3.6) or anticoagulants (adj RR 2.8; 95% CI 2.1 to 3.7). An apparent interaction was found between low-dose aspirin and use of non-aspirin-NSAIDs, coxibs or thienopyridines, which increased further the risk of UGIB in a similar way. Conclusions: Coxib use presents a lower RR of UGIB than non-selective NSAIDs. However, when combined with low-dose aspirin, the differences between non-selective NSAIDs and coxibs tend to disappear. Treatment with either non-aspirin antiplatelet or cardioprotective aspirin has a similar risk of UGIB.

1 March 2003 in Hepatology
Verified
Journal Article
Closed access
PDF file
RVRosario F Velázquez
Rosario F Velázquez
RFRosario F.
Rosario F.
MRManuel Rodríguez
Manuel Rodríguez
NANavascués
Navascués
CACarmen A.
Carmen A.
Luis RodrigoLuis Rodrigo
Luis Rodrigo
Better knowledge of the risk factors associated with the appearance of hepatocellular carcinoma (HCC) could improve the efficacy of surveillance programs. A total of 463 patients aged 40 to 65 years with liver cirrhosis in Child–Pugh class A or B were included in a program of early diagnosis. The predictive value of different risk factors was evaluated using the Kaplan–Meier method and Cox regression model. Thirty–eight patients developed HCC. In the multivariate analysis, 4 variables showed an independent predictive value for the development of HCC: age 55 years or older, antibody to hepatitis C virus (anti–HCV) positivity, prothrombin activity 75% or less, and platelet count less than 75 × 103/mm3. According to the contribution of each of these factors to the final model, a score ranging between 0 and 4.71 points was constructed to allow the division of patients into 2 different risk groups. The low–risk group included those with a score of 2.33 points or less (n = 270; 4 with HCC; cumulative incidence of HCC at 4 years, 2.3%), and the high–risk group included those with a score greater than 2.33 (n = 193; 34 with HCC; cumulative incidence of HCC at 4 years, 30.1%) (P= .0001). In conclusion, a simple score made up of 4 clinical and biological variables allowed us to distinguish 2 groups of cirrhotic patients at high and low risk for the development of HCC. We believe this score can be useful in establishing a subset of cirrhotic patients in whom a surveillance program for early detection of HCC could be unjustified.

20 February 2016 in Nutrition & Metabolism
Verified
Journal Article
Open access
PDF file
NKNazarii Kobyliak
Nazarii Kobyliak
Caterina ConteCaterina Conte
Caterina Conte
GCGiovanni Cammarota
Giovanni Cammarota
AHAndreana P. Haley
Andreana P. Haley
ISIgor Styriak
Igor Styriak
Peter KruzliakPeter Kruzliak
Peter Kruzliak
The worldwide prevalence of obesity more than doubled between 1980 and 2014. The obesity pandemic is tightly linked to an increase in energy availability, sedentariness and greater control of ambient temperature that have paralleled the socioeconomic development of the past decades. The most frequent cause which leads to the obesity development is a dysbalance between energy intake and energy expenditure. The gut microbiota as an environmental factor which influence whole-body metabolism by affecting energy balance but also inflammation and gut barrier function, integrate peripheral and central food intake regulatory signals and thereby increase body weight. Probiotics have physiologic functions that contribute to the health of gut microbiota, can affect food intake and appetite, body weight and composition and metabolic functions through gastrointestinal pathways and modulation of the gut bacterial community.