Enric Domingo

University of Oxford, Oxford, England, United Kingdom

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Publications (131)848.95 Total impact

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    Juan C Grignola · Enric Domingo
    European Respiratory Journal 06/2015; 45(6):1756-8. DOI:10.1183/09031936.00023015 · 7.13 Impact Factor
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    ABSTRACT: BRAF mutant colorectal cancer carries a poor prognosis which is thought to be related to poor response to conventional chemotherapy. BRAF mutation is associated with the serrated tumour phenotype. We hypothesised that one of the mechanisms by which BRAF mutant colorectal cancer demonstrate poor outcomes with chemotherapy is abnormal gene methylation. The Cancer Genome Atlas (TCGA) methylation data was analysed using a linear regression model with BRAF mutation as an independent variable. Expression datasets were also obtained to correlate functional changes. Top differentially methylated probes were taken forward for validation by methylation pyrosequencing. These probes were analysed on a cohort of patients enriched for BRAF mutations taken from the VICTOR and QUASAR2 studies. In an analysis of 91 tumours (9 BRAF mutant, 82 wild type), the Illumina probe cg11835197 was the probe identified as top differentially methylated (p = 2.56×10-7, Bayes Factor (BF) =6.54). This probe covered a region -413bp from the promoter region of TFAP2E. We found a complex pattern of CpG specific methylation of this region which was associated with both overall (p=0.044) and disease free (p=0.046) survival. BRAF mutant tumours may attain part of their chemoresistance from abnormal TFAP2E methylation, which has not previously been described.
    01/2015; 2(5):508-516.
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    ABSTRACT: A 63-year-old male patient with a history of stent implantation in the left anterior descending three months before. Due to the presentation of vegetative symptoms, he was referred for gated-SPECT myocardial perfusion. During acquisition of the resting images he presented chest pain and ST segment elevation, so that urgent cardiac catheterization was performed, showing stent thrombosis. Rest perfusion imaging showed a defect in anterior and apical perfusion, more severe and extensive than in the stress images, with striking left ventricular dilatation and a fall in the ejection fraction related to the acute ischemia phenomenon. Intense exercise is associated with a transient activation of the coagulation system and hemodynamic changes that might induce thrombosis, especially in recently implanted coronary stents that probably still have not become completely endothelialized.
    Revista Española de Medicina Nuclear e Imagen Molecular 08/2014; 34(2). DOI:10.1016/j.remnie.2015.01.002 · 0.86 Impact Factor
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    ABSTRACT: A 63-year-old male patient with a history of stent implantation in the left anterior descending three months before. Due to the presentation of vegetative symptoms, he was referred for gated-SPECT myocardial perfusion. During acquisition of the resting images he presented chest pain and ST segment elevation, so that urgent cardiac catheterization was performed, showing stent thrombosis. Rest perfusion imaging showed a defect in anterior and apical perfusion, more severe and extensive than in the stress images, with striking left ventricular dilatation and a fall in the ejection fraction related to the acute ischemia phenomenon. Intense exercise is associated with a transient activation of the coagulation system and hemodynamic changes that might induce thrombosis, especially in recently implanted coronary stents that probably still have not become completely endothelialized.
    Revista Española de Medicina Nuclear e Imagen Molecular 08/2014; 34(2). DOI:10.1016/j.remn.2014.07.005 · 0.86 Impact Factor
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    ABSTRACT: The angiogenic capability of colorectal carcinomas (CRC), and their susceptibility to anti-angiogenic therapy, is determined by expression of vascular endothelial growth factor (VEGF) isoforms. The intracellular protein T-cell Intracellular Antigen (TIA-1) alters post-transcriptional RNA processing and binds VEGF-A mRNA. We therefore tested the hypothesis that TIA-1 could regulate VEGF-A isoform expression in colorectal cancers. TIA-1 and VEGF-A isoform expression was measured in colorectal cancers and cell lines. We discovered that an endogenous splice variant of TIA-1 encoding a truncated protein, short TIA-1 (sTIA-1) was expressed in CRC tissues and invasive K-Ras mutant colon cancer cells and tissues but not in adenoma cell lines. sTIA-1 was more highly expressed in CRC than in normal tissues and increased with tumour stage. Knockdown of sTIA-1 or over-expression of full length TIA-1 (flTIA-1) induced expression of the anti-angiogenic VEGF isoform VEGF-A165b. Whereas flTIA-1 selectively bound VEGF-A165 mRNA and increased translation of VEGF-A165b, sTIA-1 prevented this binding. In nude mice, xenografted colon cancer cells over-expressing flTIA-1 formed smaller, less vascular tumours than those expressing sTIA-1, but flTIA-1 expression inhibited the effect of anti-VEGF antibodies. These results indicate that alternative splicing of an RNA binding protein can regulate isoform specific expression of VEGF providing an added layer of complexity to the angiogenic profile of colorectal cancer and their resistance to anti-angiogenic therapy.
    Molecular Oncology 08/2014; 9(1). DOI:10.1016/j.molonc.2014.07.017 · 5.94 Impact Factor
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    ABSTRACT: Treatment of pulmonary arterial hypertension has achieved significant progress over the past 20 years. Currently, 3 groups of drugs have proven useful for the treatment of this disease: endothelin receptor antagonist, phosphodiesterase inhibitors and prostacyclin and its analogues. It is recommended to initiate treatment with one of these drugs, the choice depending on the initial severity of patient disease and the preferences of the treating physician. When the patient does not have a satisfactory response, new drugs acting at a different pathway are most commonly added. At this time, considering referral for lung transplantation could be an alternative. Most experts recommend grouping maximum experience in what is known as expert centers. Treatment has led to better survival in these patients, but there is still a long way to cure this life-threatening disease.
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    ABSTRACT: Treatment of pulmonary arterial hypertension has achieved significant progress over the past 20 years. Currently, 3 groups of drugs have proven useful for the treatment of this disease: endothelin receptor antagonist, phosphodiesterase inhibitors and prostacyclin and its analogues. It is recommended to initiate treatment with one of these drugs, the choice depending on the initial severity of patient disease and the preferences of the treating physician. When the patient does not have a satisfactory response, new drugs acting at a different pathway are most commonly added. At this time, considering referral for lung transplantation could be an alternative. Most experts recommend grouping maximum experience in what is known as expert centers. Treatment has led to better survival in these patients, but there is still a long way to cure this life-threatening disease.
    Medicina Clínica 07/2014; 144(12). DOI:10.1016/j.medcli.2014.03.033 · 1.25 Impact Factor
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    ABSTRACT: If we were to summarize the rationale that underpins medical oncology in a Latin aphorism, it might be 'veneno ergo sum'; that is, I poison, therefore I am. The burden of chemotherapy-associated toxicity is well recognized, but we have relatively few tools that increase the precision of anticancer drug prescribing. We propose a shift in emphasis from the focussed study of polymorphisms in drug metabolic pathways in small sets of patients to broader agnostic analyses to systematically correlate germline genetic variants with adverse events in large, well-defined cancer populations. Thus, we propose the new science of 'toxgnostics' (that is, the systematic, agnostic study of genetic predictors of toxicity from anticancer therapy).
    Nature Reviews Cancer 05/2014; DOI:10.1038/nrc3729 · 29.54 Impact Factor
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    ABSTRACT: Exercise capacity is impaired in pulmonary arterial hypertension (PAH). We hypothesized that cardiovascular reserve abnormalities would be associated with impaired hemodynamic response to pharmacological stress and worse outcome in PAH. Eighteen PAH patients (p) group 1 NYHA class II/III and ten controls underwent simultaneous right cardiac catheterization and intravascular ultrasound at rest and during low dose-dobutamine (10 mcg/kg/min) with trendelenburg (DST). We estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC), and PA elastic modulus (EM). We concomitantly measured tricuspid annular plane systolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients. Based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: DeltamPAP >5 mm Hg and 2: DeltamPAP <=5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Delta) during DST compared with rest, including DeltamPAP with respect to DeltaCO (DeltamPAP/DeltaCO). All patients were prospectively followed up for 2 years. PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher DeltamPAP/DeltaCO (p < 0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest. In group 1, DST caused a higher DeltaEM, DeltamPAP/DeltaCO, DeltaPVR, and DeltaTAPSE than group 2, with a lower IVA increase and a negative DeltaSV (p < 0.05). TAPSE correlated with mPAP and RVP (p < 0.05) and, IVA and Sm correlated with CO (p < 0.05). DeltaEM correlated with DeltamPAP and DeltaIVA with DeltaCO (p < 0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p > 0.05). Pulmonary vascular reserve and RV systolic reserve are significantly impaired in patients with PAH. The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.
    BMC Pulmonary Medicine 04/2014; 14(1):69. DOI:10.1186/1471-2466-14-69 · 2.49 Impact Factor
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    ABSTRACT: Fluourouracil (FU) is a mainstay of chemotherapy, although toxicities are common. Genetic biomarkers have been used to predict these adverse events, but their utility is uncertain. We tested candidate polymorphisms identified from a systematic literature search for associations with capecitabine toxicity in 927 patients with colorectal cancer in the Quick and Simple and Reliable trial (QUASAR2). We then performed meta-analysis of QUASAR2 and 16 published studies (n = 4,855 patients) to examine the polymorphisms in various FU monotherapy and combination therapy regimens. Global capecitabine toxicity (grades 0/1/2 v grades 3/4/5) was associated with the rare, functional DPYD alleles 2846T>A and *2A (combined odds ratio, 5.51; P = .0013) and with the common TYMS polymorphisms 5`VNTR2R/3R and 3`UTR 6bp ins-del (combined odds ratio, 1.31; P = 9.4 × 10(-6)). There was weaker evidence that these polymorphisms predict toxicity from bolus and infusional FU monotherapy. No good evidence of association with toxicity was found for the remaining polymorphisms, including several currently included in predictive kits. No polymorphisms were associated with toxicity in combination regimens. A panel of genetic biomarkers for capecitabine monotherapy toxicity would currently comprise only the four DPYD and TYMS variants above. We estimate this test could provide 26% sensitivity, 86% specificity, and 49% positive predictive value-better than most available commercial kits, but suboptimal for clinical use. The test panel might be extended to include additional, rare DPYD variants functionally equivalent to *2A and 2846A, though insufficient evidence supports its use in bolus, infusional, or combination FU. There remains a need to identify further markers of FU toxicity for all regimens.
    Journal of Clinical Oncology 04/2014; 32(10):1031-9. DOI:10.1200/JCO.2013.51.1857 · 18.43 Impact Factor
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    ABSTRACT: Capecitabine is an oral 5-fluorouracil (5-FU) pro-drug commonly used to treat colorectal carcinoma and other tumours. About 35% of patients experience dose-limiting toxicity. The few proven genetic biomarkers of 5-FU toxicity are rare variants and polymorphisms, respectively, at candidate loci dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS). We investigated 1456 polymorphisms and rare coding variants near 25 candidate 5-FU pathway genes in 968 UK patients from the QUASAR2 clinical trial. We identified the first common DPYD polymorphisms to be consistently associated with capecitabine toxicity, rs12132152 (toxicity allele frequency (TAF)=0.031, OR=3.83, p=4.31×10(-6)) and rs12022243 (TAF=0.196, OR=1.69, p=2.55×10(-5)). rs12132152 was particularly strongly associated with hand-foot syndrome (OR=6.1, p=3.6×10(-8)). The rs12132152 and rs12022243 associations were independent of each other and of previously reported DPYD toxicity variants. Next-generation sequencing additionally identified rare DPYD variant p.Ala551Thr in one patient with severe toxicity. Using functional predictions and published data, we assigned p.Ala551Thr as causal for toxicity. We found that polymorphism rs2612091, which lies within an intron of ENOSF1, was also associated with capecitabine toxicity (TAF=0.532, OR=1.59, p=5.28×10(-6)). ENSOF1 is adjacent to TYMS and there is a poorly characterised regulatory interaction between the two genes/proteins. Unexpectedly, rs2612091 fully explained the previously reported associations between capecitabine toxicity and the supposedly functional TYMS variants, 5'VNTR 2R/3R and 3'UTR 6 bp ins-del. rs2612091 genotypes were, moreover, consistently associated with ENOSF1 mRNA levels, but not with TYMS expression. DPYD harbours rare and common capecitabine toxicity variants. The toxicity polymorphism in the TYMS region may actually act through ENOSF1.
    Gut 03/2014; 64(1). DOI:10.1136/gutjnl-2013-306571 · 13.32 Impact Factor
  • M Goya · M L Meseguer · C Merced · A Suy · V Monforte · E Domingo · L Cabero · A Roman
    Journal of Obstetrics and Gynaecology 02/2014; 34(2):191. DOI:10.3109/01443615.2012.706663 · 0.60 Impact Factor
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    ABSTRACT: Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) protect against colorectal cancer (CRC) and are associated with reduced disease recurrence and improved outcome after primary treatment. However, toxicities of NSAIDs have limited their use as antineoplastic therapy. Recent data have suggested that the benefit of aspirin after CRC diagnosis is limited to patients with PIK3CA-mutant cancers. We sought to determine the predictive utility of PIK3CA mutation for benefit from both cyclooxygenase-2 inhibition and aspirin. We performed molecular analysis of tumors from 896 participants in the Vioxx in Colorectal Cancer Therapy: Definition of Optimal Regime (VICTOR) trial, a large randomized trial comparing rofecoxib with placebo after primary CRC resection. We compared relapse-free survival and overall survival between rofecoxib therapy and placebo and between the use and nonuse of low-dose aspirin, according to tumor PIK3CA mutation status. We found no evidence of a greater benefit from rofecoxib treatment compared with placebo in patients whose tumors had PIK3CA mutations (multivariate adjusted hazard ratio [HR], 1.2; 95% CI, 0.53 to 2.72; P = .66; PINTERACTION = .47) compared with patients with PIK3CA wild-type cancers (HR, 0.87; 95% CI, 0.64 to 1.16; P = .34). In contrast, regular aspirin use after CRC diagnosis was associated with a reduced rate of CRC recurrence in patients with PIK3CA-mutant cancers (HR, 0.11; 95% CI, 0.001 to 0.832; P = .027; PINTERACTION = .024) but not in patients lacking tumor PIK3CA mutation (HR, 0.92; 95% CI, 0.60 to 1.42; P = .71). Although tumor PIK3CA mutation does not predict benefit from rofecoxib treatment, it merits further evaluation as a predictive biomarker for aspirin therapy. Our findings are concordant with recent data and support the prospective investigation of adjuvant aspirin in PIK3CA-mutant CRC.
    Journal of Clinical Oncology 09/2013; 31(34). DOI:10.1200/JCO.2013.50.0322 · 18.43 Impact Factor
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    ABSTRACT: OBJECTIVES:Microsatellite instability (MSI) is an established marker of good prognosis in colorectal cancer (CRC). Chromosomal instability (CIN) is strongly negatively associated with MSI and has been shown to be a marker of poor prognosis in a small number of studies. However, a substantial group of "double-negative" (MSI-/CIN-) CRCs exists. The prognosis of these patients is unclear. Furthermore, MSI and CIN are each associated with specific molecular changes, such as mutations in KRAS and BRAF, that have been associated with prognosis. It is not known which of MSI, CIN, and the specific gene mutations are primary predictors of survival.METHODS:We evaluated the prognostic value (disease-free survival, DFS) of CIN, MSI, mutations in KRAS, NRAS, BRAF, PIK3CA, FBXW7, and TP53, and chromosome 18q loss-of-heterozygosity (LOH) in 822 patients from the VICTOR trial of stage II/III CRC. We followed up promising associations in an Australian community-based cohort (N=375).RESULTS:In the VICTOR patients, no specific mutation was associated with DFS, but individually MSI and CIN showed significant associations after adjusting for stage, age, gender, tumor location, and therapy. A combined analysis of the VICTOR and community-based cohorts showed that MSI and CIN were independent predictors of DFS (for MSI, hazard ratio (HR)=0.58, 95% confidence interval (CI) 0.36-0.93, and P=0.021; for CIN, HR=1.54, 95% CI 1.14-2.08, and P=0.005), and joint CIN/MSI testing significantly improved the prognostic prediction of MSI alone (P=0.028). Higher levels of CIN were monotonically associated with progressively poorer DFS, and a semi-quantitative measure of CIN was a better predictor of outcome than a simple CIN+/- variable. All measures of CIN predicted DFS better than the recently described Watanabe LOH ratio.CONCLUSIONS:MSI and CIN are independent predictors of DFS for stage II/III CRC. Prognostic molecular tests for CRC relapse should currently use MSI and a quantitative measure of CIN rather than specific gene mutations.Am J Gastroenterol advance online publication, 17 September 2013; doi:10.1038/ajg.2013.292.
    The American Journal of Gastroenterology 09/2013; 108(11). DOI:10.1038/ajg.2013.292 · 9.21 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):3200-3200. DOI:10.1158/1538-7445.AM2013-3200 · 9.28 Impact Factor
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    ABSTRACT: Accepted treatment for severe pulmonary arterial hypertension (PAH) includes intravenous epoprostenol and lung transplantation (LT). Inhaled iloprost plus oral sildenafil (Ilo-Sil) is an alternative strategy that may also delay the need for LT. This was a long-term descriptive study in eight patients with PAH functional class (FC) IV with right heart failure, four of them potential candidates for LT, who were treated with Ilo-Sil as an alternative to epoprostenol. At the start of the study, patients (seven women; mean age, 43.8 [range, 34-66] years) were in FC IV and unable to perform the 6-minute walk test. Mean cardiac index was 1.9 (range, 1.4-2.1) L/min/m(2). Treatment with Ilo-Sil provoked a rapid and sustained improvement; mean walking distance at 3 months was 322 ± 90 m and no patient remained in FC IV. Survival at 1 and 5 years was 100% and 75%, respectively. Of the four potential LT candidates, one underwent transplantation after 6.8 years and one died after 1.2 years. These results suggest that therapy with Ilo-Sil represents an acceptable alternative in patients with severe and unstable PAH.
    Transplantation Proceedings 07/2013; 45(6):2347-50. DOI:10.1016/j.transproceed.2013.03.040 · 0.95 Impact Factor
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    Dataset: Paper-2013
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    ABSTRACT: OBJECTIVES: The spectrum of patients with 'angina and normal coronary arteries' ranges from severe vasospasm to atypical chest pain. Among those with typical angina, however, little is known about similarities in the clinical profile and circadian presentation between typical nonvasospastic angina and normal coronary arteries (tANCA) and vasospastic angina (VA). MATERIALS AND METHODS: Clinical, ECG, and angiographic features as well as the circadian characteristics of angina were compared between 384 tANCA and 273 VA patients. Follow-up events were also analyzed. RESULTS: tANCA patients had greater female predominance (61 vs. 18%), higher incidence of dyspnea to moderate exertion (49 vs. 12%), lower incidence of tobacco smoking (25 vs. 67%), but a similar low rate of diabetes (8.9 vs. 4.4%). In both groups, however, dyspnea and smoking were associated with female and male sex, respectively. tANCA patients showed lower but non-negligible frequency of early morning (25 vs. 67%) and evening angina (37 vs. 54%), similar rate of nocturnal angina (47 vs. 50%), and higher rate of emotional angina (49 vs. 31%). Moreover, a high proportion of patients gained pain relief with nitroglycerin (97% in VA, 246/253, and 76% in tANCA, 231/306). At 140 months, frequent angina (>10 episodes/year) was rare (VA: 7.1% vs. tANCA: 6.3%) as was the rate of cardiac death/myocardial infarction (7.3 vs. 6.0%, P=0.524). CONCLUSION: Despite differences in the clinical profile between VA and tANCA patients, there is notable sharing of circadian presentation of rest angina, response to nitroglycerin, and long-term presence and frequency of angina that suggests more similarities in underlying mechanisms than heretofore suspected.
    Coronary artery disease 06/2013; 24(5). DOI:10.1097/MCA.0b013e328362230e · 1.30 Impact Factor
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    ABSTRACT: Introduction: pulmonary hypertension (PH) is a hemodynamic condition defined as an increase in mean pulmonary arterial pressure (mPAP) >= 25 mmHg at rest as assessed by right heart catheterization (RHC). We report the experience in the PH diagnosis, follow-up and treatment (groups 1 and 4 of DanaPoint)of the PH polyclinic of the Hospital Maciel. Methods: we analyzed a cohort of 15 patients (p) (2009-2011). We estimated the functional class (FC), the six-minute walk distance (6MWD), the tricuspid annulus plane systolic excursion (TAPSE) and the peak systolic velocity (Sm). The hemodynamic severity was estimated by RHC. Acute vasoreactivity (AVT) positive response was defined as a decrease in mPAP≥10 mmHg, reaching an absolute mPAP≤40 mmHg with an unchanged or increased cardiac index (CI). Data were expressed as mean±SD. Student t test and Kruskal-Wallis test were used to compare the specific treatment effects and for multiple comparisons, respectively,with a p<0.05. Results: mean p aged 43±12 years, 12 (80%) women. 10 (67%) of group 1 y 5 (33%) of group 4. 20% p were in FC CF I-II and 80% in FC III-IV. The mean follow-up was 19±11 months. Basal TAPSE and Sm were 17±7 mm and 11±2 cm/s, respectively. mPAP was 54±15 mmHg, right atrial pressure 11±6 mmHg, CI 2.1±0.7 l/min/m2, pulmonary vascular resistance 1087±625 dinas.s.cm-5, pulmonary capacitance 1.3±0.6 ml/mmHg. One p (10%) presenteda positive AVT. P were treated with sildenafil (100%), bosentan (50%) and iloprost (43%), and 71% p received a combination therapy. We did not report hepatotoxicity by bosentan during the follow-up period. One p refused to receive specific therapy and died. The remaining 14 p improved their FC (3.0±0.8 versus 2.1±0.8, p<0.05), and trended towards an improved of 6MWD (381±117 versus 424±107m, p=0.1), with no change of RV function at rest. 6MWD correlated with FC, while the worse FC, the higher hemodynamic severity (non-significant tendency). Conclusions: PH affectsyoung patients, being detected in late stages of the illness and requiring sequential combination therapy.6MWD correlated with FC. We recommendthe development of early detection programs (associated conditions) and parenteral prostacyclins.
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    ABSTRACT: Abstract Objectives: To determine whether inflammation (C-reactive protein, CRP), oxidative stress (malondialdehyde, MDA) or haemodialysis (HD) affect associations between asymmetric (ADMA), symmetric (SDMA) dimethylarginine, NG-monomethyl-L-arginine (L-NMMA) and nitrite/nitrate (NOx) in end-stage renal disease (ESRD). Method: Metabolites were measured pre-HD, after 1 hour and end-HD in 40 ESRD patients (age 63 ± 14 years). Results: Positive associations between NOx and ADMA (p = 0.04), SDMA (p < 0.001) and L-NMMA (p = 0.04) were observed pre-HD. Associations weakened during HD but were not significantly influenced by CRP or MDA. Conclusions: HD, oxidative stress or inflammation did not significantly affect the positive associations between methylated arginines and NOx in ESRD.
    Biomarkers 05/2013; 18(4). DOI:10.3109/1354750X.2013.795608 · 2.52 Impact Factor

Publication Stats

4k Citations
848.95 Total Impact Points

Institutions

  • 2010–2015
    • University of Oxford
      • Wellcome Trust Centre for Human Genetics
      Oxford, England, United Kingdom
  • 1987–2015
    • University Hospital Vall d'Hebron
      • • Department of Pulmonology
      • • Department of Cardiology
      • • Centre d'Investigacions en Bioquimica i Biologia Molecular
      Barcino, Catalonia, Spain
  • 2011–2014
    • Wellcome Trust
      Londinium, England, United Kingdom
    • Hospital Valle Del Nalon
      Rianxo, Galicia, Spain
  • 1985–2014
    • Autonomous University of Barcelona
      • Department of Medicine
      Cerdanyola del Vallès, Catalonia, Spain
  • 2012
    • Medical Research Council (UK)
      • Institute of Genetics and Molecular Medicine
      London, ENG, United Kingdom
  • 2004–2011
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 2007–2008
    • London Research Institute
      Londinium, England, United Kingdom
  • 2005
    • Molecular Biology Institute of Barcelona
      Barcino, Catalonia, Spain
  • 2002
    • Vall d’Hebron Institute of Oncology
      Barcino, Catalonia, Spain