tbuckley/cabot-search huggingface dataset:
Abstract P1-14-09: Immunohistochemical classification of intrinsic subtypes as a predictive biomarker of pathological compelete response in breast cancer patients treated with preoperative chemotherapy.
Authors: A Nagayama, H Jinno, M Takahashi, T Hayashida, S Hirose, Y Kitagawa
Journal: Cancer Research (2012)

Abstract Background: Analysis of gene expression arrays has resulted in the recognition of several fundamentally different subtypes of breast cancer. These subtypes have different natural histories and different responses to systemic and local therapies. However, widespread use of gene expression profiling is limited because of its expense and of technical difficulty. Alternatively, this classification has also been reproduced in immunohistochemical studies. The objective of this study was to evaluate the clinical utility of immunohistochemical classification of breast cancer intrinsic subtypes in the prediction of pathological compelete response (pCR) in a cohort of breast cancer patients receiving the sequential combination of taxane followed by anthracycline as preoperative chemotherapy. Materials and methods: A prospective database of 150 women with stage II/ III breast cancer, who received neoadjuvant chemotherapy, was analyzed. The regimens were either four cycles of docetaxel (40 mg/m2 on day 1 every 3 weeks) with S-1 (80 mg/m2 on days 1–14 every 3 weeks) followed by four cycles of 5-fluorouracil (500 mg/m2), epirubicin (100 mg/m2) and cyclophosphamide (500 mg/m2) (FEC) or four cycles of docetaxel (60 mg/m2 on day 8 every 3 weeks) with capecitabine (1650 mg/m2 on days 1–14 every 3 weeks) followed by four cycles of FEC. Subtypes were classified into luminal A (lumA) (ER+ and/or PgR+, HER2−, Ki67&amp;lt;14%), luminal B (lumB) (ER+ and/or PgR+, HER2−, Ki67&amp;gt;14%), triple-positive (TP) (ER+ and/or PgR+, HER2+), HER2 (ER−, PgR−, HER2+), and triple-negative (TN) (ER−, PgR−, HER2−) by using immunohistochemically stained specimen obtained by core needle biopsy. Absence of invasive tumor cells in the breast at the time of surgery was defined as pCR. Results: We found 34 women in lumA, 54 in lumB, 15 in TP, 8 in HER2, 33 in TN. The median age in each group was 53, 51, 50, 57 and 53 respectively (p = .397). The mean tumor size was 3.2cm, 3.5cm, 4.4cm, 3.9cm and 3.6cm respectively (p = .158). The clinical response rate measured by physical examination (calliper) was 80.6%, 93.9%, 86.7%, 100% and 82.4% (p = .378). pCR rate was 5.9%, 14.8%. 13.3%, 50%, 21.2% respectively (p = .031). The multivariate analysis showed ER negative, PgR negative and intrinsic subtype (TN) were the significant predictive factors of pCR (p = .027, p = .003, p = .004). Conclusion: This study indicated that immunohistochemical classification of intrinsic subtype might be a useful predictive biomarker of pCR in breast cancer patients treated with preoperative chemotherapy. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-14-09.
An exonic expression profile for breast cancer diagnosis of fine needle aspiration biopsies.
Authors: S Delaloge, V Scott, S Michiels, P Dessen, V Suciu, M Spielmann, P Vielh, F André
Journal: Cancer Research (2009)

Abstract Abstract #2029 Background: Fine needle aspiration (FNA) for breast cancer diagnosis, a simple, quick and cheap procedure, is limited by a significant number of inconclusive exams. In the present study, we have analyzed whether the expression of a set of exonic probes could accurately diagnose breast cancer of FNA biopsies.&amp;#x2028; Patients and methods: cDNA from 165 breast lesions (120 cancers), obtained by FNA in 2006-2007, and for which RIN score was &amp;gt; 6, was hybridized on splice arrayTM in two separate series (training/validation)(data set Andre et al SABCS 2008). We focused on 703 680 evidenced probe sets. The actual diagnosis of breast cancer was established by pathological examination at surgery. Associations between exonic probes and diagnosis were assessed by correlation coefficients (using t-tests) and a nearest centroid prediction rule was determined on the training set of 94 samples (70 cancers) in order to classify lesions as malignant or benign. Using the validation set of 71 samples (50 cancers), the performance of the prediction rule was evaluated and the proportion of explained variation (PEV) estimated in a logistic regression model (including only variables significant by a likelihood ratio test).&amp;#x2028; &amp;#x2028; Results: In a leave-one-out cross-validation analysis, the nearest prediction rule based on the expression of 1228 exonic probes (all probes with p&amp;lt;10e-9) accurately classified all samples from the training set. In the validation set, 68 out of 71 samples were accurately classified (96%) by this exonic expression profile of 1228 probes. Sensitivity and specificity were 96% (exact 95% CI: 86-100%) and 95% (76-100%). The cytological exam failed to provide a definitive diagnosis in 5 out of 71 patients. Four out of these 5 lesions were accurately classified by the nearest prediction rule. The PEV obtained by a clinical model (age and BI-RADS classification) was 75% (bootstrap standard error +/-8%) and the PEV by the exonic profile alone 81% (+/- 10%) in the validation set. When the clinical model and the exonic profile were combined, the PEV was 87% (+/-7%).&amp;#x2028; Conclusion: We have developed a profile based on the expression of 1228 exonic probes for breast cancer diagnosis using FNA samples. This exonic profile could be a complementary tool to clinical variables and to the cytologic exam to decide about surgery in post-screening programs. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2029.
Calcification of the Aorta and Common Iliac Arteries
Authors: Kazumasa Sudo, Hiroshi Harada
Journal: New England Journal of Medicine (2011)

A 59-year-old man presented with paresthesia and weakness in both legs. Plain radiography of the abdomen showed marked calcification of the abdominal aorta, aortic bifurcation, and common iliac arteries. These findings were confirmed on CT of the lower abdomen.
The Impact of Estrogen Receptor-beta on the Actions of Endoxifen in Breast Cancer Cells.
Authors: J. Hawse, X. Wu, M. Subramaniam, V. Negron, W. Lingle, M. Goetz, T. Spelsberg, J. Ingle
Journal: Cancer Research (2009)

Abstract Background: We have previously demonstrated that endoxifen is the most potent tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing ERα (Wu, Hawse et al. Cancer Res 2009;69:1722). These studies support the clinical findings which demonstrate that women with genetically impaired CYP2D6 metabolism have significantly reduced endoxifen levels and a higher risk of breast cancer recurrence. More recently, data has emerged from several laboratories suggesting that expression of ERβ in breast tumors leads to increased benefits from tamoxifen therapy. However, the role of ERβ in mediating endoxifen action has yet to be explored.Methods: Using U2OS osteosarcoma cells, as well as Hs578T and MCF7 breast cancer cells, stably expressing ERβ, we examined the effects of endoxifen on ERβ protein levels by western blotting, ERβ transcriptional activity by real-time RT-PCR, and on ERβ inhibition of breast cancer cell growth through the use of proliferation assays.Results: We have discovered that endoxifen stabilizes ERβ protein, unlike its targeted degradation of ERα, and induces ERα/ERβ heterodimerization in a concentration dependent manner. We have also found that endoxifen is a more potent inhibitor of estrogen induced gene expression in MCF7 cells stably expressing ERβ. Concentrations of endoxifen that mimic patients with impaired CYP2D6 activity (20-40 nM) do not significantly alter E2-induced cell proliferation in MCF7 cells expressing only ERα. However, these concentrations of endoxifen significantly reduce the estrogen induced proliferation rate of MCF7 cells expressing ERβ.Conclusions: Our data demonstrate that endoxifen stabilizes ERβ protein, induces ER heterodimerization and more potently inhibits the actions of estrogen in breast cancer cells expressing ERβ. The presence of ERβ sensitizes cells to the anti-estrogenic effects of endoxifen and growth inhibition occurs at substantially lower endoxifen concentrations (20-40 nM) than in cells that express only ERα (100 nm). Our data suggest that tamoxifen therapy may be beneficial even in patients with reduced CYP2D6 metabolism when ERβ is expressed. These studies also suggest that the increased effectiveness of tamoxifen therapy in patients whose tumors express ERβ may be due to the effects of endoxifen. Finally, these findings underscore the need to further elucidate the role of ERβ in the biology and treatment of breast cancer. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 405.
P849 QUANTITATIVE AND QUALITATIVE ANALYSIS OF PLASMA FREE FATTY ACIDS AND THEIR IMPACT ON LIVER DAMAGE IN NAFLD PATIENTS
Authors: C. Saponaro, E. Vanni, M. Gaggini, C. Rosso, L. Mezzabotta, R. Gambino, E. Buzzigoli, F. Carli, M.L. Abate, F. Saba, F. Salomone, G.P. Caviglia, A. Smedile, M. Rizzetto, M. Cassader, E. Bugianesi, A. Gastaldelli
Journal: Journal of Hepatology (2014)
ANGIOGRAPHIC OUTCOMES OF PERCUTANEOUS CORONARY INTERVENTION WITH EVEROLIMUS-ELUTING STENTS FOR THE TREATMENT OF CARDIAC ALLOGRAFT VASCULOPATHY: DE NOVO LESIONS FOUND ON SUBSEQUENT SURVEILLANCE ANGIOGRAPHY
Authors: Richard Cheng, Jon Kobashigawa, Christopher Vanichsarn, Raj Makkar, Mamoo Nakamura, Jignesh Patel, Babak Azarbal
Journal: Journal of the American College of Cardiology (2016)
Abstract LB-446: Target-based therapeutic matching in patients with <i>PIK3CA</i> mutations and PTEN aberrations
Authors: Filip Janku, Jennifer J. Wheler, Sarina A. Piha-Paul, Vanda M. Stepanek, Siqing Fu, David S. Hong, Aung Naing, Gerald S. Falchook, Stacy L. Moulder, Rajyalakshmi Luthra, Apostolia M. Tsimberidou, Razelle Kurzrock
Journal: Cancer Research (2012)

Abstract Background: Activating mutations of PIK3CA or loss of PTEN function result in increased PI3K/AKT/mTOR signaling and may predict sensitivity to drugs targeting the PI3K/AKT/mTOR pathway, while simultaneous KRAS mutations may mediate resistance. Methods: From 10/2008, available tumor samples from advanced cancer patients referred to the Phase I Clinical Trials Program were screened for PIK3CA mutations and PTEN aberrations (loss of expression on immunohistochemistry or mutation) in a CLIA-certified laboratory. Patients with tumors carrying PIK3CA mutations and/or PTEN aberrations were treated, whenever possible, with agents targeting the PI3K/AKT/mTOR pathway. Results: Overall, 1,540 patients were tested, and 285 (19%) had PIK3CA mutations (n=141), PTEN aberrations (n=130), or a simultaneous PIK3CA mutation and PTEN aberration (n=14). Of these 285 patients, 131 (46%) were treated in clinical trials containing a PI3K/AKT/mTOR inhibitor (median age, 56; median number of prior therapies, 3). Of these 131 patients, 26 (20%, 95% CI 0.14-0.27) achieved a partial response (PR) (4/21 breast cancers; 4/19 endometrial cancers; 3/13 ovarian cancers; 4/9 head and neck cancers; 4/10 cervical cancers; 2/9 renal cancers; 2/4 salivary gland cancers; 1/4 sarcomas; 1/3 non-small cell lung cancers; 1/2 melanomas). Patients without known PIK3CA mutations and/or PTEN aberrations treated on the same protocols had a PR rate of 6% (26/458; 95% CI 0.04-0.08, p=0.0001). Treated patients with wild-type KRAS had a higher PR rate of 20% compared to 8% in patients with simultaneous KRAS mutations (p=0.05). Conclusion: Heavily pretreated patients with PIK3CA mutations and/or PTEN aberrations had higher PR rates on protocols with PI3K/AKT/mTOR inhibitors than patients without these aberrations (20% vs 6%; p = 0.0001). Simultaneous KRAS mutations were associated with a lower PR rate. Screening for PIK3CA mutations and PTEN aberrations merits further evaluation in making treatment decisions. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-446. doi:1538-7445.AM2012-LB-446
35% OF EMPIRIC ATRIOVENTRICULAR DELAY SETTINGS MAY BENEFIT FROM ADDITIONAL OPTIMIZATION
Authors: Gregory Sinner, Vedant Gupta, Arash Seratnahaei, Kevin Parrott, Richard Charnigo, Yousef Darrat, Samy Elayi, Steve Leung, Vincent Sorrell
Journal: Journal of the American College of Cardiology (2016)
A Patient with Fevers and Fatigue
Authors: Kevin Wei, Anand Vaidya, Peter Rohloff, Yee-Ping Sun, Yonatan Grad
Journal: New England Journal of Medicine (2013)

A 68-year-old man who lived in New England presented to the emergency department in December with a 4-week history of fevers and chills. One month before presentation, he had traveled to the Netherlands for a 3-day professional conference. A few days after he returned home, chills, temperatures as high as 38°C, and fatigue developed. The fevers had become more frequent in the week preceding presentation, . . .
Abstract 2871: Pharmacokinetics studies of anticancer gallotannin penta-O-galloyl-beta-D-glucose (PGG) in mice
Authors: Li Li, Jinhui Zhang, Ahamd Shaik, Katai Nhkata, Chengguo Xing, Junxuan Lü
Journal: Cancer Research (2010)

Abstract Studies by our group and others have shown that 1, 2, 3, 4, 6-penta-O-galloyl-beta-D-glucose (PGG) exhibits in vivo anti-cancer effects against prostate and breast cancer xenograft or lung cancer allograft when administrated by i.p injection or oral gavage. PGG has also been shown in several studies to exhibit anti-diabetic activities both in vitro and in vivo. However, no data have been published on the absorption, distribution, metabolism and elimination (ADME) to provide mechanistic correlates to account for the biological activities. In this study, we developed a method for the analysis of PGG in mouse plasma, using tea polyphenol epigallocatechin gallate (EGCG) as an internal standard (IS). A liquid-liquid extraction (LLE) protocol originally developed for tea polyphenol analyses was optimized for the extraction of PGG from mouse plasma. In brief, plasma (0.2 ml) was acidified with an equal volume of 2% acetic acid, and ethyl acetate was then applied to extract PGG and EGCG (IS). After LLE, PGG was quantitated by HPLC with a UV detection at 280 nm. The method was validated according to FDA guidelines. The extraction efficiency for spiked PGG was ∼70 % in mouse plasma. The limit of detection (LOD) for PGG was approximately 100 ng/ml and the limit of quantitation (LOQ) around 200 ng/ml when using 200 µl mouse plasma. The linear range of the method was 0.2 −25 µg/ml in mouse plasma. Pharmacokinetics of PGG following a single i.p. injection in mice was studied. The peak plasma PGG concentrations (Cmax) were found to be approximately 4 and 11 µM at administered dose of 20 and 80 mg/kg of PGG, respectively. The apparent half life of the elimination phase for PGG is 3 h. Addition of glucuronidase and sulfatase to plasma did not change extractable PGG. These data suggest that PGG exists in plasma mostly as free extractable form after a single i.p. injection and that the plasma resident time for PGG is several hours. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2871.
INDEPENDENT PREDICTORS OF MACE AT DIFFERENT TIME POINTS AFTER THE TREATMENT OF NON-SELECTED PATIENTS WITH DRUG-ELUTING STENTS: AN ANALYSIS OF THE DESIRE REGISTRY
Authors: Jose de Ribamar Costa, Amanda Sousa, Adriana Moreira, Ricardo Costa, Galo Maldonado, Manuel Cano, Cantidio Moura Neto, J. Eduardo Sousa
Journal: Journal of the American College of Cardiology (2017)
PEDIATRICS CLINICAL RESEARCH
Authors: R. Antony, M. Zagardo, M. Gujrati, J. Lin, R. Antony, M. Al-Rahawan, M. Zagardo, M. Gujrati, J. Lin, A. Broniscer, R. Bhardwaj, C. Hampton, V. Ozols, M. Chakravadhanula, E. Bouffet, C. Hawkins, K. Scheinemann, S. Zelcer, D. Johnston, L. Lafay-Cousin, V. Larouche, N. Jabado, A. S. Carret, J. Hukin, D. Eisenstat, G. Pond, K. Poskitt, B. Wilson, U. Bartels, U. Tabori, G. Dhall, K. Haley, J. Finlay, T. Rushing, R. Sposto, R. Seeger, J. Garvin, K. Rupani, E. Stark, R. Anderson, N. Feldstein, J. Grill, D. Hargrave, M. Massimino, T. Jaspan, P. Varlet, C. Jones, P. Morgan, M. C. Le Deley, A. Azizi, A. Canete, E. Bouffet, F. Saran, J. Bachir, L. Bubuteishvili-Pacaud, R. Rousseau, G. Vassal, S. Gupta, N. Robinson, N. Dhir, K. Wong, S. Zhou, J. Finlay, G. Dhall, T. Kumabe, T. Kawaguchi, R. Saito, M. Kanamori, Y. Yamashita, Y. Sonoda, T. Tominaga, T. Miyagawa, C. Nwachukwu, R. Youland, N. Laack, I. Filipek, M. Drogosiewicz, M. P.- Polnik, E. Swieszkowska, B. Dembowska-Baginska, E. Jurkiewicz, D. Perek, D. Perek, B. Dembowska-Baginska, M. Drogosiewicz, M. P.- Polnik, W. Grajkowska, M. Roszkowski, G. Sobol, K. Musiol, J. Wachowiak, B. Kazmierczak, J. P. - Pogorzelski, W. Mlynarski, B. Z.- Szewczyk, M. Wysocki, E. Niedzielska, J. Kowalczyk, H. W. - Slusarz, W. Balwierz, E. Z. - Czepko, A. Szolkiewicz, D. Perek, M. Perek-Polnik, B. Dembowska-Baginska, M. Drogosiewicz, W. Grajkowska, M. Lastowska, M. Chojnacka, I. Filipek, M. Tarasinska, M. Roszkowski, S. Perreault, K. Chao, V. Ramaswamy, D. Shih, M. Remke, B. Luu, S. Schubert, P. Fisher, S. Partap, H. Vogel, M. Taylor, L. Goumnerova, Y.-J. Cho, N. Robison, G. Dhall, R. Brown, T. Cloughesy, T. B. Davidson, M. Krieger, M. Berger, K. Wong, A. Perry, F. Gilles, J. L. Finlay, N. Robison, N. Dhir, J. Khemani, K. Wong, S. Gupta, B. Britt, J. Grimm, J. Finlay, G. Dhall, M. I. Ruge, T. Blau, V. Hafkemeyer, C. Hamisch, K. Klinger, T. Simon, Z. Sadighi, B. Ellezam, M. Guindani, J. Ater, Y. Shimizu, H. Arai, M. Miyajima, K. Shimoji, A. Kondo, E. Shinohara, S. Perkins, T. DeWees, I. Slavc, M. Chocholous, U. Leiss, C. Haberler, A. Peyrl, A. A. Azizi, K. Dieckmann, A. Woehrer, C. Dorfer, T. Czech, T. Spence, D. Picard, M. Barszczyk, S.-K. Kim, Y.-S. Ra, J. Fangusaro, H. Toledano, H. Nakamura, L. Lafay-Cousin, X. Fan, K. M. Muraszko, H.-K. Ng, E. Bouffet, W. Halliday, M. Shago, C. E. Hawkins, A. Huang, M. Suzuki, A. Kondo, M. Miyajima, H. Arai, S. V. van Zanten, M. Jansen, D. van Vuurden, E. Hulleman, S. Idema, D. Noske, N. Wolf, H. Hendrikse, P. Vandertop, G. J. Kaspers, K. Muller, A. Schlamann, M. Warmuth-Metz, T. Pietsch, S. Pietschmann, R.-D. Kortmann, C. M. Kramm, A. O. von Bueren, S. Walston, T. Williams, D. Hamstra, K. Oh, C. Pelloski, N. Zhukova, J. Pole, M. Mistry, I. Fried, U. Bartels, A. Huang, N. Lapperiere, P. Dirks, K. Scheinemann, J. An, N. Alon, P. Nathan, M. Greenberg, E. Bouffet, D. Malkin, C. Hawkins, U. Tabori
Journal: Neuro-Oncology (2013)
Estimated Effect of Breast Self-Examination and Routine Physician Examinations on Breast-Cancer Mortality
Authors: Peter Greenwald, Philip C. Nasca, Charles E. Lawrence, John Horton, Robert P. McGarrah, Thomas Gabriele, Kathleen Carlton
Journal: New England Journal of Medicine (1978)

We examined the effects of breast self-examination and breast examination by physicians on the stage of breast cancer at diagnosis. Clinical and pathological-staging information was compared to interview data on method of initial detection of 293 women. Tumors were detected in clinical Stage I 53.8% of the time when the detection method was routine physician examination, 37.7% when it was self-examination and only 27.0% when detection was accidental. Sixty-nine per cent of women practicing self-examination at the time of diagnosis discovered their tumor by this method. Differences were less apparent when pathological stage was considered. Tumors found during routine examination of the breast averaged 6.1 mm smaller in diameter than those discovered accidentally. We estimate that breast-cancer mortality might be reduced by 18.8% to 24.4% through self-examination or routine physician examination, respectively.
Abstract 194: MicroRNA-1 induces apoptosis by targeting prothymosin alpha in nasopharyngeal carcinoma cells
Authors: Cheng-Der Wu, Yuan-Sung Kuo, Han-Chung Wu, Chin-Tarng Lin
Journal: Cancer Research (2012)

Abstract MiR-1 (microRNA-1) can be used as a positive control and for optimizing transfection conditions in microRNA experiments (e.g., Ambion Pre-miR miRNA Starter Kit, QIAGEN Syn-hsa-miR-1 miScript miRNA mimic positive control). We noticed that transfection of nasopharyngeal carcinoma cells with miR-1 reveals a typical apoptotic process when observed by time-lapse microscopy. Annexin V and TUNEL staining and caspase assay confirm that miR-1 induces nasopharyngeal carcinoma cell apoptosis. MiR-1 transfection of HeLa, Cal-27, KYSE30 and NPC-TW06 cell lines which express low levels of endogenous miR-1 also induces apoptosis. However, miR-1 transfection of cell lines such as SW620, HepG2, HEK-293T, SAS and PC-13 which express high levels of endogenous miR-1 does not induce apoptosis. To determine miR-1 target genes that are involved in apoptosis, we analyzed microRNA and pathway databases, and cDNA expression microarrays from miR-1 transfected cells. Using qRT-PCR analysis and luciferase reporter vector assays, we found that miR-1 directly targets PTMA (prothymosin alpha). We used PTMA siRNA to down regulate PTMA mRNA levels and observed whether PTMA siRNA could induce apoptosis. Knocking down PTMA expression alone did not induce apoptosis but could accelerate apoptotic progression in cells treated with apoptosis inducers. We also found that transfection of miR-1 could up regulated some pro-apoptotic proteins (HTRA, SMAC, p53, TNF-R1, TNF-R2, TRAILR-1, TNF-alpha, TNF-beta). They are not miR-1 directly target genes but involve in miR-1 inducing apoptosis. We conclude that miR-1 can induced apoptosis in low levels of endogenous miR-1 cell lines. This is a novel model of microRNA-induced cell apoptosis. The apoptotic inducers including actinomycin D, camptothecin and etoposide are also the chemotherapeutic drugs in clinical cancer therapy and PTMA siRNA can accelerate apoptotic progression in cells treated with those apoptosis inducers. Therefore PTMA siRNA may have potential applications as an adjuvant in cancer chemotherapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 194. doi:1538-7445.AM2012-194
IMPACTO DIAGNOSTICO Y TERAPEUTICO DE LA CAPSULA ENDOSCOPICA EN LA RECTORRAGIA ACTIVA DE ORIGEN OSCURO
Authors: M Luján, P Suarez, R Pastor, A Monzo, E Orti, A Dura, I Bort, P Canelles, E Medina
Journal: Endoscopy (2010)

Introduccion: La capsula endoscópica (CE) es la técnica gold standard en la hemorragia digestiva de origen oscuro (HDOO), siendo más rentable cuando la hemorragia es manifiesta. En nuestro medio, ante una HDOO manifiesta por rectorragia, la primera exploración a realizar es el second look con colonoscopia (C) previo a la CE.