D Y Graham

Baylor College of Medicine, Houston, Texas, United States

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Publications (421)3452.7 Total impact

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    Dataset: feltre
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    M Rugge · M Fassan · M Pizzi · D Y Graham
    Alimentary Pharmacology & Therapeutics 04/2013; 37(7):764-5. DOI:10.1111/apt.12239 · 5.73 Impact Factor
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    D Y Graham · L A Fischbach
    Alimentary Pharmacology & Therapeutics 04/2012; 35(7):852-4; discussion 858. DOI:10.1111/j.1365-2036.2011.04944.x · 5.73 Impact Factor
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    ABSTRACT: Intestinal-type gastric cancer (GC) still ranks among the high-incidence, highly lethal malignancies. Atrophic gastritis is the cancerization field in which GC develops. The current histological reporting formats for gastritis do not include any (atrophy-based) ranking of GC risk. To test the gastritis OLGA-staging (Operative Link for Gastritis Assessment) in prognosticating neoplastic progression. Ninety-three Italian patients were followed up for more than 12 years (range: 144-204 months). Clinical examinations, pepsinogen serology, endoscopy and histology (also assessing Helicobacter pylori status) were performed both at enrolment (T1) and at the end of the follow-up (T2). All invasive or intra-epithelial gastric neoplasia were consistently associated with high-risk (III/IV) OLGA stages. There was a significant inverse correlation between the mean pepsinogen ratio and the OLGA stage (test for trend; P < 0.001). OLGA-staging at T1 predicted both the OLGA stage (Kaplan-Maier log-rank test, P = 0.001) and the neoplasia at T2 (Kaplan-Maier log-rank test, P = 0.001). This long-term follow-up study provides the first evidence that gastritis OLGA-staging conveys relevant information on the clinico-pathological outcome of gastritis and therefore for patient management. According to OLGA-staging and H. pylori-status, gastritis patients could be confidently stratified and managed according to their different cancer risks.
    Alimentary Pharmacology & Therapeutics 02/2010; 31(10):1104-11. DOI:10.1111/j.1365-2036.2010.04277.x · 5.73 Impact Factor
  • M P Dore · D Y Graham
    Endoscopy 11/2009; 42(1):38-41. DOI:10.1055/s-0029-1215314 · 5.05 Impact Factor
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    S Abudayyeh · J Hoffman · H.T. El-Zimaity · D.Y. Graham
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    ABSTRACT: Endoscopic biopsy forceps differ in the size and shape of the biopsy cup and the presence or absence of a needle. We compared four different "large cup" forceps (three with needles) designed for 2.8mm biopsy channels. A gastric antral and corpus biopsy were obtained with each. Parameters examined included: weight (mg), length (mm), orientation (poor, good), intactness (1, 2, or 3 pieces), depth (superficial, above muscularis mucosae, included muscularis mucosae), crush artefact (yes, no), and overall adequacy (inadequate, suboptimal, adequate). Twenty-four patients were enrolled (191 biopsies). The median length was approximately 5mm (range 1.1-8.2mm). Histologically inadequate specimens were present in 4% with the forceps without needle compared to 16% of those with needles (P=0.061) and there were significantly fewer specimens in three or more pieces than did the forceps with needles 2.1% vs. 12.6% (P<0.05). Current alligator style forceps provide a high proportion of acceptable specimens with only minor differences between brands. Forceps from one source were least preferred by endoscopy assistants and had the highest rates of inadequate biopsies and biopsies with crush artefact. Forceps without needles provide histologically acceptable samples slightly more frequently than those with needles.
    Digestive and Liver Disease 10/2008; 41(5):340-4. DOI:10.1016/j.dld.2008.07.317 · 2.96 Impact Factor
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    ABSTRACT: Atrophic gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for (intestinal-type) gastric cancer development and the extent/topography of the atrophic changes significantly correlates with the degree of cancer risk. The current format for histology reporting in cases of gastritis fails to establish an immediate link between gastritis phenotype and risk of malignancy. The histology report consequently does not give clinical practitioners and gastroenterologists an explicit message of use in orienting an individual patient's clinical management. Building on current knowledge of the biology of gastritis and incorporating experience gained worldwide by applying the Sydney System for more than 15 years, an international group of pathologists (Operative Link for Gastritis Assessment) has proposed a system for reporting gastritis in terms of stage (the OLGA staging system). Gastritis staging arranges the histological phenotypes of gastritis along a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). This tutorial aims to provide unequivocal information on how to consistently apply the OLGA staging system in routine diagnostic histology practice.
    Digestive and Liver Disease 09/2008; 40(8):650-8. DOI:10.1016/j.dld.2008.02.030 · 2.96 Impact Factor
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    D.Y. Graham · M Kato · M Asaka
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    ABSTRACT: The acceptance of the premise that Helicobacter pylori infection is aetiologically related to gastric cancer and peptic ulcer and that the risk of gastric cancer among Helicobacter pylori infected individuals is related to the extent, severity and duration of atrophic gastritis has led to major changes in medical and endoscopic practices. The development of non-invasive methods to detect Helicobacter pylori and to estimate the extent and severity of gastritis has reduced the need for diagnostic endoscopy in asymptomatic individuals. Here we provide recommendations regarding deciding whether non-invasive and endoscopic assessment of the gastric mucosa is preferred. We also include specific recommendations and caveats regarding the preferred biopsy number and sites as well as the identification of specimens, to allow the pathologist to reliable stage the severity and extent of gastritis, and thus provide prognostic information needed for patient managements (e.g., whether endoscopic surveillance is recommended). In summary, while there is clearly a role for gastric endoscopy and endoscopic biopsy in the Helicobacter pylori era, obtaining useful diagnostic and prognostic information is critically dependent upon attention to detail with regard to biopsy site and identification as to the location from where the specimen was taken.
    Digestive and Liver Disease 08/2008; 40(7):497-503. DOI:10.1016/j.dld.2008.02.032 · 2.96 Impact Factor
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    ABSTRACT: A number of theories regarding the aetiology of Crohn’s disease have been proposed. Diet, infections, other unidentified environmental factors and immune disregulation, all working under the influence of a genetic predisposition, have been viewed with suspicion. Many now believe that Crohn’s disease is a syndrome caused by several aetiologies. The two leading theories are the infectious and autoimmune theories. The leading infectious candidate is Mycobacterium avium subspecies paratuberculosis (Mycobacterium paratuberculosis), the causative agent of Johne’s disease, an inflammatory bowel disease in a variety of mammals including cattle, sheep, deer, bison, monkeys and chimpanzees. The evidence to support M. paratuberculosis infection as a cause of Crohn’s disease is mounting rapidly. Technical advances have allowed the identification and/or isolation of M. paratuberculosis from a significantly higher proportion of Crohn’s disease tissues than from controls. These methodologies include: (i) improved culture techniques; (ii) development of M. paratuberculosis-specific polymerase chain reaction assays; (iii) development of a novel in situ hybridization method; (iv) efficacy of macrolide and anti-mycobacterial drug therapies; and (v) discovery of Crohn’s disease-specific seroreactivity against two specific M. paratuberculosis recombinant antigens. The causal role for M. paratuberculosis in Crohn’s disease and correlation of infection with specific stratification(s) of the disorder need to be investigated. The data implicating Crohn’s as an autoimmune disorder may be viewed in a manner that supports the mycobacterial theory. The mycobacterial theory and the autoimmune theory are complementary; the first deals with the aetiology of the disorder, the second deals with its pathogenesis. Combined therapies directed against a mycobacterial aetiology and inflammation may be the optimal treatment of the disease.
    Alimentary Pharmacology & Therapeutics 07/2008; 15(3):337 - 346. DOI:10.1046/j.1365-2036.2001.00933.x · 5.73 Impact Factor
  • M P Dore · D Y Graham
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    ABSTRACT: Peptic ulcer disease remains a common problem and it most frequently due to the presence of an Helicobacter pylori infection or use of non-steroidal anti-inflammatory drugs (NSAIDs). Dyspepsia is neither sensitive or specific for diagnosing peptic ulcer disease. The approach to patients with dyspepsia is to arrive at a definitive diagnosis without unnecessary exposure to invasive or costly diagnostic procedures. Non-invasive testing is preferred with endoscopy being reserved for those with alarm markers or above a specified age (e.g., 55 years in Western countries). Patients negative for H. pylori infection should receive an empiric trial of acid suppression for 4 to 8 weeks and if beneficial it can be continued.
    Minerva medica 07/2008; 99(3):323-33. · 0.91 Impact Factor
  • S H Pang · W K Leung · D Y Graham
    Endoscopy 03/2008; 40(2):136-9. DOI:10.1055/s-2007-995318 · 5.05 Impact Factor
  • D Y Graham
    Alimentary Pharmacology & Therapeutics 03/2007; 25(3):345-6; author reply 346-7. DOI:10.1111/j.1365-2036.2006.03192.x · 5.73 Impact Factor
  • D. Y. Graham
    Alimentary Pharmacology & Therapeutics 01/2007; 25(3):345 - 346. · 5.73 Impact Factor
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    ABSTRACT: The success rate of current anti-Helicobacter pylori triple therapies in now generally 80% or less. Sequential therapy has proved superior. To test a new sequential therapy for H. pylori eradication. This was a pilot study of a sequential therapy consisting of 40 mg of esomeprazole and 1 g amoxicillin t.d.s., for 12 days. On days 6 through 12 gatifloxacin (400 mg in the morning) was added. Outcome was accessed 4 or more weeks after ending antibiotic therapy. Both naive and treatment failures were eligible. Thirty patients were entered in the study. One was lost to follow-up and one stopped early because of side effects. The success rate intention-to-treat was 80% (95% CI: 61-92%). The per-protocol eradication rate was 85.7% (95% CI: 67-95%); two of the four failures had pre-treatment gatifloxacin-resistant H. pylori. Side effects were reported by 13 patients (46%) and were generally mild with diarrhoea being most common (n = 6). Only one patient stopped medicine because of side effects of dizziness (severe) and diarrhoea (mild). Sequential therapy using the combination of a high dose of proton-pump inhibitor and amoxicillin followed gatifloxacin was effective, but pre-treatment susceptibility testing may become necessary as fluoroquinolone resistance increases.
    Alimentary Pharmacology & Therapeutics 10/2006; 24(5):845-50. DOI:10.1111/j.1365-2036.2006.03072.x · 5.73 Impact Factor
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    ABSTRACT: A number of Helicobacter pylori outer membrane proteins (OMPs) undergo phase variations. This study examined the relation between OMP phase variations and clinical outcome. Expression of H pylori BabA, BabB, SabA, and OipA proteins was determined by immunoblot. Multiple regression analysis was performed to determine the relation among OMP expression, clinical outcome, and mucosal histology. H pylori were cultured from 200 patients (80 with gastritis, 80 with duodenal ulcer (DU), and 40 with gastric cancer). The most reliable results were obtained using cultures from single colonies of low passage number. Stability of expression with passage varied with OipA > BabA > BabB > SabA. OipA positive status was significantly associated with the presence of DU and gastric cancer, high H pylori density, and severe neutrophil infiltration. SabA positive status was associated with gastric cancer, intestinal metaplasia, and corpus atrophy, and negatively associated with DU and neutrophil infiltration. The Sydney system underestimated the prevalence of intestinal metaplasia/atrophy compared with systems using proximal and distal corpus biopsies. SabA expression dramatically decreased following exposure of H pylori to pH 5.0 for two hours. SabA expression frequently switched on or off, suggesting that SabA expression can rapidly respond to changing conditions in the stomach or in different regions of the stomach. SabA positive status was inversely related to the ability of the stomach to secrete acid, suggesting that its expression may be regulated by changes in acid secretion and/or in antigens expressed by the atrophic mucosa.
    Gut 06/2006; 55(6):775-81. DOI:10.1136/gut.2005.083014 · 14.66 Impact Factor
  • W K Leung · F K Chan · DY Graham
    Endoscopy 02/2006; 38(1):2-4. DOI:10.1055/s-2005-921129 · 5.05 Impact Factor
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    ABSTRACT: Antibiotic resistance and duration of therapy influence the success of proton-pump inhibitor-containing Helicobacter pylori eradication therapy. Clarithromycin resistance is associated with treatment failure. To examine the success of a 7-day rabeprazole-clarithromycin-amoxicillin therapy in the study population. Adults from Ciudad Juarez with H. pylori infections identified by culture or histology received rabeprazole 20 mg, clarithromycin 0.5 g and amoxicillin 1 g, each b.d. for 7 days. Outcome was assessed by 13C-urea breath test carried out 4+ weeks after treatment. A total of 111 patients were enrolled and evaluated by urea breath test; 102 completed the full 7 days therapy. Two deviated from protocol, and five stopped because of adverse events. The cure rate (intention-to-treat) was 85% (95% CI: 78-91%); the per-protocol cure rate was 85% (95% CI: 78-91%). Side-effects were not serious and only 6.6% of those with adverse events stopped medication. Only three isolates were clarithromycin-resistant and none was cured. Compliance explained most of the successes. In the study population a 7-day rabeprazole triple eradication therapy was both effective and well-tolerated. Clarithromycin resistance was uncommon. We observed a slightly better outcome but consistent with results from recent large studies in US populations.
    Alimentary Pharmacology & Therapeutics 02/2006; 23(2):295-301. DOI:10.1111/j.1365-2036.2006.02755.x · 5.73 Impact Factor
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    The Journal of Infectious Diseases 01/2006; 194(5):714-716. · 6.00 Impact Factor
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    ABSTRACT: Helicobacter pylori associated gastric cancer arises via a multistage process, with atrophic gastritis being the precursor lesion. Helicobacter pylori is typically acquired in childhood, yet little is known of the prevalence of atrophic gastritis in childhood. To study atrophic gastritis among children from countries with high gastric cancer incidence. Sections from topographically mapped gastric biopsy specimens from children undergoing clinically indicated endoscopy in Korea and Colombia were evaluated using visual analogue scales. Atrophy was defined as loss of normal glandular components, including replacement with fibrosis, intestinal metaplasia (IM), and/or pseudopyloric metaplasia of the corpus (identified by the presence of pepsinogen I in mucosa that was topographically corpus but phenotypically antrum). One hundred and seventy three children, 58 from Korea (median age, 14 years) and 115 from Colombia (median age, 13 years), were studied. Helicobacter pylori was present in 85% of Colombian children versus 17% of Korean children (p<0.01). Atrophic mucosa near the antrum-corpus border was present in 16% of children, primarily as pseudopyloric metaplasia (31%, IM; 63%, pseudopyloric metaplasia; 6%, both). The median age of children with corpus atrophy was 15 (range, 7-17) years. Gastric atrophy occurs in H pylori infected children living in countries with high gastric cancer incidence. Identification and characterisation of the natural history of H pylori gastritis requires targeted biopsies to include the lesser and greater curve of the corpus, starting just proximal to the anatomical antrum-corpus junction, in addition to biopsies targeting the antrum and cardia.
    Journal of Clinical Pathology 12/2005; 58(11):1189-93. DOI:10.1136/jcp.2005.026310 · 2.92 Impact Factor
  • DY Graham
    Endoscopy 11/2005; 37(10):1006-7. DOI:10.1055/s-2005-870351 · 5.05 Impact Factor

Publication Stats

20k Citations
3,452.70 Total Impact Points


  • 1979–2013
    • Baylor College of Medicine
      • • Department of Medicine
      • • Veterans Affairs Medical Center
      • • Department of Molecular Virology & Microbiology
      Houston, Texas, United States
  • 2001–2006
    • The Chinese University of Hong Kong
      • Department of Medicine and Therapeutics
      Hong Kong, Hong Kong
    • Università degli studi di Parma
      Parma, Emilia-Romagna, Italy
    • William Beaumont Army Medical Center
      El Paso, Texas, United States
  • 1991–2006
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States
    • University of Utah
      • School of Medicine
      Salt Lake City, Utah, United States
    • Arkansas Children's Hospital
      Little Rock, Arkansas, United States
  • 1992–2004
    • United States Department of Veterans Affairs
      Бедфорд, Massachusetts, United States
  • 1999–2003
    • Università degli Studi di Sassari
      • Dipartimento di Scienze Biomediche
      Sassari, Sardinia, Italy
    • Università degli Studi di Siena
      Siena, Tuscany, Italy
  • 1998–2001
    • Technische Universität Dresden
      • Medizinische Klinik und Poliklinik I
      Dresden, Saxony, Germany
    • The University of Calgary
      Calgary, Alberta, Canada
  • 1982–2001
    • Spokane VA Medical Center
      Spokane, Washington, United States
  • 2000
    • Social Insurance Chukyo Hospital
      Nagoya, Aichi, Japan
    • University of Texas MD Anderson Cancer Center
      • Department of Bioimmunotherapy
      Houston, TX, United States
  • 1997–1999
    • Hospital San Juan de Dios Pamplona
      Quilichao, Cauca, Colombia
  • 1994–1996
    • Louisiana State University in Shreveport
      Shreveport, Louisiana, United States
  • 1995
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States
  • 1993
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 1990
    • Baylor University
      Waco, Texas, United States
  • 1988–1990
    • Texas Medical Center
      Houston, Texas, United States
    • Houston medical Center
      Ворнер Робинс, Georgia, United States
  • 1989
    • Case Western Reserve University
      Cleveland, Ohio, United States
  • 1986
    • Colorado State University
      • College of Veterinary Medicine and Biomedical Sciences
      Fort Collins, Colorado, United States