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Dive into the research topics where Brendan Drumm is active.

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Featured researches published by Brendan Drumm.


The New England Journal of Medicine | 1990

Intrafamilial Clustering of Helicobacter pylori Infection

Brendan Drumm; Guillermo I. Perez-Perez; Martin J. Blaser; Philip M. Sherman

Colonization of the gastric antrum by Helicobacter pylori (formerly Campylobacter pylori) has been associated with primary gastritis. We determined the frequency of colonization by H. pylori in gastric-antrum biopsy specimens from 93 children undergoing gastroscopy for the evaluation of upper gastrointestinal symptoms. We also determined H. pylori IgG antibody levels by enzyme-linked immunosorbent assay in coded serum samples from these children, family members, and control subjects of comparable ages. Among 27 children with primary, or unexplained, gastritis, H. pylori was identified by silver staining in 24 biopsy specimens and by culture in 22; specific antibodies were present in 23 children (96 percent). Three children with unexplained gastritis had no evidence of H. pylori in the antrum, nor did any of 13 children with secondary gastritis or any of 53 children with normal antral histologic features; specific antibodies were present in only 1 of these 69 children. H. pylori antibody was detected in 25 of 34 parents of colonized children, but in only 8 of 33 parents of noncolonized children (P less than 0.001). Of 22 siblings of children colonized by H. pylori, 18 had specific antibodies, as compared with only 5 of 37 controls (P less than 0.001). We conclude that H. pylori-specific IgG antibodies are associated with bacterial colonization of the gastric antrum by this organism. The intrafamilial clustering of H. pylori infection suggests that there may be person-to-person spread of these bacteria.


Clinical Gastroenterology and Hepatology | 2004

Clinical and genetic characteristics of hereditary pancreatitis in Europe.

Nathan Howes; Markus M. Lerch; William Greenhalf; Deborah D. Stocken; Ian Ellis; Peter Simon; Kaspar Truninger; Rudi Ammann; G. Cavallini; Richard Charnley; G. Uomo; Miriam Delhaye; Julius Spicak; Brendan Drumm; Jan B.M.J. Jansen; Roger Mountford; David C. Whitcomb; John P. Neoptolemos

BACKGROUND & AIMS Hereditary pancreatitis is an autosomal dominant disease that is mostly caused by cationic trypsinogen (PRSS1) gene mutations. The aim was to determine phenotype-genotype correlations of families in Europe. METHODS Analysis of data obtained by the European Registry of Hereditary Pancreatitis and Pancreatic Cancer was undertaken using multilevel proportional hazards modelling. RESULTS There were 112 families in 14 countries (418 affected individuals): 58 (52%) families carried the R122H, 24 (21%) the N29I, and 5 (4%) the A16V mutation, 2 had rare mutations, and 21 (19%) had no PRSS1 mutation. The median (95% confidence interval [CI]) time to first symptoms for R122H was 10 (8, 12) years of age, 14 (11, 18) years for N29I, and 14.5 (10, 21) years for mutation negative patients (P = 0.032). The cumulative risk (95% CI) at 50 years of age for exocrine failure was 37.2% (28.5%, 45.8%), 47.6% (37.1%, 58.1%) for endocrine failure, and 17.5% (12.2%, 22.7%) for pancreatic resection for pain. Time to resection was significantly reduced for females (P < 0.001) and those with the N29I mutation (P = 0.014). The cumulative risk (95% CI) of pancreatic cancer was 44.0% (8.0%, 80.0%) at 70 years from symptom onset with a standardized incidence ratio of 67% (50%, 82%). CONCLUSIONS Symptoms in hereditary pancreatitis start in younger patients and endpoints take longer to be reached compared with other forms of chronic pancreatitis but the cumulative levels of exocrine and endocrine failure are much higher. There is an increasingly high risk of pancreatic cancer after the age of 50 years unrelated to the genotype.


The New England Journal of Medicine | 1987

Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children

Brendan Drumm; Philip M. Sherman; Ernest Cutz; Mohamed A. Karmali

We investigated the presence of Campylobacter pylori colonization of the gastric mucosa and of histologic evidence of gastritis in a prospective study of 71 consecutive children undergoing upper gastrointestinal tract endoscopy and gastric biopsies because of gastrointestinal symptoms. Two tissue samples from the gastric antrum were obtained from 67 of the 71 children (mean age [+/- SD], 11.4 +/- 3.8 years). One sample was evaluated for evidence of gastritis and stained with silver to detect organisms morphologically resembling campylobacter. The second sample was cultured for C. pylori, and a portion was used to perform a urease-screening test for the presence of C. pylori. Antral gastritis was diagnosed histologically in 18 of 67 patients. C. pylori was identified by both culture and silver staining on the antral mucosa in 7 of 10 patients with unexplained gastritis (primary gastritis) but in none of 8 patients with gastritis associated with an identifiable underlying cause (secondary gastritis). C. pylori was not identified in any of the 49 cases with normal histologic features. The urease-screening test was positive in only three of six patients with a positive culture for C. pylori. Duodenal ulcers were diagnosed by endoscopy in five patients. Each of the five had C. pylori on the antral mucosa, but organisms were not identified on the duodenal mucosa. We conclude that the presence of C. pylori on the antral mucosa is specifically associated with primary antral gastritis and may also be associated with primary duodenal ulceration.


The American Journal of Gastroenterology | 2002

Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis

F Sharif; Michael McDermott; M Dillon; Brendan Drumm; Marion Rowland; Cameron Imrie; Suzanne Kelleher; Sinead Harty; Billy Bourke

OBJECTIVES:Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohns disease. However, the utility of FEG for distinguishing Crohns disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohns disease.METHODS:This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System.RESULTS:FEG was present in 28 of 43 (65.1%) children with Crohns disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohns disease and in 12 of 24 (50%) patients with ulcerative colitis.CONCLUSIONS:The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohns disease, it does not reliably differentiate between Crohns disease and ulcerative colitis.


Clinical Gastroenterology and Hepatology | 2005

A Prospective Study of the Oral Manifestations of Crohn's Disease

Sinead Harty; Padraig Fleming; Marion Rowland; Ellen Crushell; Michael McDermott; Brendan Drumm; Billy Bourke

BACKGROUND & AIMS Recent studies suggest that the mouth may be involved frequently in patients with Crohns disease (CD). The aim of this study was to document prospectively the proportion of children with oral lesions at diagnosis of CD, to describe the type of lesions found, and to examine the ability of gastroenterologists to identify correctly oral Crohns manifestations. METHODS In a prospective 3-year study, systematic dental examinations were performed on all children with suspected inflammatory bowel disease. Each child underwent upper endoscopy, colonoscopy, and barium follow-through radiography. RESULTS Forty-eight of 49 children with CD were examined by the dentist. Oral CD was found in 20 patients (41.7%). Oral findings included mucogingivitis (12 patients), mucosal tags (4 patients), deep ulceration (4 patients), cobblestoning (3 patients), lip swelling (3 patients), and pyostomatitis vegetans (1 patient). Noncaseating granulomas were found in all 8 oral biopsy specimens from oral CD lesions (100%). Two patients with granulomas in oral biopsy specimens had no granulomas found in any other biopsy specimens. The presence of oral manifestations was associated with perianal disease. In only 9 patients (45%) with oral CD was the mouth found to be abnormal by the consultant gastroenterologists. Only nonspecific oral changes were seen in children with ulcerative colitis and indeterminate colitis. CONCLUSIONS More than one third of all children presenting with CD had involvement of the mouth. The ability of physicians to recognize oral lesions was poor. Expert dental evaluation may be useful during the investigation of patients with suspected inflammatory bowel disease.


The Journal of Pediatrics | 1995

Association of symptoms with Helicobacter pylori infection in children

Siobhan M. Gormally; Nan Prakash; Marie T. Durnin; Leslie Daly; Marguerite Clyne; Barry M. Kierce; Brendan Drumm

The aim of this study was to determine prospectively whether Helicobacter pylori-associated gastritis is associated with specific symptoms by evaluating whether these symptoms are relieved by treatment of the infection. Symptoms resolved after the eradication of H. pylori in only three of eight children with H. pylori-associated gastritis alone, in comparison with all six children with duodenal ulcer disease.


Helicobacter | 2007

Results from the pediatric European register for treatment of Helicobacter pylori (PERTH).

Giuseppina Oderda; Peter Shcherbakov; Patrick Bontems; Pedro Urruzuno; Claudio Romano; Frédéric Gottrand; M. Jose Martinez Gómez; A. Ravelli; P. Gandullia; Elefteria Roma; Sami Cadranel; Costantino De Giacomo; Roberto Berni Canani; V. Rutigliano; Ender Pehlivanoglu; Nicolas Kalach; Paola Roggero; Danuta Celinska-Cedro; Brendan Drumm; Thomas Casswall; Marja Ashorn; Sanda Nousia Arvanitakis

Background and Aim:  Data on the eradication treatment for childhood Helicobacter pylori are scanty. A register was established on the European Society for Pediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) website to collect data on treatment performed by European pediatricians to ascertain what is practiced in the field.


The New England Journal of Medicine | 1999

Treatment of Fistulas with Granulocyte Colony-Stimulating Factor in a Patient with Crohn's Disease

David Vaughan; Brendan Drumm

To the Editor: An adolescent boy with Crohns disease and enterocutaneous fistulas had a response to treatment with granulocyte colony-stimulating factor (filgrastim) after all standard treatments ...


Pediatric Dermatology | 1999

Bullous mastocytosis : A fatal outcome

M. Murphy; D. Walsh; Brendan Drumm; Rosemarie Watson

Abstract: A 6‐week‐old boy was referred with a generalized bullous rash since birth. Examination revealed bullous mastocytosis with initially no evidence of systemic involvement. Hepatosplenomegaly was noted at 6 months, and at 12 months he was found to have generalized lymphadenopathy. He developed bouts of vomiting associated with increased blistering. At 17 months he had sudden collapse following a brief bout of vomiting and was apneic and asystolic on arrival at the emergency department. The cause of death was attributed to massive hypotension secondary to mast cell degranulation. Although childhood mastocytosis has a favorable course in general, the subset of children with congenital bullous mastocytosis is at higher risk of sudden death and a more guarded prognosis should be given.


Pediatrics | 1998

Colonoscopy Under General Anesthesia in Children

Michelle Dillon; Siobhan Brown; William Casey; Deirdre Walsh; Marie T. Durnin; Kabir Abubaker; Brendan Drumm

Objective. In children, colonoscopy is usually performed using deep sedation that may be associated with significant risks. The purpose of this study was to evaluate the safety of colonoscopy performed under general anesthesia. Methods. All patients undergoing colonoscopy during a 3-year period were reviewed for the study. One hundred and thirty-six procedures were performed. Colonoscopies were performed by a pediatric gastroenterologist. Anesthesia was administered by a pediatric anesthetist in a gastroenterology procedure room, adjacent to the operating recovery area. Results. Three patients had significant abdominal pain and tenderness after the procedure, 1 of whom suffered a perforation of the sigmoid colon. This patient had severe ulcerative colitis. The gastrointestinal complication rate was no higher than reported in adult patients undergoing colonoscopy under sedation. No significant complications relating to the administration of anesthesia were encountered. Conclusion. We conclude that colonoscopy performed under general anesthesia in children is a very safe procedure. It is superior to the use of sedation because the child is not placed at risk of respiratory compromise. Furthermore, the procedure is less worrisome for children when performed under a general anesthetic.

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Marion Rowland

University College Dublin

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Billy Bourke

University College Dublin

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Leslie Daly

University College Dublin

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Cameron Imrie

University College Dublin

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David Vaughan

University College Dublin

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D Walsh

University College Dublin

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