![]() | Ingvar T BjarnasonShow email addressDepartment of Gastroenterology, King’s College Hospital, London, UK | Department of Gastroenterology, King's College Hospital, London, UK | Gastroenterology, King’s College ... |
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Ingvar T Bjarnason:Expert Impact
Concepts for whichIngvar T Bjarnasonhas direct influence:Intestinal permeability,Intestinal inflammation,Idiopathic parkinsonism,Ulcerative colitis,Coeliac disease,Inflammatory bowel disease,Large intestine,Elemental diet.
Ingvar T Bjarnason:KOL impact
Concepts related to the work of other authors for whichfor which Ingvar T Bjarnason has influence:Inflammatory bowel disease,Intestinal permeability,Ulcerative colitis,Fecal calprotectin,Gut microbiota,Small intestine,Irritable bowel syndrome.
KOL Resume for Ingvar T Bjarnason
Year | |
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2022 | Department of Gastroenterology, King’s College Hospital, London, UK |
2020 | Gastroenterology, King’s College Hospital, London SE5 9RS, UK;, (B.H.H.);, (I.B.) |
2019 | Gastroenterology, King's College Hospital, London, United Kingdom Departments of Gastroenterology At King’S College Hospital, Denmark Hill, SE59RS, London, UK |
2017 | Department of Gastroenterology, King's College Hospital, London, United Kingdom. King’s College Hospital, Denmark Hill, SE5 9RS, London, UK |
2016 | Department of Colorectal Surgery, King's College Hospital NHS Foundation Trust, Denmark Hill, London, U.K |
2015 | Department of Minimally Invasive Colorectal Surgery, King's College Hospital, Denmark Hill, London, UK |
2014 | Department of Endoscopy and Gastroenterology, King's College Hospital, Denmark Hill, London, United Kingdom |
2013 | Department of Endoscopy and Gastroenterology, King’s College Hospital, London, UK |
2012 | Endoscopy and Gastroenterology, King’s College Hospital, London, UK |
2011 | Institute of Pharmaceutical Sciences, King’s College London, The Maudsley Hospital, Department of Gastroenterology, King’s College Hospital, and, Statistics Unit, Health Protection Agency, London, UK Biomedical Research Centre, Sheffield Hallam University, Sheffield |
2010 | Clinical Biochemistry, Kings College, London, UK |
2009 | Department of Medicine, King's College Hospital, Denmark Hill, London, United Kingdom |
2008 | Department of Gastroenterology, King's College Hospital, London SE5 9RS, UK FT Sigurbjörnsson is a Medical Student in his final year at the University of Iceland, Reykjavik, Iceland. Biochemistry Unit, King's College Hospital, Denmark Hill |
2007 | GKT Medical School, London, UK Department of Medicine, King’s College Hospital, London, United Kingdom |
2006 | Department of Internal Medicine, Guy’s, King’s, St Thomas’ Medical School, London, United Kingdom Guy’s, King’s, St Thomas’s Medical School, Denmark Hill Campus, Bessemer Road, SE5 9PJ, London, UK |
2005 | Department of Gastroenterology, Guy's, King's, St Thomas’ School of Medicine, GKT Medical School, London, United Kingdom |
2004 | Dept. of Gastroenterology, King's College Hospital, London, UK Department of Gastroenterology, King’s College Hospital, Denmark Hill, England |
2003 | Department of Medicine, GKT Medical School, London, England Division of Gastroenterology, University Hospital Nottingham, Nottingham, UK AstraZeneca Sodertalje, Sweden |
2002 | bResearch Fellow, Department of Gastroenterology, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden cResearch Fellow, Department of Medicine, Guy's, King's, St Thomas' School, Bessemer Road, London SE5 9PJ Department of Medicine, Guy's, Kings, St. Thomas' Medical School St Mark's Hospital, Northwick Park, Harrow, Middlesex HA1 3JU, UK |
2001 | Department of Medicine, Guy’s, King’s and St Thomas’ Medical School, London, UK, |
2000 | Department of Medicine |
1999 | Departments of Child Health and Medicine, Kings College Hospital, Denmark Hill, London SE5 9RS Department of Clinical Biochemistry, King’s College School of Medicine and Dentistry, London, UK |
1998 | Department of Clinical Biochemistry. King's College School of Medicine and Dentistry, Bessemer Road, London SE5 9PJ |
1997 | Depts. of Clinical Biochemistry and Medicine, King's College School of Medicine and Dentistry, London, UK Ciba-Geigy Pharmaceuticals, Basel, Switzerland Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, London, UK. Dept. Medicine, King's College School of Medicine, London, UK |
Concept | World rank |
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controls anthropometric measurements | #1 |
melibiose rhamnose | #1 |
food gastric damage | #1 |
drugs small | #1 |
microbiome patients | #1 |
medicationinduced symptoms | #1 |
radioisotopes crohn | #1 |
uncoupling pathogenesis | #1 |
nsaid carboxyl moiety | #1 |
experimentation cyclooxygenase | #1 |
51cr cells day | #1 |
pscibd n20 | #1 |
111indium white cells | #1 |
crossrisk ratios relatives | #1 |
psc findings | #1 |
nabumetone 24 | #1 |
pscibd correlation | #1 |
endoscopy 11 | #1 |
fcal biliary calprotectin | #1 |
scientific basis experimentation | #1 |
cai colonoscopy female | #1 |
cotraceptive pill | #1 |
visualized source | #1 |
liver disease sepsis | #1 |
permeability relapse | #1 |
corticosteroids δfcal | #1 |
calprotectin discriminating | #1 |
indometacin drug humans | #1 |
rhamnose adult | #1 |
nonparametric adenoma biomarkers | #1 |
differential urine excretion | #1 |
tests intestinal permeability | #1 |
indium111 nsaid | #1 |
nimesulide intestinal inflammation | #1 |
misoprostol −15 | #1 |
efficacy refractory colitis | #1 |
reduced duodenum injury | #1 |
proinflammatory cd14cd16 increase | #1 |
histological study prostaglandins | #1 |
ulcerative colitis symprove | #1 |
diseased jejunum | #1 |
large intestinal ulcers | #1 |
clinical relapse disease | #1 |
positive rome criteria | #1 |
absorptive capacity children | #1 |
additional factor effects | #1 |
specificity cyclooxygenase | #1 |
probes intestinal function | #1 |
modified nsaids | #1 |
ileostomy intestine restorative | #1 |
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Prominent publications by Ingvar T Bjarnason
BACKGROUND: Acute and chronic use of non-steroidal anti-inflammatory drugs can increase intestinal permeability. Rofecoxib, which selectively inhibits cyclooxygenase 2 (COX-2), is a novel anti-inflammatory drug with the potential to produce minimal gastrointestinal toxic effects while retaining clinical efficacy.
AIMS: To assess the potential for rofecoxib to affect the intestine adversely, in comparison with placebo and indomethacin.
SUBJECTS: Thirty nine healthy subjects (aged 24-30 ...
Known for Intestinal Permeability | Rofecoxib Placebo | 2 Cyclooxygenase | Crossover Study | Greater Increases |
Use of surrogate markers of inflammation and Rome criteria to distinguish organic from nonorganic intestinal disease
[ PUBLICATION ]
BACKGROUND & AIMS: Differentiating symptoms of irritable bowel syndrome (IBS) from those of organic intestinal disease is a familiar problem for physicians. The aim of this study was to assess the sensitivity, specificity, and odds ratios (ORs) of fecal calprotectin, small intestinal permeability, Rome I criteria, and laboratory markers of inflammation (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], blood count) in distinguishing organic from nonorganic intestinal ...
Known for Intestinal Disease | Rome Criteria | Sensitivity Specificity | Surrogate Markers | Antiinflammatory Agents |
Faecal calprotectin and faecal occult blood tests in the diagnosis of colorectal carcinoma and adenoma
[ PUBLICATION ]
BACKGROUND AND AIMS: Testing for faecal occult blood has become an accepted technique of non-invasive screening for colorectal neoplasia but lack of sensitivity remains a problem. The aim of this study was to compare the sensitivity and specificity of faecal calprotectin and faecal occult blood in patients with colorectal cancer and colonic polyps.
METHODS: Faecal calprotectin and occult blood were assessed in 62 patients with colorectal carcinoma and 233 patients referred for ...
Known for Faecal Calprotectin | Occult Blood | Colorectal Carcinoma | Sensitivity Detection | Colonic Polyps |
COX-1 and 2, intestinal integrity, and pathogenesis of nonsteroidal anti-inflammatory drug enteropathy in mice
[ PUBLICATION ]
BACKGROUND & AIMS: The pathogenesis of nonsteroidal anti-inflammatory drug-induced enteropathy is controversial, but it is thought that cyclooxygenase-1 (COX-1) inhibition is of pivotal importance. We compared small intestinal function and morphology in untreated wild-type, COX-1- and COX-2-deficient mice and the effect of indomethacin, selective COX-1 (SC-560), and COX-2 (celecoxib) inhibition.
METHODS: Intestinal permeability ((51)CrEDTA), inflammation (fecal granulocyte marker ...
Known for Cox1 Cox2 | Intestinal Integrity | Nonsteroidal Anti | Inflammatory Drug | Mice Indomethacin |
Surrogate markers of intestinal inflammation are predictive of relapse in patients with inflammatory bowel disease
[ PUBLICATION ]
BACKGROUND & AIMS: Prediction of relapse of inflammatory bowel disease has important implications for therapeutic strategies. We assessed whether measurement of intestinal permeability and inflammation could predict relapse of inflammatory bowel disease (IBD).
METHODS: Forty-three patients with Crohn's disease (CD) and 37 with ulcerative colitis (UC) in clinical remission provided a stool sample to be assayed for calprotectin (a neutrophil-specific marker), and patients with CD ...
Known for Relapse Patients | Inflammatory Bowel Disease | Surrogate Markers | Intestinal Inflammation | Sensitivity Specificity |
Intestinal permeability in patients with Crohn's disease and their first degree relatives.
[ PUBLICATION ]
It has been reported that intestinal permeability to polyethylene glycol 400 is increased in patients with Crohn's disease and their apparently unaffected first degree relatives. Because of the implications that these findings have for the aetiology of Crohn's disease these studies were repeated. Patients with Crohn's disease (n = 28) and 32 first degree relatives from 11 families underwent a polyethylene glycol 400 (PEG400) intestinal permeability test and a hyperosmotic (1500 mosmol/l) ...
Known for Degree Relatives | Intestinal Permeability | Crohns Disease | Polyethylene Glycol | Patients Crohn |
Mitochondrial damage: a possible mechanism of the “topical” phase of NSAID induced injury to the rat intestine
[ PUBLICATION ]
BACKGROUND: The "topical" effect of non-steroidal anti-inflammatory drugs (NSAIDs) seems to be an important cause of NSAID induced gastrointestinal damage.
AIM: To examine the possible mechanism of the "topical" phase of damage in the small intestine.
METHODS: Electron microscopy and subcellular organelle marker enzyme studies were done in rat small intestine after oral administration of indomethacin (doses varied between 5 and 30 mg/kg). The effect of conventional and non-acidic NSAIDs ...
Known for Mitochondrial Damage | Rat Intestine | Electron Microscopy | Nsaids Nsaid | Oxidative Phosphorylation |
Mucosal antibodies in inflammatory bowel disease are directed against intestinal bacteria.
[ PUBLICATION ]
In contrast with normal subjects where IgA is the main immunoglobulin in the intestine, patients with active inflammatory bowel disease (IBD) produce high concentrations of IgG from intestinal lymphocytes, but the antigens at which these antibodies are directed are unknown. To investigate the specificities of these antibodies mucosal immunoglobulins were isolated from washings taken at endoscopy from 21 control patients with irritable bowel syndrome, 10 control patients with intestinal ...
Known for Intestinal Bacteria | Bowel Disease | Active Uc | Ibd Controls | Colitis Ulcerative |
OBJECTIVE: It has been suggested that increased intestinal permeability plays a pathogenic role in bacterial infections, such as spontaneous bacterial peritonitis, in patients with liver cirrhosis. The aim of this study was to assess whether intestinal permeability is altered in cirrhotic patients with and without ascites.
MATERIAL AND METHODS: Intestinal permeability was assessed by a (51)Cr-EDTA permeability test in 20 cirrhotic patients (10 with and 10 without ascites) along with 20 ...
Known for Intestinal Permeability | Cirrhotic Patients | Liver Cirrhosis | Bacterial Infections | 51cr Edta |
BACKGROUND AND AIMS: Assessing the presence and degree of intestinal inflammation objectively, simply, and reliably is a significant problem in gastroenterology. We assessed faecal excretion of calprotectin, a stable neutrophil specific marker, as an index of intestinal inflammation and its potential use as a screening test to discriminate between patients with Crohn's disease and those with irritable bowel syndrome.
METHODS: The validity of faecal calprotectin as a marker of intestinal ...
Known for Intestinal Inflammation | Crohns Disease | Irritable Bowel Syndrome | Faecal Calprotectin Patients | Screening Test |
BACKGROUND: The diagnosis of non-steroidal anti-inflammatory drug (NSAID) induced enteropathy is difficult, requiring enteroscopy or the use of four day faecal excretion of (111)In labelled white cells.
AIMS: To assess faecal calprotectin (a non-degraded neutrophil cytosolic protein) as a method for diagnosing NSAID enteropathy.
METHODS: Single stool faecal calprotectin concentrations were compared with the four day faecal excretion of (111)In labelled white cells in 47 patients taking ...
Known for Nsaid Enteropathy | Antiinflammatory Agents | Faecal Calprotectin | Rheumatoid Arthritis | 47 Patients |
BACKGROUND: The frequency with which non-steroidal anti-inflammatory drugs (NSAIDs) increase small intestinal permeability and cause inflammation is uncertain.
AIMS: To examine small intestinal permeability and inflammation in a large number of patients on long term NSAIDs.
METHODS: Sixty eight patients receiving six different NSAIDs for over six months underwent combined absorption-permeability tests at three different test dose osmolarities (iso-, hypo-, and hyperosmolar). Two hundred ...
Known for Intestinal Permeability | Patients Nsaids | Antiinflammatory Agents | Small Bowel | Steroidal Anti |
BACKGROUND: The predicted gastrointestinal tolerability of specific cyclooxygenase-2 inhibitors could be due to either a lack of 'topical' irritation and/or lack of effect on cyclooxygenase-1.
METHODS: Key pathophysiologic steps (in vitro and in vivo uncoupling, intestinal prostanoid levels (prostaglandin E, thromboxane B2, and 6-keto-prostaglandin F1alpha), intestinal permeability (51Cr-ethylenediaminetetraacetic acid), inflammation (faecal excretion of a granulocyte marker protein), ...
Known for Nimesulide Indomethacin | Intestinal Permeability | Inflammatory Drug | Inflammation Ulcers | Key Pathophysiologic |
Inflammatory and/or autoimmune diseases like ulcerative colitis (UC) or Crohn's disease (CD) are debilitating chronic disorders that poorly respond to pharmacological interventions. Further, drug therapy has adverse effects that add to disease complications. The current thinking is that disorders like inflammatory bowel disease (IBD) reflect an over exuberant immune activation driven by cytokines including TNF-alpha. Major sources of cytokines include myeloid leukocytes (granulocytes, ...
Known for Drug Therapy | Selective Leukocytapheresis | Ulcerative Colitis Uc | Monocytes Macrophages | Major Sources |
Prevalence and Mechanism of Nonsteroidal Anti-Inflammatory Drug–Induced Clinical Relapse in Patients With Inflammatory Bowel Disease
[ PUBLICATION ]
BACKGROUND & AIMS: It has been variably suggested that nonselective NSAIDs and cyclooxygenase (COX)-2 selective inhibitors aggravate or ameliorate clinical disease activity in patients with inflammatory bowel disease. We assessed the effect of these drugs in patients with inflammatory bowel disease (n = 209) and the possible mechanisms.
METHODS: First, patients with quiescent Crohn's disease and ulcerative colitis received the non-NSAID analgesic acetaminophen (n = 26) and the ...
Known for Inflammatory Bowel | Clinical Relapse | Nonselective Nsaids | Disease Cyclooxygenase | Lowdose Aspirin |