G. N. J. Tytgat

Erasmus MC, Rotterdam, South Holland, Netherlands

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Publications (992)5302.46 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The annual Gastro Highlights training event, held at the university Hospital Zurich last autumn, also celebrated the 60th birthday of prof.Dr.med. Michael Fried, who initiated this widely recognized event 17 years ago. Featured at the symposium was a round up of the most important new discoveries in the field of gastroenterology and hepatology to be published during the course of the previous year or represented at the Digestive Disease Week (DDW). To mark the birthday of Prf. Dr. med. Michael Fried, two international experts made a special report on the key developments in the gastroenterology to emerge over the past decades.
    Praxis 02/2013; 102(4):197-210. DOI:10.1024/1661-8157/a001224
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    Guido N J Tytgat ·
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    ABSTRACT: The incidence of gastroesophageal reflux disease (GERD) and esophageal columnar metaplasia is rising worldwide. Both mechanical and functional factors perturb the double sphincter barrier at the esophagogastric junction (EGJ). Discovery of the acid pocket is fundamental in understanding postprandial acid reflux. Adding impedencemetry to pH measurements allows detection of non-acid or weakly acidic reflux. Histologic and endoscopic injury of the squamous mucosa rises from dilation of the intercellular spaces, papillary extension, accentuated intrapapillary looping, red streaks, erosive tissue loss, etc., graded with the Los Angeles system. Seventy percent of patients have no recognizable abnormalities (non-erosive or neGERD). Treatment of GERD mainly relates to the control of acid secretion but a revival of alginate/antacid obliterating the acid pocket is to be expected. Weaker heartburn control in neGERD is a misnomer because most studies included patients with no evidence of reflux disease. Traditional (delayed-release) proton pump inhibitors (PPIs) are powerful suppressors of acid secretion but do have limitations such as gradual build up of acid control, weak control of nocturnal acid recovery, possibility of rebound, occasional need for dose escalation, etc. Barrett's esophagus (BE) is endoscopically diagnosed also in the absence of intestinal metaplasia. A prerequisite is the precise location of the EGJ (proximal end of gastric folds, esophageal sphincter pinch, distal extent of palisade vessels). BE is graded with the Prague C & M system. Barrett's cancer develops usually via low-grade and high-grade dysplasia. Endoscopic examination may indicate suspicious areas, amenable for targeted biopsy. Otherwise, four quadrant biopsies are obtained when searching for neoplasia. Low-grade dysplasia, especially when it is multifocal and p53 positive, high-grade dysplasia and mucosal cancer should be treated with endoscopic resection of the target area, followed by radiofrequency ablation of the adjacent non-neoplastic columnar mucosa, followed with powerful acid suppressant therapy. The long-term results of the combination of resection and ablation are exiting and at least comparable to surgical resection.
    Journal of Digestive Diseases 06/2012; 13(6):291-5. DOI:10.1111/j.1751-2980.2012.00598.x · 1.96 Impact Factor
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    Guido N.J. TYTGAT ·
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    ABSTRACT: No abstract is available for this article.
    Journal of Digestive Diseases 05/2012; 13(5):243. DOI:10.1111/j.1751-2980.2012.00586.x · 1.96 Impact Factor

  • European journal of gastroenterology & hepatology 04/2012; 9 Suppl 1:S27-9. DOI:10.1097/00042737-201204001-00007 · 2.25 Impact Factor
  • G N J Tytgat ·
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    ABSTRACT: Ulceration corresponds to tissue loss, breaching the muscularis mucosae. When ulcers develop in the acid-peptic environment of the gastroduodenum, they are traditionally called peptic ulcer (PUD). Ulcers never develop spontaneously in a healthy gastroduodenal mucosa. Ulceration is the ultimate consequence of a disequilibrium between aggressive injurious factors and defensive mucosa-protective factors. The dominant aggressors are strong acid and high proteolytic (pepsin) activity in gastric secretions. The dominant defensors are the phospholipid surfactant layer, covering the mucus bicarbonate gel, the mucus bicarbonate layer covering the epithelium, the tight junctional structures between the epithelial cells, restricting proton permeability, and the epithelial trefoil peptides, contributing to healing after injury. Initially, acid-peptic aggression was considered the overwhelming cause of PUD, supported by the pioneering work of Schwartz, launching the dictum 'no acid, no ulcer'. This led to the universal therapy directed against intragastric acidity, also interfering with peptic activity when the pH was >4. The therapeutic sequence went from large doses of antacids to H(2)-receptor antagonists and finally to proton pump inhibitors (PPIs). The longer the intragastric pH was >3, the quicker ulcer healing was seen. Unfortunately, ulcers often recurred after stopping therapy, demanding maintenance therapy to keep the ulcers healed and to prevent the need for surgery (vagotomy, partial gastric resection). Later on, the emphasis gradually shifted to weakening/failing of the defensive factors, raising the vulnerability of the gastroduodenal mucosa to luminal secretions. Leading injurious mechanisms jeopardizing the mucosal integrity are numerous: infections, especially Helicobacter pylori, drug-induced injury, particularly acetylsalicylic acid (ASA) and non-steroidal anti-inflammatory drugs (NSAIDs), physicochemical and caustic injury, vascular disorders, interfering with perfusion, etc. Currently the leading cause of PUD is H. pylori infection. Standard triple eradication therapy is losing interest in favor of quadruple therapy (PPI, bismuth, tetracycline, metronidazole). H. pylori-induced PPI is rapidly disappearing in the Western world, in contrast to drug-induced ulcer disease and what is called idiopathic PUD. Partial prophylaxis of ASA/NSAID-induced ulceration is possible with PPI maintenance therapy, but novel ways to strengthen the mucosal defense are urgently awaited.
    Digestive Diseases 11/2011; 29(5):454-8. DOI:10.1159/000331520 · 2.18 Impact Factor
  • Ernst J Kuipers · Guido N J Tytgat ·

    Best practice & research. Clinical gastroenterology 04/2011; 25 Suppl 1:S1. DOI:10.1016/S1521-6918(11)00052-7 · 3.48 Impact Factor
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    ABSTRACT: Background/Aims: Although considerable information exists regarding gastroesophageal reflux disease with erosions, much less is known of non-erosive reflux disease (NERD), the dominant form of reflux disease in the developed world. Methods: An expert international group using the modified Delphi technique examined the quality of evidence and established levels of agreement relating to different aspects of NERD. Discussion focused on clinical presentation, assessment of clinical outcome, pathobiological mechanisms, and clinical strategies for diagnosis and management. Results: Consensus was reached on 85 specific statements. NERD was defined as a condition with reflux symptoms in the absence of mucosal lesions or breaks detected by conventional endoscopy, and without prior effective acid-suppressive therapy. Evidence supporting this diagnosis included: responsiveness to acid suppression therapy, abnormal reflux monitoring or the identification of specific novel endoscopic and histological findings. Functional heartburn was considered a separate entity not related to acid reflux. Proton pump inhibitors are the definitive therapy for NERD, with efficacy best evaluated by validated quality-of-life instruments. Adjunctive antacids or H2 receptor antagonists are ineffective, surgery seldom indicated. Conclusions: Little is known of the pathobiology of NERD. Further elucidation of the mechanisms of mucosal and visceral hypersensitivity is required to improve NERD management.
    Digestion 10/2009; 80(2):74-88. DOI:10.1159/000219365 · 2.10 Impact Factor
  • W. Hameeteman · H. J. Houthoff · G. N. J. Tytgat ·
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    ABSTRACT: Barrett's esophagus (BE) is a complication of long-standing pathologic gastroesophageal reflux and is found in approximately 10% of patients with reflux esophagitis. As it is a premalignant condition with a 30- to 100-fold increased risk of developing adenocarcinoma, detection is important. Endoscopy is most sensitive for diagnosing BE. Biopsy specimens should be taken at various levels to look for intestinal-type epithelium, dysplasia, or carcinoma. Although an early carcinoma may present as a small ulcer or a small polypoid mass, carcinoma may be present without any endoscopic suspicion. No histologic markers have so far been found that are useful in screening for dysplasia, but flow cytometry may prove of use in the future. As dysplasia and carcinoma are almost always related to intestinal-type epithelium, patients with this epithelium may benefit from an endoscopic follow-up program.
    Scandinavian Journal of Gastroenterology 07/2009; 23(s154). DOI:10.3109/00365528809095944 · 2.36 Impact Factor
  • G. N. J. Tytgat · R. H. Hunt ·

    Scandinavian Journal of Gastroenterology 07/2009; 23(s146):225-230. DOI:10.3109/00365528809099149 · 2.36 Impact Factor
  • A. A. M. Geraedts · M. R. Esseveld · G. N. J. Tytgat ·
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    ABSTRACT: Chronic diarrhoea is a commonly occurring complaint. In a prospective study of 100 consecutive patients with chronic diarrhoea we established the proportions of the appearance of organic and functional diarrhoea, and, secondly, we investigated by means of a few low-stress procedures the possibility of screening for organic or functional diarrhoea. In this paper we describe the results of our study. It appears that, of the cases of chronic diarrhoea, 40% are of organic and 60% of functional origin. An overview of the value of the different procedures for use in diagnosis is presented. It appears that no single method alone could be used to distinguish with almost complete certainty patients with diarrhoea of organic origin and those with irritable bowel syndrome. A combination of several anamnestic data, laboratory findings, and other examinations made it possible to state with some certainty about patients with chronic diarrhoea that its cause was organic. At the end of the paper we propose an order in which tests of patients with chronic diarrhoea should be made.
    Scandinavian Journal of Gastroenterology 07/2009; 23(s154):46-56. DOI:10.3109/00365528809095950 · 2.36 Impact Factor
  • K. Huibregtse · J. Cheng · E. A. J. Rauws · G. N. J. Tytgat ·
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    ABSTRACT: Postoperative biliary strictures usually present with jaundice and/or cholangitis. Surgical reconstruction of these mostly proximal strictures is often associated with high morbidity and mortality. In addition, restenosis after surgery is common. We attempted endoscopic therapy in 63 consecutive patients with benign biliary strictures, by the placement of one or multiple 10 French endoprostheses. The procedure was successful in 54 out of 63 (86%) patients. All 54 had rapid clearance of jaundice and/ or cholangitis. Follow-up study during a median period of 32.5 (range, 1-96) months after stent removal of 35 patients showed 4 recurrent strictures and 5 recurrent stones. There was low morbidity and mortality associated with the procedures. Although placement of an endoprosthesis in this group of patients is technically difficult, we believe it should be considered as the initial therapeutic modality. The stents should preferably be multiple and left in situ for 1 year to avoid restenosis.
    Scandinavian Journal of Gastroenterology 07/2009; 24(s171):50-56. DOI:10.3109/00365528909091373 · 2.36 Impact Factor
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    ABSTRACT: Acute studies suggested a therapeutic benefit for fundus-relaxing drugs in functional dyspepsia (FD) with visceral hypersensitivity (VH) to gastric distention or impaired accommodation (IA), but long-term studies are lacking. R-137696 is a serotonin-1A (5-HT(1A)) receptor agonist which relaxes the proximal stomach in man. Our aim was to investigate the influence of R-137696 on symptoms in FD with VH or IA. Randomized, double-blind, placebo-controlled, parallel group study of 4 weeks R-137696 2 mg t.i.d. in FD with VH or IA. Symptoms were assessed using the patient assessment of upper gastrointestinal symptom severity index (PAGI-SYM) total score and individual symptom subscales. Barostat studies were performed before and after 4 weeks of treatment. Fifty-three patients (33 VH and 20 IA), 18 men, mean age 40 +/- 13 years were recruited. Twenty-four received placebo and 29 received R-137696. In VH patients, both placebo and R-137696 improved total symptom scores, with a tendency for superiority of placebo (-1.12 vs-0.51, P = 0.07). Placebo was superior for the subscales of early satiety, bloating, fullness and discomfort (all P < 0.05). In IA, both placebo and R-137696 had no significant influence on total or individual symptom scores (-0.08 and -0.27). In VH, both placebo and R-137696 increased the discomfort volume, without a statistical difference between both arms (+120 and +164 mL). In IA, both placebo and R-137696 enhanced accommodation, without a statistical difference between both (+77 and +159 mL). Adverse events were similar for drug and placebo. A 4-week administration of the fundus-relaxing 5-HT(1A) agonist R-137696 failed to significantly improve symptoms, VH or gastric accommodation compared to placebo.
    Neurogastroenterology and Motility 02/2009; 21(6):619-26, e23-4. DOI:10.1111/j.1365-2982.2008.01260.x · 3.59 Impact Factor
  • G N J Tytgat ·

    Best practice & research. Clinical gastroenterology 02/2009; 23(5):621. DOI:10.1016/j.bpg.2009.06.007 · 3.48 Impact Factor
  • Guido N Tytgat ·
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    ABSTRACT: Being a quaternary ammonium compound derived from scopolamine, the alkaloid hyoscine butylbromide (HBB) exerts anticholinergic effects without side effects related to the central nervous system because it does not pass the blood-brain barrier. Clinical experience with this antispasmodic dates back to the 1950s and led to its registration for treating abdominal cramps/spasm and for diagnostic imaging purposes. OBJECTIVES AND SCOPE: This review focuses on the therapeutic efficacy and safety of the parenteral administration of HBB for treating biliary and renal colic and acute spasm in the genito-urinary tract. In addition, its value for diagnostic or therapeutic procedures in the abdomen, as well as for labour and palliative care, is reviewed. With the generic and trade name of the drug combined with various search terms related to the relevant clinical applications, a thorough literature search was performed in the Medline and EMBASE databases in April 2008. In most clinical studies, recommended doses of 20-40 mg HBB were injected, mainly intravenously. Fast pain reduction was achieved by HBB in renal colic; about 90% of the patients showed good to moderate analgesic responses after 30 min and the onset of action was noticeable within 10 min. Similarly, a pain reduction of 42-78% was observed in patients with biliary colic within 30 min after a single intravenous injection of 20 mg. In contrast, no analgesic efficacy of a single injection of 20 mg was found after surgical or shock-wave procedures in the urogenital area. Administration of HBB prior to, or during, radiological imaging distended the gastrointestinal (GI) tract in double-contrast barium and computed tomographic colonography studies and reduced motion artefacts in magnetic resonance imaging. This improved diagnostic image quality and organ visualisation. Pre-medication led to shorter and easier endoscopy in some, but not all, studies. Because of cervical relaxation, HBB shortened total labour duration with 17-67%. It also relieved pain and reduced GI secretions in terminal cancer patients with inoperable bowel obstruction. With regard to its safety profile, parenteral administration of HBB is associated with mild and self-limiting adverse events, typical for anticholinergic drugs. These clinical results of rapid action and beneficial efficacy combined with good tolerability support the use of HBB in a range of indications related to acute abdominal spasm, in labour and palliative care and for supporting diagnostic and therapeutic abdominal procedures, where spasm may be a problem.
    Current Medical Research and Opinion 11/2008; 24(11):3159-73. DOI:10.1185/03007990802472700 · 2.65 Impact Factor
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    ABSTRACT: In the developed world, most patients with gastroesophageal reflux disease (GERD) do not exhibit erosions when examined by standard white light endoscopy. Despite the high prevalence of such non-erosive reflux disease (NERD), relatively little is known of its underlying pathophysiology, hence there is no clear guide to clinical management. To establish areas of agreement or uncertainty in NERD, an international meeting was held in Vevey, Switzerland, in late 2007. The goal was to document current thinking in the areas of clinical presentation, assessment of clinical outcome, pathobiological mechanisms, and define optimal clinical strategies to diagnose and manage NERD. After extensive debates, the modified Delphi technique was utilized to reach a consensus on 85 specific statements. In addition, it was proposed that NERD be defined as ‘a subcategory of GERD characterised by troublesome reflux-related symptoms in the absence of esophageal mucosal erosions/breaks at conventional endoscopy and without recent acid suppressive therapy’. Evidence in support of this diagnosis may include responsiveness to acid suppression therapy, abnormal reflux monitoring or the identification of specific novel endoscopic findings. Defining the current state of knowledge in NERD should help improve the elucidation and management of this condition in the future.
    Digestion 10/2008; 78(1):1-5. DOI:10.1159/000151248 · 2.10 Impact Factor
  • B D J van den Elzen · G N J Tytgat · G E E Boeckxstaens ·
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    ABSTRACT: Distal oesophageal acid exposure has been shown to increase visceral sensitivity of the proximal oesophagus via central sensitization. Here we evaluated whether acidification of the distal oesophagus also affects the sensorimotor function of the proximal stomach. A gastric barostat study combined with a 30-min acid (HCl 0.15 mol L(-1)) or saline infusion in the distal oesophagus was performed in 18 healthy volunteers. Gastric and cutaneous sensitivity was assessed before and up to 2 h after the start of infusion. Directly after acid infusion, but not after saline, the threshold for discomfort decreased (-6.4 +/- 1.7 vs 0.4 +/- 0.4 mmHg; P = 0.028) and distension-induced symptoms increased significantly compared with the baseline (122 +/- 49% vs -3 +/- 9%). Cutaneous sensitivity remained unaffected by acid infusion. In contrast, when the infused liquid was aspirated 3 cm more distally, at the level of the lower oesophageal sphincter, the effect of acid infusion on gastric sensitivity was abolished and the increase in distension-induced symptoms was reduced (61 +/- 24%). Distal oesophageal acid infusion induces visceral hypersensitivity without affecting somatic sensitivity arguing against a similar mechanism of central sensitization as observed in non-cardiac chest pain. As reduction of the acid load to the stomach prevented this effect, our findings indicate that either gastric and/or duodenal acidification is involved. It should be emphasized though that aspiration from distal oesophagus may have attenuated the effect by reducing the acid-exposed area or by reducing the contact time.
    Neurogastroenterology and Motility 09/2008; 21(2):160-9. DOI:10.1111/j.1365-2982.2008.01172.x · 3.59 Impact Factor
  • Guido N J Tytgat ·
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    ABSTRACT: Histologic markers of reflux-induced mucosal injury are demonstrable in patients with nonerosive gastroesophageal reflux disease (neGERD). They include papillary elongation, basal cell hyperplasia, and dilation of intercellular spaces, especially of the prickle layer. These abnormalities are responsive to acid-suppressive therapy. Unfortunately, the longitudinal and circumferential distributions of these anomalies are nonuniform. They are presumably focalized on top of the esophageal folds, where the brunt of acid exposure and injury occurs. Therefore, based on current evidence, routine, random, nontargeted biopsies of the distal esophagus cannot be recommended in patients with neGERD. This may change if future studies reveal a high sensitivity and specificity of biopsies obtained from the squamocolumnar junction and the tops of the mucosal folds at 2 cm and 4 to 5 cm in patients with neGERD.
    Current Gastroenterology Reports 07/2008; 10(3):231-4. DOI:10.1007/s11894-008-0048-1
  • G. N. J. TYTGAT ·

    Journal of Gastroenterology and Hepatology 03/2008; 6(2):103 - 103. DOI:10.1111/j.1440-1746.1991.tb01447.x · 3.50 Impact Factor
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    ABSTRACT: Gastro-oesophageal reflux disease (GERD) is associated with a variety of typical and atypical symptoms. Patients often present in the first instance to a pharmacist or primary care physician and are subsequently referred to secondary care if initial management fails. Guidelines usually do not provide a clear guidance for all healthcare professionals with whom the patient may consult. To update a 2002-treatment algorithm for GERD, making it more applicable to pharmacists as well as doctors. A panel of international experts met to discuss the principles and practice of treating GERD. The updated algorithm for the management of GERD can be followed by pharmacists, for over-the-counter medications, primary care physicians, or secondary care gastroenterologists. The algorithm emphasizes the importance of life style changes to help control the triggers for heartburn and adjuvant therapies for rapid and adequate symptom relief. Proton pump inhibitors will remain a prominent treatment for GERD; however, the use of antacids and alginate-antacids (either alone or in combination with acid suppressants) is likely to increase. The newly developed algorithm takes into account latest clinical practice experience, offering healthcare professionals clear and effective treatment options for the management of GERD.
    Alimentary Pharmacology & Therapeutics 03/2008; 27(3):249-56. DOI:10.1111/j.1365-2036.2007.03565.x · 5.73 Impact Factor
  • M E van Leerdam · G N J Tytgat ·

    Baillière&#x027 s Best Practice and Research in Clinical Gastroenterology 02/2008; 22(2):207-8. DOI:10.1016/j.bpg.2007.12.002 · 3.48 Impact Factor

Publication Stats

35k Citations
5,302.46 Total Impact Points


  • 2011
    • Erasmus MC
      • Department of Internal Medicine
      Rotterdam, South Holland, Netherlands
  • 1973-2011
    • University of Amsterdam
      • • Department of Gastroenterology and Hepatology
      • • Department of Surgery
      • • Department of Pharmacy
      • • Department of Internal Medicine
      • • Department of Medicine
      Amsterdamo, North Holland, Netherlands
  • 1991-2009
    • Academic Medical Center (AMC)
      Amsterdamo, North Holland, Netherlands
    • Università degli Studi di Bari Aldo Moro
      Bari, Apulia, Italy
  • 1984-2009
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • • Department of Gastroenterology and Hepatology
      • • Academic Medical Center
      • • Department of Nuclear Medicine
      Amsterdamo, North Holland, Netherlands
  • 2008
    • Royal Adelaide Hospital
      • Department of Gastroenterology and Hepatology
      Tarndarnya, South Australia, Australia
  • 1982-2008
    • University of Leuven
      Louvain, Flemish, Belgium
  • 2001
    • Second Military Medical University, Shanghai
      Shanghai, Shanghai Shi, China
    • Bernhoven Hospital
      Os, North Brabant, Netherlands
  • 1996-2001
    • Onze Lieve Vrouwe Gasthuis
      • Department of Intensive Care
      Amsterdamo, North Holland, Netherlands
    • United States Department of Veterans Affairs
      Бедфорд, Massachusetts, United States
    • Het Oogziekenhuis Rotterdam
      Rotterdam, South Holland, Netherlands
    • University Medical Center Utrecht
      • Division of Pediatrics
      Utrecht, Provincie Utrecht, Netherlands
  • 1999
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
    • University of Michigan-Dearborn
      • Department of Behavioral Sciences
      Dearborn, MI, United States
    • University of Sydney
      Sydney, New South Wales, Australia
    • University of Bologna
      Bolonia, Emilia-Romagna, Italy
  • 1998
    • Slotervaartziekenhuis
      Amsterdamo, North Holland, Netherlands
    • Columbia University
      New York City, New York, United States
  • 1997
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 1995
    • GGD Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 1994
    • Utrecht University
      • Department of Gastroenterology and Hepatology
      Utrecht, Utrecht, Netherlands
  • 1992-1994
    • Georgetown University
      • Division of Gastroenterology
      Washington, Washington, D.C., United States
  • 1990
    • VU University Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 1989
    • Leiden University
      Leyden, South Holland, Netherlands
  • 1987-1989
    • Netherlands Cancer Institute
      Amsterdamo, North Holland, Netherlands
  • 1988
    • Leiden University Medical Centre
      • Department of Pathology
      Leiden, South Holland, Netherlands
  • 1985
    • Académie Universitaire Wallonie-Bruxelles
      Bruxelles, Brussels Capital, Belgium
  • 1981
    • University of Washington Seattle
      • Department of Medicine
      Seattle, Washington, United States