Jan Paul Ottervanger
Erasmus University Rotterdam
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Featured researches published by Jan Paul Ottervanger.
The Lancet | 1993
Jan Paul Ottervanger; B.H.Ch. Stricker; H.J.A. Paalman; G.L. Boxma
For sumatriptan, tightness in the chest caused by an unknown mechanism has been reported in 3-5% of users. We describe a 47-year-old woman with an acute myocardial infarction after administration of sumatriptan 6 mg subcutaneously for cluster headache. The patient had no history of underlying ischaemic heart disease or Prinzmetals angina. She recovered without complications.
The Journal of Allergy and Clinical Immunology | 1996
Jan Paul Ottervanger; Rita A.S. Phaff; Erik G.J. Vermeulen; Bruno H. Stricker
respiratory arrest in young patients with asthma. N Engl J Med 1991;324:359-63. 4. Malling HJ. Diagnosis and immunotherapy of mould allergy. Allergy 1986;41:342-50. 5. Beaumont F, Kauffman H, Sluiter H, de Vries K. Sequential sampling of fungal air spores inside and outside the homes of mold-sensitive asthmatic patients: a search for a relationship to obstructive reactions. Ann Allergy 1983;55: 740-6. 6. Hasnain S, Wilson J, Newhook F. Fungal allergy and respiratory disease. N Z Med J 1985;98:342-6. 7. Darke CS, Knowelden J, Lacey J. Respiratory disease of workers harvesting grain. Thorax 1976;31:294-302. 8. Harries MG, Lacey J, Tee TD, Cayley GR, Newman Taylor AI. Didymella exitialis and late summer asthma. Lancet 1985;1:1063-6. 9. Klaustermeyer WB, Bardana EJ, Hale FC. Pulmonary hypersensitivity to Alternaria and Aspergillus in bakers asthma. Clin Allergy 1977;7:227-33. 10. Fink JN. Hypersensitivity pneumonitis. In: Middleton E Jr, Reed CE, Ellis EF, Yunginger JW, Busse WW, eds. Allergy: principles and practice. 4th ed. St. Louis: Mosby, 1993;2:1415-31. 11. C6t6 J, Chan H, Brochu G, Chan-Yeung M. Occupational asthma caused by exposure to Neurospora in a plywood factory worker. Br J Ind Med 1991;48:279-82. 12. Malloch D. Moulds, their isolation, cultivation and identification. Toronto: University of Toronto Press, 1981. 13. von Arx JA. On Monilia sitophila and some families of Ascomycetes. Sydowia 1981;34:13-29. 14. Yassin S, Wheals A. Neurospora species in bakeries. J Appl Bacteriol 1992;72:377-80. 15. Shaw DE. Honeybees collecting Neurospora spores from steamed Pinus logs in Queenslan& The Mycologist 1993;7: 182-5. 16. Abdel-Rahman TMA, Salama AAM, Ali MIA, Tharwat NAH. Fibrinolytic activity of some fungi isolated from self-heated composted fertilizer. Mag Tokyo 1990;103: 313-24. 17. Song HS, Min KH. Microfungal flora of Tricholoma matsutake producing and nonproducing sites in the forest of Pinus densiflora. Korean J Mycol 1991;19:109-19.
CNS Drugs | 1995
Jan Paul Ottervanger; Bruno H. Stricker
SummaryThe serotonin (5-hydroxytryptamine; 5-HT) 5-HT1-receptor agonist sumatriptan is a relatively new antimigraine drug. Some clinical trials and postmarketing surveillance studies of sumatriptan have demonstrated the occurrence of angina pectoris, cardiac arrhythmias and myocardial infarction that can be attributed to the use of the drug.At present the mechanisms of these adverse effects have not be determined. However, a possible relationship between migraine per se and cardiovascular disease, and an association between serotonin and cardiovascular disease, do exist. There are data to suggest that sumatriptan causes constriction of coronary arteries. In contrast, some investigators believe that the chest pains experienced by some patients who take sumatriptan are not of cardiac origin, but are due to oesophageal contractions. Whatever the cause, it can be concluded that, although severe cardiovascular adverse reactions to sumatriptan may be rare, every case of chest pain after administration of sumatriptan requires careful evaluation.
European Journal of Clinical Pharmacology | 1996
Jan Paul Ottervanger; Hans A. Valkenburg; Diederick E. Grobbee; Bruno H. Stricker
Objective:To investigate the frequency of use and misuse of sumatriptan, and to explore the characteristics of patients reporting overuse.Setting:A postmarketing cohort study on adverse reactions to sumatriptan, performed with the assistance of drug-dispensing general practitioners in the Netherlands.Methods:Questionnaires were sent to patients on sumatriptan of drug-dispensing general practitioners in the Netherlands. Use of sumatriptan was classified into five groups: < 1, 1–10, 11–20 and 21–30 times per month and a group of patients who reported daily use of sumatriptan more than 10 times per week. Patients in the latter group were regarded as “overusers”.Results:The request to the 1720 patients yielded a response rate of 1202 (70%). Of 952 (79%) of these patients, details of their sumatriptan intake were available. Most patients (718, 75%) took sumatriptan 1–10 times each month. However, 36 patients (4%, 95% CI 2.8–5.2%) took sumatriptan daily or more than 10 times each week. The group with the highest intake consisted mainly of males, and many patients who reported a poor efficacy of sumatriptan. Age was not related to use of sumatriptan.Conclusions:A small group of patients (4%) used sumatriptan too often. A high intake was associated with both male gender and a reported poor efficacy of sumatriptan, but not with age, reported adverse reactions, or headache attributed to sumatriptan. It is important to explain to patients that sumatriptan is only for the treatment of acute attacks, and not for prophylactic use. Drug consumption patterns have to be evaluated, in particular in patients who report low efficacy of sumatriptan.
Journal of Clinical Epidemiology | 1994
B.H.Ch. Stricker; M.M. van der Klauw; Jan Paul Ottervanger; F.G.A. Van Der Meché
The Guillain-Barré syndrome is an inflammatory demyelinating polyneuropathy with an acute or subacute onset. The current case-control study was performed to investigate the possible role of drugs and other determinants in the causation of the Guillain-Barré syndrome. Patients were included as cases if they fulfilled the criteria for acute Guillain-Barré syndrome and were unable to walk 10 m independently and had been admitted to the hospital within 2 weeks of onset of the neuropathy. For every case, two controls without the disease were obtained from the general practitioner (GP) of the patient with Guillain-Barré syndrome. Controls had the same type of health care insurance, were of the same gender and age (within 5 years), and resident in the same area. By telephone, the GPs of the patients with Guillain-Barré syndrome were interviewed. There were 71 female and 75 male cases and 142 female and 149 male controls. Significantly more cases than controls had been prescribed drugs in the 3 months prior to the index date and also diagnoses or symptoms in cases were more common. Case patients used significantly more frequently antipropulsives (loperamide), penicillins (amoxicillin with or without clavulanic acid) and vaccines. Female controls used significantly more often oral contraceptives. More cases than controls suffered from infections of the respiratory, gastrointestinal or urinary tract prior to the onset of neurological symptoms. In a logistic regression analysis, symptoms concerning the gastrointestinal and respiratory system were strongly associated with the Guillain-Barré syndrome. The use of oral contraceptives was significantly lower in female cases which could be compatible with the hypothesis that these drugs are protective.
Netherlands Journal of Medicine | 1997
Bruno H. Stricker; J. Feenstra; Jan Paul Ottervanger; A. J. Porsius; Diederick E. Grobbee
BACKGROUND A recent interim analysis of the PRIME II placebo-controlled study showed a significantly higher mortality in the group treated with ibopamine than in the control group. The objective was to study mortality in patients on ibopamine, and to assess risk factors for death. METHODS All 2147 drug-dispensing outlets (DDO) in the Netherlands were asked to provide a printout of the complete medication history of users of ibopamine. A reaction was received from 92% of the DDO. From the 14,024 identified former or current users of ibopamine, a sample of 3148 patients (22%) was enrolled in the follow-up study. All general practitioners (GP) of these patients received an enquiry pertaining to the vital status of their patient, cause of death, primary cause and NYHA classification of heart failure, echo- and electrocardiographic data, serum creatinine, admissions and the effects of ibopamine. Cases were defined as patients who died during the follow-up period which ended on the day of return of the questionnaire or the day of decease (index date). Two random controls were obtained for each case from the non-deceased patients at the index date. The design was a follow-up study with risk factor assessment in a nested case-control design. RESULTS Questionnaires were returned regarding almost 70% of the sample. Mortality in this group was 25%. A case-control analysis was performed with the first 104 cases and 208 random controls. Patients with NYHA class IV had a 3-times increased risk of dying. In patients with a serum-creatinine level in the highest quartile the risk of dying was increased threefold. Higher doses of ibopamine seemed to have a protective effect. Significantly more cases than controls used amiodarone. Also, opioids were used more often, which may be related to their use in terminal cardiac failure. CONCLUSION NYHA classification and serum-creatinine levels were independent risk factors for death in patients with heart failure on ibopamine. Although there were increased risk estimates for current use of ibopamine and amiodarone, these did not reach statistical significance. This may be related, however, to the fact that this analysis was restricted to the first 20% of cases.
JAMA Internal Medicine | 1998
Eibert R. Heerdink; Hubert G. M. Leufkens; Ron M. C. Herings; Jan Paul Ottervanger; Bruno H. Stricker; Albert Bakker
British Journal of Clinical Pharmacology | 2003
B.H.Ch. Stricker; M.M. van Riemsdijk; Miriam Sturkenboom; Jan Paul Ottervanger
European Journal of Clinical Pharmacology | 1994
Jan Paul Ottervanger; T.B. vanWitsen; Hans A. Valkenburg; Diederick E. Grobbee; Bruno H. Stricker
JAMA Neurology | 1997
Jan Paul Ottervanger; Hans A. Valkenburg; Diederick E. Grobbee; Bruno H. Stricker