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Bernard Bannwarth

Publications and source records attributed to Bernard Bannwarth.

27 records · Page 2Linked to original sources
PubMed2003

Adverse events associated with rofecoxib therapy: results of a large study in community-derived osteoarthritic patients.

OBJECTIVE: To evaluate the safety profile of rofecoxib, a selective cyclo-oxygenase-2 inhibitor, in patients with osteoarthritis who are receiving care in non-hospital practice settings. DESIGN: All patients participating in a large 24-week, open-label, nonpharmacological intervention trial were given rofecoxib for painful osteoarthritis of the knee or hip. They started at a dose of 12.5mg once daily for the first month, with the option of increasing to 25mg daily thereafter, if needed for efficacy. Adverse events were closely monitored. We considered all adverse events that occurred during treatment and within 14 days of discontinuation of rofecoxib. PATIENT GROUP STUDIED: 2896 patients (861 males and 2035 females) were involved in the safety analysis. Their mean (SD) age was 66.8 (9.9) years, and 631 patients (21.8%) were aged >/=75 years. There were 913 patients (31.5%) with hypertension and 151 (5.2%) with diabetes mellitus at the start of the study; 78 patients (2.7%) had a prior medical history of angina and/or myocardial infarction. The mean (SD) duration of rofecoxib treatment was 139 (62) days. RESULTS: A total of 519 patients (17.9%) discontinued rofecoxib. The main reasons for discontinuation were dyspepsia (4.4%), nausea (2.4%) and dizziness (2.1%). The annualised incidence rates (95% CI) of complicated and uncomplicated upper gastrointestinal ulcers, myocardial infarction, and stroke were 1.36 (0.76-2.23), 0.09 (0-0.50) and 0.45 (0.16-1.05), respectively. CONCLUSION: This study conducted in conditions close to daily practice confirms that the use of rofecoxib is associated with a low rate of serious adverse events in patients with osteoarthritis.

Administration, Oral↗
PubMed2003

[Adverse drug effects observed at French admissions departments and emergency services (Prospective study of the National Educational Association for Teaching Therapeutics and proposals for preventive measures].

Various studies have shown that adverse drug events (ADE) are a substantial cause of hospital admissions. However, little is known about the incidence and severity of ADE resulting in hospital visits. To address this issue, we conducted a prospective survey in 10 primary care and emergency departments of French public hospitals. This study was performed over two periods of one week, one in June 1999 and one in December 1999, in primary care and emergency departments of five university hospitals and five general hospitals throughout France. Out of a total of 1,937 patients consulting, 1,562 were taking at least one drug during the previous week and were included for analysis according to the protocol. Altogether, 328 (21%; 95% confidence interval 19% to 23%) of these patients receiving at least one drug consulted because of an ADE. The sex ratio (M/F) was the same in both groups with or without ADE (1.04 vs 1.02, respectively, P = 0.83). Patients with ADE were older than those without (63.5 vs 54.8 years, P < 0.0001). Furthermore, ADR patients were more likely to have a higher severity score than no-ADE group (P = 0.019). The outcome seemed to be worse in patients with an ADE. The percentage of patients treated with 2 or more drugs and the number of drug exposures were significantly higher in patients with ADE than in those without (90.9% vs 75.0%, P < 0.0001, and 5.17 vs 3.82, P < 0.0001, respectively). The most frequent causes of visits for ADE-patients were digestive (n = 53, 16.2%), neurological (n = 52, 15.9%), cardiovascular (n = 49, 14.9%) and malaise (n = 49, 14.9%) events. In total, 410 drugs were incriminated in the occurrence of 328 ADE. The most frequently incriminated drug classes were (1) psychotropic agents, including anxiolytics and/or hypnotics, antidepressants and antipsychotics (n = 84, 20.5%), (2) diuretics (n = 48, 11.7%), (3) anticoagulants (n = 38, 9.3%), (4) other cardiovascular drugs (n = 63, 15.4%), and (5) analgesics, including non steroidal antiinflammatory agents (n = 57, 13.9%). The avoidability of ADE could be estimated by an external expert panel in 280 of the 328 cases. In 106 cases (37.9%), ADE was considered to be preventable because a contra-indication or a warning about drug use had not been respected.

Adult↗
PubMed2003

[Pharmacologic basis for using paracetamol: pharmacokinetic and pharmacodynamic issues].

The advantage of paracetamol (acetaminophen) is that it can be administered via the oral, intravenous or rectal routes. The last mentioned differs from the oral route in the slow and irregular absorption of the active substance. At therapeutic concentrations, the pharmacokinetics of paracetamol are linear--that is, independent of the dose, and constant with repeated administration. The efficacy of paracetamol has been demonstrated in a wide variety of acute or chronic painful syndromes. In adults, the optimum unit dose is 1 g. The maximum daily dosage is 4 g, consistent with the decline in analgesic activity, which is usually over 6 hours. With effervescent tablets, drug absorption and onset of action are more rapid than with conventional tablets. However, there is no direct correlation between serum concentrations of paracetamol and its analgesic or antipyretic effect. Paracetamol is the non-opiate analgesic of choice in elderly persons or patients with chronic renal insufficiency, and it is usually not necessary to reduce the dosage in such individuals, even though clearance is reduced. Although the bioavailability of paracetamol is not impaired in patients with chronic, benign liver diseases, the agent is contraindicated in those with hepatic insufficiency. It can be used during pregnancy and lactation. The very low level of paracetamol binding to plasma proteins, together with its hepatic metabolism, mainly through glucuronide or sulphate conjugation, account for the low risk of drug interactions with paracetamol, particularly with antivitamin K. When added to a traditional non-steroidal anti-inflammatory drug, paracetamol enhances the analgesic effect or allows the use of lower doses. It is more difficult to define the ideal dosage of paracetamol in children, because of the influence of age on its pharmacokinetics, and the relatively erratic bioavailability of suppositories. An oral dose of 15 mg/kg every 4 hours, up to a total of 60 mg/kg/day, is usually sufficient to achieve the desired analgesic or antipyretic effect.

Acetaminophen↗
PubMed2002

[Anti-inflammatory non-steroidal selective cyclooxygenase 2 inhibitors and gastroduodenal lesions].

NSAID CATEGORIES: Contrary to classical NSAIDs, which inhibit the 2 isoforms of cyclo-oxygenase (COX), coxibs do not affect COX-1, which catalyses the synthesis of cytoprotective prostaglandins in the stomach. ULCER COMPLICATIONS: The probability of developing a symptomatic, uncomplicated or complicated (perforation, gastric outlet obstruction, bleeding) gastroduodenal ulcer is significantly lower with a COX-2 selective inhibitor (Celecoxib, rofecoxib) than with a traditional NSAIDs, with a reduction in absolute risk of around 1-1.5 for 100 patient-years in clinical trials. The gastrointestinal toxicity of coxibs is greater than that of a placebo. THE INFLUENCE OF A CO-PRESCRIPTION OF ASPIRIN: Patients for whom low-dose aspirin is indicated to offset known thrombotic risk must continue this therapy if a COX-2 selective inhibitor is introduced. In that case, however, coxibs expose the patient to almost the same risk of severe gastroduodenal complications as with classical NSAIDs. TARGET POPULATION: In view of the lesser ulcerogenic potential of coxibs, patients at risk of gastrointestinal complications are the population of choice for these drugs. In the case of concomitant ingestion of aspirin for prevention of thrombosis, some authors prefer the association of classical NSAIs with proton pump inhibitors (omeprazole, lansoprazole) or misoprostol.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Drug-induced myopathies.

Drug-induced muscle disorders represent a broad clinical spectrum, from asymptomatic elevated serum creatine kinase levels to life-threatening myopathies. An increasing number of drugs have been suspected or identified as myotoxic. It would be unrealistic to attempt to list them. In clinical practice, an iatrogenic origin must be discussed in any patient presenting with muscle symptoms in as much as drug-induced myopathies are usually reversible after discontinuation of the offending compound. The clinical and histopathological features depend on the causative agent and individual susceptibility to a given compound. Apart from isolated myalgias, drug-induced myopathies can be divided into five major categories: necrotising myopathies mainly due to lipid-lowering drugs; inflammatory myopathies, including polymyositis (especially associated with thiol compounds) and maphrophagic myofasciitis; mitochondrial myopathies, mainly due to antiretroviral nucleoside analogues; corticosteroid myopathy; and various forms of painless neuromyopathies. In some cases (e.g., statin-induced myopathies), risk factors have been clearly identified and preventive measures have been recommended.

Adrenal Cortex Hormones↗
PubMed2002

Influence of Helicobacter pylori eradication therapy on the occurrence of gastrointestinal events in patients treated with conventional nonsteroidal antiinflammatory drugs combined with omeprazole.

OBJECTIVE: To evaluate the effect of eradication treatment of Helicobacter pylori and the influence of H. pylori status on the incidence of gastrointestinal (GI) events in rheumatic patients receiving longterm conventional nonsteroidal antiinflammatory drug (NSAID) therapy combined with omeprazole. METHODS: Patients (n = 919) requiring longterm NSAID therapy entered this multicenter, open label, parallel group study. H. pylori positive patients were randomized to receive either eradication therapy (omeprazole 20 mg bid, amoxicillin 1 g bid, and clarithromycin 500 mg bid for 7 days) or no therapy. Both these groups and the H. pylori negative patients were given omeprazole, 20 mg once daily, along with NSAID for the study duration (5-8 weeks). Treatment failure (primary outcome variable) was defined as the occurrence of severe GI event (symptomatic ulcer, bleeding, perforation) or dyspepsia leading to discontinuation of NSAID therapy, unscheduled consultation, or upper GI tract endoscopy. RESULTS: Treatment failure was recorded in 9/294 (3.06%) infected patients receiving eradication therapy, 8/219 (3.65%) infected patients receiving omeprazole alone, and 5/391 (1.28%) H. pylori negative patients (p > 0.05). H. pylori eradication did not appear to influence the incidence and severity of dyspeptic symptoms in infected patients. CONCLUSION: Our results do not support the use of H. pylori eradication therapy in rheumatic patients receiving conventional NSAID along with omeprazole.

Adult↗