[Alternative account of therapeutic effects in osteoporosis].
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Biomedical subjects
Publications and source records attributed to H Liedholm.
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The purpose of drug information from the pharmaceutical industry is to increase sales. The message is often simplified, short, with emphasis on Unique Selling Points (USP). Information is often given in a pleasant environment, food is served, gifts handed out. The same information is repeated in advertising campaigns. However, the information is often incomplete and the level of evidence not discussed. The purpose of producer independent information is to give scientific facts according to the principles practiced by evidence-based medicine. This information focuses on the level of evidence of published papers but is often more lengthy, may be difficult to understand and may even be regarded as boring. There are, however, useful principles to apply when analysing the information given by the pharmaceutical industry on specific drugs. There are also several sources of independent drug information to turn to.
OBJECTIVE: Individual-based studies on restricted geographical settings have suggested that non-steroidal anti-inflammatory drugs (NSAIDs) may precipitate congestive heart failure. As NSAID use is very extensive, it might increase the occurrence of symptomatic heart failure in the general population. Therefore, in order to study the impact of NSAID utilisation (prescribed and over the counter) on hospitalised heart failure in an entire country (Sweden), we performed an ecological analysis, a design appropriate for studying large geographical areas. METHODS: We employed weighted (population size) ecological linear regression to study the association between outpatient utilisation of NSAIDs during 1989-1993 and hospitalised heart failure in 1993 in 283 of Sweden's 288 municipalities. Data were adjusted for age and gender proportions, socio-economic factors, latitude and utilisation of cardiovascular drugs, aspirin, low-dose aspirin and paracetamol. RESULTS: The unadjusted relative risk of hospitalised heart failure for each increase of one standard deviation of NSAID utilisation (5.8 defined daily doses/1000 inhabitants/day) was 1.23 [95% confidence interval (CI) 1.18, 1.27]. After adjustments, the relative risk was 1.08 (95% CI 1.04, 1.12); the corresponding values if aspirin (non-low-dose) was included as an NSAID were 1.26 (95% CI 1.23, 1.28) and 1.07 (95% CI 1.04, 1.10). There was no such adjusted association with the utilisation of paracetamol-0.95 (95% CI 0.92, 0.98). CONCLUSION: The NSAID--heart failure association already established by individual-based studies on restricted geographical settings was corroborated in the present ecological study based on the whole population of an entire country (Sweden). Efforts should be made to promote a rational use of NSAIDs in the general population.
In a randomised, controlled trial, patients with joint diseases and concomitant treatment with NSAIDs and diuretics received systematic education. The intervention group was given information by a self-conducted, interactive Kodak Photo-CD program in addition to personal drug information and non-commercial drug leaflets. Awareness of drug interactions and encouragement of self-adjustment of treatment was focused on. Control patients received conventional information. Three months after randomisation, knowledge was tested by means of a questionnaire. At 3 months there was a significant difference in attained score between the intervention group and the control group. Greater knowledge was achieved, especially on drug interaction, in the intervention group. In conclusion, less than 1 h of systematic education significantly improved patients' knowledge on essential issues of concomitant treatment with NSAIDs and diuretics. Knowledge of effects, side-effects and interactions of drugs is essential for self-adjustment of treatment. The method employed, which is standardised and produces a reproducible quantity of education, might be applicable to several other medical conditions.
STUDY OBJECTIVE: Although national variation in short-term prognosis (that is, 30 day mortality) after a patient's first hospitalisation for heart failure may depend on individual differences between patients, dissimilarities in hospital practices may also influence prognosis. This study, therefore, sought to disentangle patient determinants from institutional factors that might explain such variation. DESIGN: A multilevel logistic regression modelling was performed with patients (1st level) nested in hospitals (2nd level). Institutional effects (that is, 2nd level variance and intra-hospital correlation) were calculated unadjusted and adjusted for specific patient (that is, age and previous diseases) and institutional (that is, size of hospital) characteristics. Patients were followed up until death or 30 days from hospital admission. SETTING: Hospitals in Sweden. PATIENTS: The study identified all the 20420 men and 17923 women (ages 65 to 85) admitted to the 90 acute care hospitals in Sweden during the period 1992-1995 for their first hospitalisation attributable to heart failure. MAIN RESULTS: Patient age and previous diseases (particularly senile dementia) were major determinants of impaired prognosis. Institutional factors explained only 1.6% and 2.3% of the total variation in 30 day mortality in men and women, respectively. These modest institutional effects remained after adjusting for patient age and previous diseases, but were in part explained by hospital size. CONCLUSIONS: National variation in short-term prognosis after an initial hospitalisation for heart failure was mainly explained by differences between patients, with hospital factors playing a minor part. Of the latter, hospital size seemed to emerge as one determinant (that is, the greater the number of patients, the better the individual prognosis).
BACKGROUND: Heart failure is a serious syndrome with a bad prognosis. Hospitalisation is common and readmittance rate is high; factors which influence the cost of care and treatment. Only scarce data on detailed patient materials regarding health care costs are known. AIMS: To describe in detail the health care costs for heart failure patients. METHODS: Costs for patients (n=108) who completed a randomised education trial were studied for 6 months after hospital discharge. Costs for hospital stay, out-patient visits, diagnostic tests and procedures, laboratory analyses and drug treatment were calculated. Official unit prices list used to reimburse providers of cross-boundary health services and prices for drugs in the Swedish Drug Compendium were employed. RESULTS: The total cost for a heart failure patient was approximately 20000 SEK (2564 US$, 7.80 SEK=1 US$) for 6 months. There was a 27-fold variation between patients. There was no relation between age or sex and cost. In decreasing order cost for hospitalisation was followed by costs for out-patient visits, diagnostic tests and procedures, laboratory analyses and drugs. CONCLUSION: Hospitalisation was the largest part of the total cost and there was a large inter-individual variation. Efforts to reduce the economic burden should be focused on hospitalisation. Due to skewed distribution, individual data must be considered in the analysis of the efforts.
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BACKGROUND: Many procedures for patient education are introduced in clinical practice without proper evaluation in randomised trials. AIMS: To compare systematic nurse and pharmacist led education including an interactive Kodak Photo-CD Portfolio technique with conventional information regarding heart failure patients' knowledge. METHODS: One hundred and thirty heart failure patients discharged from hospital were randomised to receive either conventional information or additional structured education with a follow-up of 6 months. Difference in knowledge was tested by questionnaire after 6 months. RESULTS: At the end of the study there was a significant difference in the intervention group (n = 50) compared to the control group (n = 58) regarding knowledge as tested by a questionnaire. Of maximal 28 points the intervention group attained 17.2 points (mean) and the control group 14.3 points (mean), 95% confidence interval for difference 1.0-4.7 points (P = 0.0051). CONCLUSIONS: Two to 3 hours of systematic education improved heart failure patients' knowledge on essential issues. High age does not preclude the introduction of a new technique for patient education.
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The influence of food on presystemic metabolism of single doses of amitriptyline (AMI) and nortriptyline (NT) was examined. In randomised order 25 mg tablets of each drug was given to 9 healthy, female volunteers both in the fasting state and together with a standardised breakfast. Concentrations of the drugs and of their dealkylated, hydroxylated and conjugated metabolites were measured by gas chromatography--mass spectrometry (AMI experiment) or high-pressure liquid chromatography (NT experiment). Standard pharmacokinetic parameters were calculated. Food intake did not consistently or significantly influence the bioavailability of either AMI or NT, nor the demethylation of AMI, nor the hydroxylation or the primary or secondary conjugation of NT. There were large interindividual changes in AUC of AMI after food (+94% to -44%). A significant negative correlation between AUC of AMI but not of NT during fasting conditions and per cent change in AUC after food was found (r = -0.72, P = 0.029). The implication of this (negative) correlation for an individual patient might be to keep the intake of the drug in standardised relation to food to avoid undue heavy changes in drug concentration, which might just occur with a change in time relation between intake of drug and food. From a mechanistic view the results argue against a direct and selective influence of food on the presystemic oxidation and conjugation of weakly basic drugs but does not exclude that food may reduce the presystemic metabolism of some such drugs indirectly, by enhancing their rate of hepatic delivery. Presentation of data from food interaction studies should not be restricted to general descriptions. It seems equally important to present the variability of individual data to allow inspection of the extent and direction of effects. This should be of interest for patient, prescriber as well as the regulatory agency.
OBJECTIVE: To analyse the association between use of antihypertensive treatment, diastolic blood pressure, and long term incidence of ischaemic cardiac events in elderly men. DESIGN: Population based cohort study. Baseline examination in 1982-3 and follow up for up to 10 years. SETTING: Malmŏ, Sweden. SUBJECTS: 484 randomly selected men born in 1914 and living in Malmŏ during 1982. MAIN OUTCOME MEASURES: Observational comparisons of incidence rates and rate and hazard ratios of ischaemic cardiac events (myocardial infarction or death due to chronic ischaemic cardiac disease). RESULTS: The crude incidence rate of ischaemic cardiac events was higher in those subjects who were taking antihypertensive drugs than in those who were not (rate ratio 2.6 (95% confidence interval 1.7 to 3.9)). After adjustment for potential confounders (differences in baseline smoking habits, blood pressure, time since diagnosis of hypertension, ischaemic or other cardiovascular disease, hypercholesterolaemia, hypertriglyceridaemia, diabetes mellitus, obesity, and raised serum creatinine concentration) this rate was reduced but still raised (hazard ratio 1.9 (1.0 to 3.7)). In men with diastolic blood pressure > 90 mm Hg, antihypertensive treatment was associated with a twofold increase in the incidence of ischaemic cardiac events (rate ratio 2.0 (1.1 to 3.6)), which vanished after adjustment for potential confounders (hazard ratio 1.1 (0.5 to 2.6)). In those subjects with diastolic blood pressure < or = 90 mm Hg, antihypertensive treatment was associated with fourfold increase in incidence (rate ratio 3.9 (2.1 to 7.1)), which remained after adjustment for potential confounders (hazard ratio 3.8 (1.3 to 11.0)). CONCLUSION: Antihypertensive treatment may increase the risk of myocardial infarction in elderly men with treated diastolic blood pressures < or = 90 mm Hg.
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