The Swedish system for the classification of fetal risk of drugs was the first of its kind and was implemented in 1978. Drugs for use in pregnant women are classified in 4 general categories--A to D. The US Food and Drug Administration (FDA) introduced a system in 1979 also using the letters A to D, together with an X category. However, the definitions differ considerably between the FDA system and the Swedish system, resulting in a very different allocation of drugs to the respective categories. In the Swedish system, category A includes drugs that have been extensively used and/or for which there are reliable clinical data indicating no evidence of disturbance of the reproductive process. Category B includes drugs for which data from pregnant women are insufficient for making any solid estimation of human teratogenic risk, and classification is therefore based on animal data, with allocation to 3 subgroups. For products in category C, the pharmacological action of the drug may have undesirable effects on the human fetus or newborn infant. Finally, category D contains drugs for which human data indicate an increased incidence of malformations. The categorisation statement is always followed by a short explanatory text. In contrast to the FDA system, the Swedish system has been well accepted, as judged by an interview study including 934 physicians and pharmacists. We believe that much of the American dissatisfaction may be a consequence of shortcomings in the category definitions of the FDA system. The FDA system requires an unrealistically high quality of data, e.g. the availability of controlled studies in pregnant women that fail to demonstrate a risk to the fetus are needed for a drug to be assigned to category A. Consequently, the majority of drugs on the US market are allocated to category C, interpreted as 'risk cannot be ruled out'. The distribution of drugs into the various categories is thus very different between the Swedish and FDA systems. We think that the issue of this debate reflects a fundamental problem related to public health information: how should a large, compounded, changing and difficult to evaluate databank be organised before it is made available to professionals and secondarily to lay people?
(i) to compare Helicobacter pylori serology in two 70-year-old cohorts in Gothenburg, Sweden, born 21 years apart, (ii) to study H. pylori serology in a 70-year-old cohort over 20 years.
H. pylori serology at the age of 70 was investigated in 98 men and 132 women born in 1901/02 and in 77 men and 113 women born in 1922. In 21 men and 40 women Helicobacter serology was monitored longitudinally with examinations at 70, 81, and 90 years of age. The analyses were performed on frozen samples by use of an in-house enzyme immunoassay with a sensitivity of 0.99, specificity of 1.00 and positive and negative predictive values of 0.96 and 1.00, respectively. Absorbance values or = 0.700 were interpreted as positive, and values in between as inconclusive.
The 70-year-old cohort, born in 1922, showed a significantly lower proportion of subjects with positive H. pylori serology in both men (57.1% vs 80.6%) and women (48.7% vs 75.8%) compared with 70-year-olds born in 1901/02. There were no significant sex differences in either cohort. No longitudinal increase or decrease could be demonstrated in those who were examined at 70, 81 and 90 years of age.
The difference in H. pylori prevalence between the two cohorts may reflect a rapid change in socio-economic conditions in Sweden during this 20-year period.
The aim of the present work was to investigate the effect of adrenergic alpha- and beta-1-receptor stimulation on the peripheral platelet count. The experiments were carried out on 8 healthy male volunteers using radioisotopically labelled platelets. 3 subjects received i.v. infusions of adrenaline (0.09 microgram X kg-1 X min-1) before and after the ingestion of 40 mg propranolol. In response to the first infusion there was an instant increase in the venous platelet-bound radioactivity (PBR) which amounted to 12% over basal value. This effect of adrenaline seemed to be potentiated by propranolol pretreatment. 5 subjects received i.v. infusions of the highly selective beta-1-receptor agonist H 133/22 (prenalterol, Hässle, Sweden). In response to a cumulative dose of 4.75 mg prenalterol a slight but significant (P less than 0.05) decrease in PBR occurred. It is concluded that alpha-receptor stimulation causes a depletion of platelets from the exchangeable splenic platelet pool resulting in a concomitant increase in the peripheral platelet count. Beta-receptor stimulation has an opposite effect on the spleen. The trapping of platelets by the spleen is mediated both via beta-1- and beta-2-receptors, but the effect of beta-2-receptor stimulation seems to predominate.