Genetic database initiatives have given rise to considerable debate about their potential harms and benefits. The question arises as to whether existing ethical frameworks are sufficient to mediate between the competing interests at stake. One approach is to strengthen mechanisms for obtaining informed consent and for protecting confidentiality. However, there is increasing interest in other ethical frameworks, involving solidarity--participation in research for the common good--and the sharing of the benefits of research.

Certain properties of the atypical serum lipoprotein, referred to as pre‐β1‐lipoprotein, suggested that it might be identical to the lipoprotein carrying the Lp(a) antigen: Lp(a) lipoprotein. Both lipoprotein phenomena are under genetic control and occur in a certain proportion of healthy people. Pre‐β1‐lipoprotein occurs more frequently in patients with coronary heart disease (CHD) than in the healthy population. The present study of Finnish CHD patients was undertaken to investigate whether a close relationship could be revealed between pre‐β1‐lipoprotein and Lp(a) lipoprotein, as well as between Lp(a) lipoprotein and CHD. Both expectations were realised, and we conclude that pre‐β1‐lipoprotein is very closely related, if not identical to Lp(a) lipoprotein. If the present results are confirmed in future studies, serum analysis for Lp(a) lipoprotein/pre‐β1‐lipoprotein may become a useful tool for the identification in early life of members of a subpopulation which is particularly at risk for developing CHD.

A significant fraction (30%) of the genetically determined variance in plasma concentration of the von Willebrand factor antigen (vWf:Ag) has been shown to be related to ABH determinants. Individuals with blood group O, who have the highest amounts of blood group H substance, have the lowest concentration of vWf:Ag. The Lewis substances, Le(a) and Le(b), are biochemically closely related to the ABH substances as both can be produced from the same precursor substance. We studied the effect of the presence of the Lewis antigens on the plasma concentration of vWf:Ag and factor VIII antigen (VIII:Ag) in 323 individuals of different ABO groups from a series of twins and in 58 blood donors of blood group O. Among persons belonging to blood group O, those with the Le(a) antigen had a higher concentration of both vWf:Ag and VIII:Ag than individuals lacking Le(a). Le(a+b-) people are nonsecretors and Le(a-b+) people are secretors of ABH substance. Thus, the lowest concentration of vWf:Ag and VIII:Ag was found in group O secretors. The effect is most likely due to an effect of the secretor locus. This finding may be of importance for the detection of carriers of hemophilia A and for the diagnosis of type I von Willebrand disease.

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Abstract. Djurovic S, Os I, Hofstad AE, Abdelonoor M, Westheim A, Berg K (Ulleva Êl University Hospital and the University of Oslo, Oslo, Norway). Increased plasma concentrations of TGF-b 1 after hormone replacement therapy. J Intern Med 2000; 247: 279± 285.Objectives and design. Hormone replacement therapy (HRT) in postmenopausal women may reduce the cardiovascular risk. A dominant protective role of transforming growth factor beta (TGF-b 1 ) on coronary arteries has been proposed. Lp(a) lipoprotein may block the activation of latent TGFb 1 . Given this background, we examined the effects of HRT on TGF-b 1 and Lp(a) lipoprotein in 99 postmenopausal women. The women had angiographically documented coronary heart disease (CHD) and were randomized to either sequential transdermal 17b-oestradiol for 14 weeks and then medroxyprogesterone (MPA) for 14 days (HRT) or to a control group (C).Results. Serum levels of TGF-b 1 were increased in the HRT group compared with the C group after 3 months' treatment and this effect was sustained after 12 months. There was a significant reduction in Lp(a) lipoprotein serum levels after 3 months' treatment in the HRT group compared with the C group. However, after 12 months, no significant difference in changes in Lp(a) lipoprotein serum levels was detected between the two groups. Conclusion. The novel observation that transdermal 17b-oestradiol in postmenopausal women increases levels of TGF-b 1 and lowers the concentration of Lp(a) lipoprotein suggests yet another possible mechanism for the cardioprotective effect of HRT. Whereas combination therapy of oestradiol and MPA preserves the beneficial effect on TGF-b 1 , it reduces the unopposed oestradiol effects on Lp(a) lipoprotein.