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The etiology of multisomatoform disorder (MSD) is largely unknown, but an influence of genetic factors is likely. Since pain is a major component of MSD and dopamine as well as serotonin are involved in pain pathways, genes of the dopaminergic and serotonergic system are promising candidate genes and we assumed that polymorphisms could be associated with MSD. One hundred forty-nine patients with MSD and 149 age- and gender-matched healthy controls participated in this study. DNA from all participants was genotyped for 22 single nucleotide polymorphisms (SNPs) within genes of the dopaminergic and serotonergic system by polymerase chain reaction, a restriction enzyme analysis, and pyrosequencing. The distribution of SNP alleles, genotypes, and haplotypes was compared between patients and controls. Neither an allelic nor a genotypic association was found for any individual SNP, but testing for a haplotypic association revealed that a haplotype of the serotonergic genes HT(1B) and HT(1D) indicated a lower risk. However, this statistically insignificant protective effect became highly significant on the background of two DAT1 haplotypes. Interestingly, if these two DAT1 haplotypes are analyzed without considering the serotonergic genes as confounders, they are significantly associated with an enhanced risk. Taking into account observations from recent publications, this apparent contradiction might be explained with the complex interaction of the dopaminergic and serotonergic systems. To conclude, our results reveal an involvement of polymorphisms in dopaminergic and serotonergic genes in the etiology of MSD in patients of German descent, but their exact role in MSD requires further investigation.

In the course of the prospective, randomized, double-blind trial the influence of a high-dose riboflavin substitution on the risk for preeclampsia was studied in a high-risk collective 1. The present contribution evaluates supplementary data from the already published PROPER trial. The patients were from the two study centers M?rida, Venezuela, and Moshi, Tanzania, they were randomized from the 20th week of pregnancy and received either 15?mg riboflavin daily or placebo. Clinical and laboratory checks were carried out at four-week intervals up to childbirth. Concerning the question of whether there is a relationship between the serum levels of antioxidative vitamins and the risk of developing preeclampsia, it was found that no relationship could be detected between the measured laboratory values of vitamins E, A and B2 and the total risk of developing a hypertensive disease of pregnancy. On comparisons between patients with severe preeclampsia, those with a mild form, and the general healthy population, however, significant differences in the levels of antioxidative vitamins E and A as well as the FAD level were seen. The patients from Tanzania showed on the whole significantly lower vitamin levels than those from Venezuela, possibly due to the better nutritional situation in Venezuela. Considering the results altogether, the role of antioxidative parameters in the pathophysiology of preeclampsia remains unclear. However, the collected data provide valuable hints for future preventative strategies.

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