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Context Risk-reducing salpingo-oophorectomy (RRSO) is performed in BRCA1 or 2 mutant carriers to minimize ovarian cancer risk. Although studies have been performed investigating sex steroid levels, menopausal complaints and sexual functioning in relation to RRSO, their exact relationship remains unknown. Objectives To investigate the impact of RRSO on serum sex steroid levels and their association with menopausal complaints and sexual functioning. Methods This prospective observational cohort study included 57 pre- and 37 postmenopausal women at risk of ovarian cancer and opting for RRSO. Data collection involved validated questionnaires on sexual functioning and menopausal complaints. Testosterone, androstenedione, estradiol and estrone levels in serum determined by liquid chromatography-tandem mass spectrometry were obtained one day before, six weeks and seven months after RRSO. Results In premenopausal women, all four steroids were decreased both six weeks (p<0.01) and seven months (p<0.01) after RRSO. Furthermore, in these women, decreases in estrogens were associated with a decrease in sexual functioning seven months after RRSO (p<0.05). In postmenopausal women, only testosterone was decreased six weeks and seven months (p<0.05) after RRSO, which was associated with an increase in menopausal complaints at seven months post-RRSO (p<0.05). Conclusion Our results suggest that in premenopausal women, decreases in estrogens are related to a decrease in sexual functioning and that in postmenopausal women, testosterone is decreased after RRSO, which indicates that postmenopausal ovaries maintain some testosterone production. Furthermore, in postmenopausal women, a strong decrease of testosterone was associated with more menopausal complaints indicating that future studies investigating testosterone supplementation are warranted.

Background In vitro haemolysis is a major operational challenge for medical laboratories. A new experimental design was used to investigate under what conditions algorithms could be designed to report either quantitative or qualitative aspartate aminotransferase and lactate dehydrogenase results outside the manufacturer’s haemolysis specifications. Quantitative corrections were required to meet prespecified quality specifications. Methods Twenty-five patient samples were used to design reporting algorithms and another 41 patient samples were used to validate the algorithms. Aspartate aminotransferase, lactate dehydrogenase and haemolysis index were determined using a Cobas 6000 analyser (Roche diagnostics, Mannheim, Germany). Correction factors were determined, and the accuracy of the correction was investigated. Reporting algorithms were designed based on (i) the manufacturer’s cut-off for the haemolysis index, (ii) corrections within the total allowable error specification and (iii) qualitative reporting based on obtained results. The impact of the reporting algorithms was retrospectively determined by recalculating six months of aspartate aminotransferase and lactate dehydrogenase results. Results No correction for aspartate aminotransferase/lactate dehydrogenase was possible for results below the upper reference interval limit, while results equal to or greater than the upper reference interval limit could, up to mild haemolysis, be corrected within the total error criterion. All samples generated from the validated patient cohort fulfilled the set criteria. The algorithms allowed reporting 88.5% and 85.9% of otherwise unreported aspartate aminotransferase and lactate dehydrogenase results, respectively. Conclusions An approach is presented that allows to generate and validate reporting algorithms for aspartate aminotransferase and lactate dehydrogenase compatible with prespecified quality specifications. The designed algorithms resulted in a significant reduction of otherwise unreported aspartate aminotransferase and lactate dehydrogenase results.

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