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High-value laboratory testing in erectile dysfunction, reduced sexual desire, and suspected hypogonadism: analytical
Marek Broul1, Petr Kelbich2, Adéla Jizerová2
1Department of Sexology, Krajská zdravotní, a.s. - Masaryk Hospital in Ústí nad Labem, Stará 1799/1, 400 01 Ústí nad Labem, Czech Republic; Department of Urology, Krajská zdravotní, a.s. - Litoměřice Hospital, Žitenická 2084, 412 01 Litoměřice, Czech Republic; Faculty of Health Studies, Jan Evangelista Purkyně University in Ústí nad Labem, Sociální péče 3652/13, 400 11 Ústí nad Labem, Czech Republic.
Abstract:
In men presenting with erectile dysfunction, reduced sexual desire, or suspected hypogonadism, laboratory work-up frequently oscillates between indiscriminate hormone panels and underuse of high-yield metabolic testing. From a clinical biochemistry perspective, the key question is not how many biomarkers can be ordered, but which tests are analytically fit for purpose and likely to change management. This evidence-informed narrative review examines biomarkers commonly used in erectile dysfunction and androgen-deficiency phenotypes, with emphasis on glycemic biomarkers, lipids, testosterone, sex hormone-binding globulin (SHBG), calculated free testosterone, prolactin, thyroid function tests, and selectively indicated estradiol. The review focuses on preanalytical control, assay limitations, interpretative pitfalls, and laboratory stewardship. In most men with erectile dysfunction, the highest-value initial laboratory panel consists of fasting glucose and/or hemoglobin A1c (HbA1c), a lipid profile, and early-morning fasting testosterone, provided recent results are unavailable. Low or borderline testosterone should be confirmed on a second independent early-morning fasting sample before biochemical classification, with attention to assay performance and to SHBG with calculated free testosterone when indicated. Prolactin testing is reserved for selected endocrine phenotypes and must account for medication use, macroprolactin, and the hook effect. Thyroid tests and estradiol should be phenotype driven rather than routine. A selective, analytically robust testing strategy can reduce misclassification, support cardiovascular and endocrine phenotyping, and better align biomarker results with clinically actionable decisions.
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