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Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels
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Journal Article
Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels
2017
Overview
Benefits associated with lowered serum DHT levels after 5α-reductase
inhibitor (5AR-I) therapy in men have contributed to a misconception that circulating DHT
levels are an important stimulus for androgenic action in target tissues
(e.g., prostate). Yet evidence from clinical studies indicates that
intracellular concentrations of androgens (particularly in androgen-sensitive tissues) are
essentially independent of circulating levels. To assess the clinical significance of
modest elevations in serum DHT and the DHT/testosterone (T) ratio observed in response to
common T replacement therapy, a comprehensive review of the published literature was
performed to identify relevant data. Although the primary focus of this review is about
DHT in men, we also provide a brief overview of DHT in women. The available published data
are limited by the lack of large, well-controlled studies of long duration that are
sufficiently powered to expose subtle safety signals. Nonetheless, the preponderance of
available clinical data indicates that modest elevations in circulating levels of DHT in
response to androgen therapy should not be of concern in clinical practice. Elevated DHT
has not been associated with increased risk of prostate disease (e.g.,
cancer or benign hyperplasia) nor does it appear to have any systemic effects on
cardiovascular disease safety parameters (including increased risk of polycythemia) beyond
those commonly observed with available T preparations. Well-controlled, long-term studies
of transdermal DHT preparations have failed to identify safety signals unique to markedly
elevated circulating DHT concentrations or signals materially different from T.Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not
correlate with those found in androgen sensitive tissue due to homeostatic control of
intracellular DHT.
Publisher
Endocrine Society,Oxford University Press
