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Glucocorticoid-induced cardiomyopathy: unexpected conclusion
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    Misguided case study

    Exogenous anabolic steroids are not a direct causative factor of glucocorticoid excess as stated by the authors. Although the phenotypes of injury (i.e., collagen infiltration, fibrosis, lowered ejection fraction via LVH) are similar as mentioned per Youssef et al. (2011), the primary evidence (reference #1; Delivanis et al., 2020) used to claim that glucocorticoid excess results from AAS does not mention exogenous androgen derivatives (AAS) anywhere in the entire Chapter 15. Let us not forget the AAS are androgens, not mineralocorticoids. Endogenous androgen increases (or excess) from pathological disorders were the only androgens mentioned in Delivanis et al. (2020) and the only citations (Delivanis et al., 2020; #189-191) in this primary cited evidence, in no manner, shape, or form, supports the inclusion of AAS to make an extrapolation that glucocorticoid resistance results from exogenous androgens (AAS) but only that glucocorticoid resistance can result from excess endogenous androgens due to various pathologies.

    Using high-index value topics like anabolic-androgenic steroids to support a case report that does not involve AAS, seems to be more of either ignorance of the AAS literature or misinterpretation of endogenous androgen excess and exogenous androgen abuse.

    The case does draw nice parallels between the phenotypes of injury (cortisol excess) and anabolic-androgenic steroid abuse, particularly activation of the RAAS. However, Youssef et al. (2011)...

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    Conflict of Interest:
    None declared.