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• Misguided case study
  Dr. Scott Howell
  Published on: 18 February 2021

• Published on: 18 February 2021

  Misguided case study

  • Dr. Scott Howell, Researcher/SME Trident University

  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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  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) does not mention that AAS bind to “mineralocorticoid receptors on cardiac and skeletal
  myocytes, causing hypertrophy via upregulation of the RAAS pathway, a pathway similar to cortisol,” but instead states verbatim “AAS bind to androgen receptors and may directly cause hypertrophy, via tissue upregulation of the renin angiotensin system.”

  Delivanis, D. A. (2020) Chapter 15 - Advances in the Diagnosis and Medical Management
  of Cushing’s Syndrome. Advances in Treatment and Management in Surgical
  Endocrinology, 151–174.

  189. Malchoff, C. D. & Malchoff, D. M. (2005). Glucocorticoid resistance and hypersensitivity. Endocrinol Metab Clin N Am, 34(2), 315e326.

  190. Bronnegard, M., Werner, S., & Gustafsson, J. A. (1986). Primary cortisol resistance associated with a thermolabile glucocorticoid receptor in a patient with fatigue as the only symptom. J Clin Investig, 78(5), 1270e1278.

  191. Lawson, E.A. et al. (2009). Adrenal glucocorticoid and androgen precursor dissociation in anorexia nervosa. J Clin Endocrinol Metab, 94(4),1367e1371.

  Youssef, M. Y. Z., Alqallaf, A., & Abdella, N. (2011). Anabolic androgenic steroid-induced
  cardiomyopathy, stroke and peripheral vascular disease. BMJ Case Rep, bcr1220103650.

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  Conflict of Interest:
  None declared.

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