Deconstructing the androgen function in active perianal infection: Investigating inflammation-driven hypogonadal state

Table 1 Testosterone changes in acute and chronic perianal inflammatory diseases

Disease	Pathophysiological features	Testosterone alteration	Proposed mechanisms	Clinical implications
Acute perianal abscess	Acute suppurative infection; strong systemic inflammation[60]; elevated WBC, CRP, IL-6, TNF-α	Significant decrease; inflammation-induced hypogonadism	Cytokine-mediated Leydig cell suppression; acute HPG axis inhibition; obesity-related effects	Reduced testosterone may reflect inflammatory burden and systemic stress
Complex anal abscess (horseshoe, ischiorectal)	Extensive multi-space infection; higher inflammatory load	Marked decrease	Higher inflammatory stress amplifies endocrine suppression	May assist in risk stratification
Simple Intersphincteric abscess	Localized infection; moderate systemic response	Moderate decrease	Cytokine-driven but less severe	Distinguishes simple vs complex abscess inflammation
Cryptoglandular anal fistula (chronic)	Chronic low-grade inflammation[61]; persistent tract	Generally unchanged or mildly reduced	Low-grade inflammation insufficient for HPG suppression	Limited endocrine involvement
High-transsphincteric/suprasphincteric fistula	Higher internal opening; more complex anatomy	Mild decrease in selected cases	Subtle endocrine modulation with chronic inflammation	May correlate with fistula complexity

All concepts presented in this table are hypothesis-generating. WBC: White blood cell; CRP: C-reactive protein; IL: Interleukin; TNF-α: Tumor necrosis factor-α; HPG: Hypothalamic-pituitary-gonadal.