Pediatric Urology Academy is an evidence-based educational podcast hosted by Amin Afrasiabi, MD, Pediatric Urologist. Each episode explores pediatric urology through clinical cases, landmark studies, practical decision-making, surgical principles, and emerging research. Topics include posterior urethral valves, vesicoureteral reflux, hydronephrosis, UPJO, megaureter, neurogenic bladder, hypospadias, disorders of sexual development, pediatric stone disease, and reconstructive surgery. Designed for pediatric urologists, urologists, residents, fellows, and healthcare professionals worldwide.
Season 6, Episode 11 — Complete Androgen Insensitivity Syndrome: Testosterone Without a Biological Audience
A 46,XY child can have testes, no uterus, female-typical external genitalia, and normal or even high testosterone.
The androgen is present.
The target cannot respond.
In this episode of Pediatric Urology Academy, we examine complete androgen insensitivity syndrome as a disorder of androgen action rather than androgen production.
We explore:
• why normal testosterone does not guarantee normal androgen effect
• how preserved AMH explains Müllerian regression despite female-typical external genitalia
• why Wolffian structures are often absent or poorly developed
• how the androgen receptor converts hormone binding into gene transcription
• why normal breast development can coexist with sparse pubic and axillary hair
• how CAIS differs from Leydig cell hypoplasia, HSD17B3 deficiency, and SRD5A2 deficiency
• why an inguinal testis in a phenotypic girl should trigger diagnostic reconsideration
• how current evidence has changed the timing of gonadectomy
• why prepubertal tumor risk appears low, but surveillance cannot eliminate uncertainty
• how retained gonads, spontaneous puberty, hormone replacement, autonomy, and fertility preservation shape shared decision-making
The central framework:
The hormone is made.
The target receives it.
But the receptor cannot convert the signal into biological action.
Season 6 — Differences of Sex Development: Reconstruct the Biology
Hosted by Amin Afrasiabi, MD
Pediatric Urology Academy
10 Oct 2026
Season 6, Episode 10 — The Backdoor Androgen Pathway: How the Fetus Can Reach DHT Without the Main Road
The classic androgen pathway is not the whole story.
A fetus can generate androgen effect through an alternative biochemical route that bypasses testosterone as the obligatory intermediate.
In this episode of Pediatric Urology Academy, we examine the human backdoor androgen pathway and why it matters when genotype, serum hormones, and genital phenotype do not seem to fit neatly together.
We explore:
• how fetal tissues can reach DHT through more than one biochemical route
• why serum testosterone does not fully represent androgen exposure at the target tissue
• the role of androsterone in human fetal backdoor androgen biology
• how AKR1C2 and AKR1C4 defects can produce 46,XY undervirilization
• why POR deficiency can produce both 46,XY undervirilization and 46,XX virilization
• how excess steroid precursors can be redirected through alternative androgen pathways
• why placenta, adrenal, liver, testis, and peripheral tissues should be viewed as a distributed fetal steroidogenic system
• when urinary steroid profiling and molecular testing become particularly useful
• why the backdoor pathway should be used to localize biology, not as a catch-all diagnosis
The central framework:
The classic pathway is the main road.
The backdoor pathway is the side road.
External genital development reflects the total androgen signal that reached the target during the critical developmental window.
Season 6 — Differences of Sex Development: Reconstruct the Biology
Hosted by Amin Afrasiabi, MD
Pediatric Urology Academy
9 Oct 2026
Season 6, Episode 9 — Testosterone Is Not DHT: SRD5A2 Deficiency and Androgen Amplification
A 46,XY child can have testes, no uterus, preserved Wolffian structures—and markedly undervirilized external genitalia.
The testosterone may even be normal.
The missing signal is DHT.
In this episode of Pediatric Urology Academy, we examine SRD5A2 deficiency as a disorder of tissue-specific androgen amplification rather than simply “low androgen.”
We explore:
• why testosterone and DHT are not biologically interchangeable
• how Wolffian structures can masculinize while external genital virilization remains incomplete
• why SRD5A2 acts as a local androgen amplifier during fetal development
• how the testosterone-to-DHT ratio helps localize the defect, but cannot reliably confirm or exclude it
• why hCG stimulation and urinary steroid profiling can add diagnostic information
• how SRD5A2 deficiency differs from HSD17B3 deficiency and complete androgen insensitivity
• why substantial virilization may occur at puberty despite severe fetal undervirilization
• why puberty cannot recreate developmental windows that were missed in fetal life
• what current evidence suggests about fertility, gonadal preservation, and tumor risk
The central framework:
Testosterone delivers the androgen signal.
DHT amplifies it in selected tissues.
Season 6 — Differences of Sex Development: Reconstruct the Biology
Hosted by Amin Afrasiabi, MD
Pediatric Urology Academy
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