How do I install the Endo Hirsutism Assess Urinary Corticoid Metabolites skill?

Run npx skillmds@latest add dromlakhani/endo-hirsutism-assess-urinary-corticoid-metabolites in your terminal (requires Node.js), paste this page's agent-chat prompt into Claude, Cursor, or any MCP-connected agent, or download the SKILL.md file and copy it into your agent's skills directory.

Which AI agents work with Endo Hirsutism Assess Urinary Corticoid Metabolites?

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Who published Endo Hirsutism Assess Urinary Corticoid Metabolites?

dromlakhani (@dromlakhani) published this skill. Their other Agent Skills are listed on their SkillMD profile.

Endo Hirsutism Assess Urinary Corticoid Metabolites by dromlakhani

Name: Endo Hirsutism Assess Urinary Corticoid Metabolites
Rating: 4.2 (5 reviews)
Author: dromlakhani

Endo Hirsutism Assess Urinary Corticoid Metabolites

Assess urinary corticoid metabolites by mass spectrometry to exclude apparent cortisone reductase deficiency. Indicated when a woman presents with moderate/severe hirsutism or mild hirsutism accompanied by clinical evidence of a hyperandrogenic endocrine disorder such as menstrual disturbance, progression despite therapy, or signs of virilization.

dromlakhani Updated Sep 8, 2026 10 repo stars

File contents

Assess urinary corticoid metabolites to rule out cortisone reductase deficiency

STEP 1 — Gather Information

Collect detailed hirsutism assessment (Ferriman–Gallwey score), menstrual history, signs of virilization (e.g., oligomenorrhea, clitoromegaly, rapid progression), and baseline androgen labs (serum total and free testosterone, 17‑hydroxyprogesterone, DHEAS). If total and free testosterone are normal but there is clinical evidence of hyperandrogenism, proceed to urinary corticoid metabolite testing.

STEP 2 — Rule In / Rule Out

Is the urinary corticoid metabolite profile showing an elevated tetrahydrocortisone/tetrahydrocortisol ratio consistent with cortisone reductase deficiency?

Yes → Rule in cortisone reductase deficiency.
No → Rule out cortisone reductase deficiency.

STEP 3 — Classify or Stratify

If ruled in, classify as biochemical cortisone reductase deficiency (await genetic confirmation).
If ruled out, stratify remaining hyperandrogenic etiologies (e.g., PCOS, nonclassic congenital adrenal hyperplasia, androgen‑secreting tumor) based on clinical clues and further testing.

STEP 4 — Decide

If cortisone reductase deficiency is confirmed, initiate low‑dose glucocorticoid therapy (e.g., dexamethasone 0.25 mg nightly) and arrange genetic counseling; if ruled out, continue androgen excess workup per guideline (e.g., ACTH stimulation, adrenal imaging) and consider condition‑specific management.

Clinical Guardrails / Mimics / Pitfalls

Do not diagnose cortisone reductase deficiency on metabolite results alone; confirm with CYP11B1 genotyping. Avoid glucocorticoid empiric therapy without biochemical proof due to risk of iatrogenic Cushingoid changes. Ensure first‑morning, uncontaminated urine collection; stress or illness can alter corticoid metabolites. Do not mistake this defect for 11‑oxygenated androgen excess, which requires different testing.

Concrete Clinical Example

A 28‑year‑old woman with Ferriman–Gallwey score 18, oligomenorrhea, normal total and free testosterone, and mild hirsutism that worsened despite 6 months of oral contraceptive therapy undergoes urinary corticoid metabolite analysis, revealing an elevated tetrahydrocortisone/tetrahydrocortisol ratio. Genetic testing confirms heterozygous CYP11B1 mutation; she is started on dexamethasone 0.25 mg nightly with clinical improvement in hirsutism over 3 months.

Source: Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline, Endocrine Society, 2018, DOI:10.1210/jc.2018-00241

---name: endo-hirsutism-assess-urinary-corticoid-metabolitesdescription: Assess urinary corticoid metabolites by mass spectrometry to exclude apparent cortisone reductase deficiency. Indicated when a woman presents with moderate/severe hirsutism or mild hirsutism accompanied by clinical evidence of a hyperandrogenic endocrine disorder such as menstrual disturbance, progression despite therapy, or signs of virilization.---# Assess urinary corticoid metabolites to rule out cortisone reductase deficiency## STEP 1 — Gather InformationCollect detailed hirsutism assessment (Ferriman–Gallwey score), menstrual history, signs of virilization (e.g., oligomenorrhea, clitoromegaly, rapid progression), and baseline androgen labs (serum total and free testosterone, 17‑hydroxyprogesterone, DHEAS). If total and free testosterone are normal but there is clinical evidence of hyperandrogenism, proceed to urinary corticoid metabolite testing.## STEP 2 — Rule In / Rule OutIs the urinary corticoid metabolite profile showing an elevated tetrahydrocortisone/tetrahydrocortisol ratio consistent with cortisone reductase deficiency? - Yes → Rule in cortisone reductase deficiency. - No → Rule out cortisone reductase deficiency.## STEP 3 — Classify or StratifyIf ruled in, classify as biochemical cortisone reductase deficiency (await genetic confirmation). If ruled out, stratify remaining hyperandrogenic etiologies (e.g., PCOS, nonclassic congenital adrenal hyperplasia, androgen‑secreting tumor) based on clinical clues and further testing.## STEP 4 — DecideIf cortisone reductase deficiency is confirmed, initiate low‑dose glucocorticoid therapy (e.g., dexamethasone 0.25 mg nightly) and arrange genetic counseling; if ruled out, continue androgen excess workup per guideline (e.g., ACTH stimulation, adrenal imaging) and consider condition‑specific management.## Clinical Guardrails / Mimics / PitfallsDo not diagnose cortisone reductase deficiency on metabolite results alone; confirm with CYP11B1 genotyping. Avoid glucocorticoid empiric therapy without biochemical proof due to risk of iatrogenic Cushingoid changes. Ensure first‑morning, uncontaminated urine collection; stress or illness can alter corticoid metabolites. Do not mistake this defect for 11‑oxygenated androgen excess, which requires different testing.## Concrete Clinical ExampleA 28‑year‑old woman with Ferriman–Gallwey score 18, oligomenorrhea, normal total and free testosterone, and mild hirsutism that worsened despite 6 months of oral contraceptive therapy undergoes urinary corticoid metabolite analysis, revealing an elevated tetrahydrocortisone/tetrahydrocortisol ratio. Genetic testing confirms heterozygous CYP11B1 mutation; she is started on dexamethasone 0.25 mg nightly with clinical improvement in hirsutism over 3 months.**Source:** Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline, Endocrine Society, 2018, DOI:10.1210/jc.2018-00241

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