테스트·보안 스킬

This skill recommends using biochemical tests to screen for hypercortisolism to detect recurrence in patients with ACTH-dependent Cushing's syndrome after surgical remission. It is triggered during postoperative follow-up when the HPA axis has recovered, annually, or sooner if clinical signs of hypercortisolism (e.g., weight gain, hypertension, glucose intolerance) or abnormal late-night salivary cortisol/UFC appear.

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This skill recommends discontinuing glucocorticoid when the response to HPA axis recovery tests (morning cortisol, ACTH stimulation, or insulin-induced hypoglycemia) is normal, indicating adequate adrenal function recovery. Use in postoperative Cushing’s syndrome patients with at least one intact adrenal gland when test results are available.

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Work up Malignancy-Associated Hypercalcemia (MAH) — distinguish humoral hypercalcemia of malignancy (HHM, PTHrP-driven), local osteolytic hypercalcemia, 1,25(OH)2D-mediated lymphoma hypercalcemia, ectopic PTH secretion, and multiple myeloma — and pick the right confirmatory tests and therapy direction. Trigger when a clinician asks "is this hypercalcemia from cancer", "PTHrP positive what now", "hypercalcemia in lung cancer / breast cancer / lymphoma / myeloma", "humoral hypercalcemia of malignancy", "MAH workup", or any hypercalcemia case with suppressed PTH and a known or suspected malignancy.

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This skill recommends against initiating treatments aimed at normalizing cortisol or its action when only borderline biochemical abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis are present without specific signs of Cushing's syndrome. Use when encountering borderline urinary free cortisol, late-night salivary cortisol, or dexamethasone suppression test results without classic Cushingoid features; triggers include borderline UFC (1-2× ULN), equivocal late-night salivary cortisol, or nondiagnostic low-dose DST.

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This skill recommends lifelong follow-up tests for cardiac myxoma and associated disease (testicular tumors, acromegaly, thyroid lesions) in patients with Carney complex. Use when managing a Cushing’s syndrome patient with a confirmed or suspected Carney complex diagnosis (e.g., spotty skin lentigines, cardiac myxoma, endocrine tumors).

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This skill suggests follow-up tests for specific comorbidities associated with Cushing's syndrome in patients with adrenal adenoma when CT density is less than 10 Hounsfield units. Use when managing a post-adrenalectomy Cushing's syndrome patient with confirmed adrenal adenoma pathology and low-density imaging (<10 HU).

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This skill recommends localizing and resecting ectopic ACTH-secreting tumors with node dissection when ectopic ACTH secretion is suspected or confirmed. Clinical triggers include unexplained persistent hypercortisolism after pituitary surgery, elevated ACTH with negative pituitary MRI, or identification of occult ectopic ACTH syndrome (EAS) on biochemical testing.

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This skill recommends follow-up morning cortisol and/or ACTH stimulation tests or insulin-induced hypoglycemia to assess HPA axis recovery in postoperative Cushing's syndrome patients with at least one intact adrenal gland. Triggers include postoperative remission (morning cortisol <5 µg/dL or UFC <28–56 nmol/d) and the need to evaluate HPA recovery before glucocorticoid discontinuation.

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This skill recommends re-evaluating the need for treatment of other pituitary hormone deficiencies in the postoperative period following surgical intervention for Cushing's syndrome. It is triggered when assessing a post-op CS patient for ongoing pituitary function, evaluating for hypopituitarism, or checking HPA axis recovery with morning cortisol/ACTH stimulation tests and pituitary MRI within 1–3 months.

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Determines when to pursue genetic testing for glucocorticoid-remediable aldosteronism (FH-I/GRA) in patients with confirmed primary aldosteronism (PA). Indicated when PA onset is before age 20 or there is a family history of PA or stroke before age 40.

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Identifies patients with adrenal tumors on CT who should undergo dexamethasone suppression test to evaluate for autonomous cortisol co-secretion. Triggers include when a clinician finds an adrenal tumor on CT and asks 'Should I test for cortisol co-secretion?' or is planning AVS for a tumor >3.0 cm.

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Identifies patients with a positive aldosterone-to-renin ratio screening who may proceed directly to subtype testing without confirmatory testing based on specific clinical criteria. Triggers include spontaneous hypokalemia, baseline plasma aldosterone concentration >100 pg/mL (CLEIA), renin suppression, or a clinician questioning the need for a confirmatory test after a positive screen.

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Determines when to test for germline KCNJ5 mutations indicating familial hyperaldosteronism type III in very young patients with primary aldosteronism. Triggered by severe early-onset hypertension with hypokalemia in infants or young children (<20 years) with confirmed PA.

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Determines if PAC/PRA ratio and PAC levels indicate positive or provisionally positive screening for primary aldosteronism. Triggered when a clinician has PAC and PRA results and asks “Is this screening test positive for PA?” or needs to interpret borderline results.

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Recommends antihypertensive therapy including mineralocorticoid receptor antagonists (MRAs) for patients with a positive primary aldosteronism (PA) screening test who decline confirmatory testing. Triggers include when a patient has positive screening but refuses additional tests and asks "What should I treat with?" or initiates empiric therapy, with preference for MRAs in typical PA presentations (e.g., spontaneous hypokalemia, resistant hypertension, adrenal tumor on CT).

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This skill determines whether confirmatory testing can be omitted after a positive aldosterone-to-renin ratio (ARR) in patients with suspected primary aldosteronism. It is applied when a patient exhibits spontaneous hypokalemia, undetectable renin, and a plasma aldosterone concentration ≥20 ng/dL (550 pmol/L).

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Guides selection of the optimal confirmatory test (CCT, SIT, FUT, OSLT) for primary aldosteronism based on patient safety and feasibility. Triggers include when a clinician asks “Which confirmatory test should I use?” or evaluates patient comorbidities before testing.

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This skill interprets the oral sodium loading test for primary aldosteronism by evaluating 24‑hour urinary aldosterone excretion after a high‑sodium diet. Use when reviewing results of an "oral sodium loading test" for PA diagnosis; trigger phrases include "urinary aldosterone excretion ≤10 g/24 h" (PA unlikely) or "≥12 g/24 h (Mayo) / ≥14 g/24 h (Cleveland)" (PA highly likely).

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Differentiates aldosterone-producing adenoma from idiopathic adrenal hyperplasia based on 18-hydroxycorticosterone levels, with APA patients generally having levels >100 ng/dL at 8:00 a.m. and IAH patients usually having levels <100 ng/dL. Use when reviewing 18-OHB test results to help subtype PA; triggers include 18-OHB >100 ng/dL (suggesting APA) or <100 ng/dL (suggesting IAH).

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Recommends confirmatory testing with corticotropin stimulation test in patients presenting with clinical symptoms or signs suggesting PAI (e.g., fatigue, hypotension, hyponatremia, hyperpigmentation) when the patient's condition permits safe testing. Use when a clinician identifies suggestive features and circumstances allow outpatient stimulation testing without imminent need for emergency glucocorticoids.

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Recommends performing a dexamethasone suppression test to evaluate for autonomous cortisol secretion in patients with primary aldosteronism and adrenal adenoma. Triggered when a clinician considers whether to perform a dexamethasone suppression test in a patient with PA and adrenal adenoma.

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Recommends initiating glucocorticoid therapy in all patients with confirmed primary adrenal insufficiency (PAI). Use when PAI diagnosis is confirmed by subnormal cortisol response to ACTH stimulation test or elevated ACTH with low cortisol.

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Suggests using a low-dose (1 µg) corticotropin stimulation test to diagnose primary adrenal insufficiency when the standard 250 µg corticotropin is unavailable due to drug shortage. Consider this approach when clinicians encounter a corticotropin shortage or when the standard dose cannot be obtained.

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Suggests using morning cortisol ≤140 nmol/L (5 µg/dL) in combination with ACTH as a preliminary test suggestive of primary adrenal insufficiency when a corticotropin stimulation test is not feasible. Use when patients present with indicative symptoms such as hypotension, hyponatremia, hyperkalemia, or fatigue and corticotropin stimulation testing cannot be performed.

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