{"id":4422389,"date":"2025-01-11T16:06:58","date_gmt":"2025-01-11T22:06:58","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/topics\/cushing-syndrome\/"},"modified":"2025-01-12T18:11:48","modified_gmt":"2025-01-13T00:11:48","slug":"cushing-syndrome","status":"publish","type":"oen_topic","link":"https:\/\/myendoconsult.com\/learn\/topics\/cushing-syndrome\/","title":{"rendered":"Cushing Syndrome"},"content":{"rendered":"\n<h2 class=\"wp-block-heading\">CUSHING SYNDROME\u2014CLINICAL FINDINGS<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Definition<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Cushing syndrome<\/strong>: A symptom complex from prolonged exposure to <strong>supraphysiologic glucocorticoids<\/strong>.\n<ul class=\"wp-block-list\">\n<li><strong>Exogenous (Iatrogenic)<\/strong>: Due to administration of synthetic glucocorticoids (most common overall).<\/li>\n\n\n\n<li><strong>Endogenous (Spontaneous)<\/strong>: Rare; due to ACTH hypersecretion (ACTH-dependent) or primary adrenal hypersecretion (ACTH-independent).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Clinical Approach<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Recognize<\/strong> signs\/symptoms of Cushing syndrome.<\/li>\n\n\n\n<li><strong>Confirm<\/strong> endogenous hypercortisolism biochemically.<\/li>\n\n\n\n<li><strong>Identify<\/strong> the underlying cause (e.g., pituitary, ectopic ACTH, adrenal).<\/li>\n\n\n\n<li><strong>Definitive Cure<\/strong> (surgical or otherwise).<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">Common Signs and Symptoms<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Weight Gain with Central (Centripetal) Obesity<\/strong>\n<ul class=\"wp-block-list\">\n<li>Fat deposition in <strong>face<\/strong> (\u201cmoon face,\u201d temporal fossae, cheeks), <strong>supraclavicular areas<\/strong>, <strong>dorsocervical region (\u201cbuffalo hump\u201d)<\/strong>.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Skin Changes<\/strong>\n<ul class=\"wp-block-list\">\n<li>Easy bruising (ecchymoses).<\/li>\n\n\n\n<li>Thin, fragile skin (\u201ccigarette paper\u201d skin) with visible subcutaneous vessels.<\/li>\n\n\n\n<li>Poor wound healing.<\/li>\n\n\n\n<li><strong>Red-purple wide striae<\/strong> (&gt;1 cm), often on abdomen, flanks, axilla, breasts, hips, inner thighs.<\/li>\n\n\n\n<li>Hyperpigmentation (only in markedly increased ACTH).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Hair and Muscle<\/strong>\n<ul class=\"wp-block-list\">\n<li>Scalp hair thinning.<\/li>\n\n\n\n<li><strong>Proximal muscle weakness<\/strong> (thin extremities).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Neuropsychiatric<\/strong>\n<ul class=\"wp-block-list\">\n<li>Emotional lability, depression, insomnia, restlessness, irritability.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Androgen Excess (in women)<\/strong>\n<ul class=\"wp-block-list\">\n<li>Hirsutism, acne, possible scalp hair recession.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Cardiovascular and Metabolic<\/strong>\n<ul class=\"wp-block-list\">\n<li>Hypertension.<\/li>\n\n\n\n<li>Osteopenia\/osteoporosis, vertebral compression fractures, low back pain.<\/li>\n\n\n\n<li>Glucose intolerance, <a href=\"https:\/\/myendoconsult.com\/learn\/diabetes-mellitus\/\" data-wpil-monitor-id=\"160\">diabetes mellitus<\/a> (insulin resistance).<\/li>\n\n\n\n<li>Renal lithiasis.<\/li>\n\n\n\n<li>Hyperlipidemia.<\/li>\n\n\n\n<li>Increased risk of opportunistic &amp; fungal infections.<\/li>\n\n\n\n<li>Menstrual dysfunction (oligomenorrhea, amenorrhea), infertility.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Children<\/strong>: May show obesity + <strong>growth retardation<\/strong>.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Additional Clues<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Gradual Onset<\/strong>: Compare current appearance to old photos.<\/li>\n\n\n\n<li><strong>Nonspecific Signs<\/strong>: Obesity, HTN, glucose intolerance, menstrual irregularities are common in general population.<\/li>\n\n\n\n<li><strong>Characteristic Features<\/strong>: Supraclavicular fat pads, wide purple striae, proximal myopathy.<\/li>\n\n\n\n<li><strong>Weakness<\/strong>: Difficulty climbing stairs, rising from a chair without arms.<\/li>\n\n\n\n<li><strong>ACTH-Dependent<\/strong> Cases: Often more androgen excess (e.g., hirsutism) in women, hyperpigmentation if ACTH is very high.<\/li>\n\n\n\n<li><strong>Laboratory Findings<\/strong>:\n<ul class=\"wp-block-list\">\n<li><strong>Hyperglycemia<\/strong>, <strong>Hyperlipidemia<\/strong>.<\/li>\n\n\n\n<li><strong>Hypokalemia<\/strong> (if cortisol has mineralocorticoid activity).<\/li>\n\n\n\n<li><strong>Leukocytosis<\/strong> with lymphopenia, possible albuminuria.<\/li>\n\n\n\n<li>Severe <strong>HTN<\/strong> and profound <strong>hypokalemia<\/strong> more typical with ectopic ACTH or adrenal carcinoma.<\/li>\n\n\n\n<li><strong>Osteoporosis<\/strong> on bone density scans.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Prognosis<\/strong>: Untreated Cushing syndrome can be fatal.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">TESTS USED IN THE DIAGNOSIS OF CUSHING SYNDROME<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">General Strategy<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Case-Detection Testing<\/strong> (screening).<\/li>\n\n\n\n<li><strong>Confirmatory Testing<\/strong> (to establish autonomous hypercortisolism).<\/li>\n\n\n\n<li><strong>Subtype Testing<\/strong> (to pinpoint the cause).<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">1. Case-Detection Tests<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>24-hour Urinary Free Cortisol (UFC)<\/strong>\n<ul class=\"wp-block-list\">\n<li>Measures <strong>free cortisol<\/strong> excretion; normal or slightly elevated results do not exclude cyclical hypercortisolism.<\/li>\n\n\n\n<li><strong>Multiple collections<\/strong> may be needed (10\u201315% false negatives).<\/li>\n\n\n\n<li><strong>Elevated<\/strong> by alcoholism, depression, severe illness, high urine volume.<\/li>\n\n\n\n<li>Upper limit of normal is ~45 \u03bcg (124 nmol) by tandem mass spec.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Late-Night (11 pm) Salivary Cortisol<\/strong>\n<ul class=\"wp-block-list\">\n<li>Loss of normal diurnal rhythm (cortisol should be low at night).<\/li>\n\n\n\n<li>~92% sensitivity.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Serum Cortisol Diurnal Pattern<\/strong>\n<ul class=\"wp-block-list\">\n<li>Loss of normal <strong>morning\/evening<\/strong> differential supports Cushing\u2019s.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Overnight 1-mg <a href=\"https:\/\/myendoconsult.com\/learn\/dexamethasone-suppression-test-interpretation\/\" data-wpil-monitor-id=\"164\">Dexamethasone Suppression Test<\/a> (DST)<\/strong>\n<ul class=\"wp-block-list\">\n<li>1 mg dexamethasone at 11 pm \u2192 measure <strong>8 am<\/strong> serum cortisol.<\/li>\n\n\n\n<li>Healthy individuals suppress <strong>&lt;1.8 \u03bcg\/dL<\/strong> (50 nmol\/L).<\/li>\n\n\n\n<li><strong>False positives<\/strong>: Estrogen therapy (\u2191CBG), pregnancy, obesity, certain drugs (enzyme inducers), severe stress, depression, etc.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"3000\" height=\"2100\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic.png\" alt=\"\" class=\"wp-image-4422818\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic.png 3000w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic-300x210.png 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic-768x538.png 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic-1536x1075.png 1536w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/DST-infographic-2048x1434.png 2048w\" sizes=\"auto, (max-width: 3000px) 100vw, 3000px\" \/><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">2. Confirmatory Testing<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Not required if very high UFC (e.g., &gt;200 \u03bcg\/24 h or &gt;552 nmol\/24 h) plus strong clinical picture.<\/li>\n\n\n\n<li><strong>2-Day Low-Dose DST<\/strong>\n<ul class=\"wp-block-list\">\n<li>0.5 mg dexamethasone q6h for 48 hours \u2192 measure UFC.<\/li>\n\n\n\n<li>UFC &gt;10 \u03bcg\/24 h (28 nmol\/24 h) = diagnostic.<\/li>\n\n\n\n<li>Sensitivity ~79%, specificity ~74%.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li>If suspicion is high, normal suppression with low-dose DST does <strong>not<\/strong> exclude mild pituitary disease.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">3. Subtype Testing<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Performed only after<\/strong> confirming Cushing syndrome.<\/li>\n\n\n\n<li><strong>Plasma ACTH<\/strong>: Distinguishes ACTH-dependent (normal-high) vs. ACTH-independent (undetectable).<\/li>\n\n\n\n<li><strong>Pituitary MRI<\/strong> (with gadolinium) if ACTH-dependent.\n<ul class=\"wp-block-list\">\n<li>Lesions \u22654 mm with typical presentation often confirm pituitary cause; no further studies needed.<\/li>\n\n\n\n<li>If lesion &lt;4 mm or normal pituitary MRI (~50% of pituitary Cushing\u2019s), consider <strong><a href=\"https:\/\/myendoconsult.com\/learn\/inferior-petrosal-sinus-sampling-ipss-testing-procedure-for-evaluating-cushings-syndrome\/\" data-wpil-monitor-id=\"165\">inferior petrosal sinus sampling<\/a><\/strong> (IPSS).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Adrenal CT<\/strong> if ACTH-independent to identify adenoma, carcinoma, macronodular hyperplasia, or PPNAD.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">CUSHING SYNDROME: PATHOPHYSIOLOGY<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Mechanisms<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>ACTH-Dependent Cushing Syndrome<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Bilateral <a href=\"https:\/\/myendoconsult.com\/learn\/non-classical-adrenal-hyperplasia\/\" data-wpil-monitor-id=\"161\">Adrenal Hyperplasia<\/a><\/strong> due to ACTH excess.<\/li>\n\n\n\n<li><strong><a href=\"https:\/\/myendoconsult.com\/learn\/topics\/nonfunctioning-pituitary-adenoma\/\" data-wpil-monitor-id=\"162\">Pituitary Adenoma<\/a><\/strong> (Cushing disease) most common endogenous cause.<\/li>\n\n\n\n<li><strong>Ectopic ACTH<\/strong> (small cell lung cancer, bronchial carcinoid, medullary <a href=\"https:\/\/myendoconsult.com\/learn\/topics\/thyroid-carcinomas\/\" data-wpil-monitor-id=\"163\">thyroid carcinoma<\/a>, thymic carcinoid, pancreatic NET, pheochromocytoma).<\/li>\n\n\n\n<li><strong>Ectopic CRH<\/strong> (rare).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>ACTH-Independent Cushing Syndrome<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Adrenal Adenoma<\/strong> or <strong>Carcinoma<\/strong> (unilateral).<\/li>\n\n\n\n<li><strong>Adrenal Macronodular Hyperplasia<\/strong> (AIMAH).<\/li>\n\n\n\n<li><strong>Primary Pigmented Nodular Adrenocortical Disease<\/strong> (PPNAD).<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">Clinical Variation by Etiology<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Ectopic ACTH or Adrenal Carcinoma<\/strong>: Marked androgen excess \u2192 severe hirsutism, acne, possibly severe HTN\/hypokalemia.<\/li>\n\n\n\n<li><strong>Slow Onset<\/strong> (e.g., Pituitary microadenoma, AIMAH, PPNAD): Gradual central obesity, osteoporosis, proximal myopathy.<\/li>\n\n\n\n<li><strong>Very High ACTH<\/strong>: Skin hyperpigmentation (ectopic ACTH, pituitary macroadenoma).<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h3 class=\"wp-block-heading\">ACTH-Dependent<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Pituitary-Dependent (Cushing Disease)<\/strong>\n<ul class=\"wp-block-list\">\n<li>~70% of endogenous cases.<\/li>\n\n\n\n<li>95% are <strong>microadenomas<\/strong> (\u226410 mm); half invisible on MRI.<\/li>\n\n\n\n<li>Bilateral <a href=\"https:\/\/myendoconsult.com\/learn\/topics\/congenital-adrenal-hyperplasia-cah\/\"  data-wpil-monitor-id=\"337\">adrenal hyperplasia<\/a> \u2192 mild to moderate adrenal enlargement (6\u201312 g each).<\/li>\n\n\n\n<li>Excess cortisol \u00b1 moderate androgen elevations (DHEA-S mildly \u2191).<\/li>\n\n\n\n<li>Pituitary histology: ACTH-staining adenoma cells + <strong>Crooke hyaline change<\/strong> in non-tumorous corticotrophs.<\/li>\n\n\n\n<li><strong>Selective transsphenoidal surgery<\/strong> = treatment of choice.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Ectopic ACTH Syndrome<\/strong>\n<ul class=\"wp-block-list\">\n<li>Marked hypercortisolism + bilateral large adrenal glands (&gt;12 g each).<\/li>\n\n\n\n<li>Common source: <strong>Bronchial <a href=\"https:\/\/myendoconsult.com\/learn\/topics\/carcinoid\/\"  data-wpil-monitor-id=\"338\">carcinoid<\/a><\/strong> (others: SCLC, MTC, thymic carcinoid, pancreatic NET, pheochromocytoma).<\/li>\n\n\n\n<li>Commonly severe: HTN, hypokalemia, hyperpigmentation if ACTH is extremely high.<\/li>\n\n\n\n<li>Definitive therapy: <strong>Surgical resection<\/strong> of ectopic tumor if possible, else bilateral adrenalectomy.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Ectopic CRH Syndrome<\/strong>\n<ul class=\"wp-block-list\">\n<li>Rare. CRH secreted by ectopic tumor \u2192 pituitary hyperplasia \u2192 excess ACTH.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h3 class=\"wp-block-heading\">ACTH-Independent<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Adrenal Adenoma<\/strong>\n<ul class=\"wp-block-list\">\n<li>Usually secretes only <strong>cortisol<\/strong>, leading to suppressed ACTH and contralateral gland atrophy.<\/li>\n\n\n\n<li>Typically \u22652.5 cm for clinical hypercortisolism.<\/li>\n\n\n\n<li>Mild androgen elevation is uncommon.<\/li>\n\n\n\n<li><strong>Unilateral laparoscopic adrenalectomy<\/strong> = curative approach.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Adrenal Carcinoma<\/strong>\n<ul class=\"wp-block-list\">\n<li>May produce cortisol \u00b1 androgen \u00b1 mineralocorticoid.<\/li>\n\n\n\n<li>Often large (5\u201320 cm), can metastasize to LN, liver, lungs.<\/li>\n\n\n\n<li>DHEA-S often very high.<\/li>\n\n\n\n<li><strong>Open en bloc resection<\/strong> if possible, though recurrences are common. 5-year survival ~30%.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>AIMAH (ACTH-Independent Macronodular Adrenal Hyperplasia)<\/strong>\n<ul class=\"wp-block-list\">\n<li>Bilateral massive nodular adrenal enlargement (each 100\u2013500 g).<\/li>\n\n\n\n<li>Often ectopic or overexpressed receptors (GIP, \u03b2-adrenergic, vasopressin, LH, etc.) leading to cortisol secretion.<\/li>\n\n\n\n<li>Typically mild, slowly progressive.<\/li>\n\n\n\n<li><strong>Bilateral adrenalectomy<\/strong> often needed if symptomatic hypercortisolism.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>PPNAD (Primary Pigmented Nodular Adrenocortical Disease)<\/strong>\n<ul class=\"wp-block-list\">\n<li>May be <strong>sporadic<\/strong> or <strong>familial<\/strong> (Carney complex).<\/li>\n\n\n\n<li>Multiple pigmented nodules in both glands; normal or slightly enlarged weight.<\/li>\n\n\n\n<li><strong>Slow, mild<\/strong> hypercortisolism, often cyclical.<\/li>\n\n\n\n<li>Low ACTH, low DHEA-S, paradoxical \u2191cortisol with dex suppression.<\/li>\n\n\n\n<li><strong>Bilateral laparoscopic adrenalectomy<\/strong> = curative.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">PRIMARY PIGMENTED NODULAR ADRENOCORTICAL DISEASE (PPNAD)<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Overview<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Rare<\/strong> ACTH-independent Cushing syndrome with multiple, pigmented, autonomously functioning nodules.<\/li>\n\n\n\n<li>Presents with <strong>mild hypercortisolism<\/strong>, frequent <strong>osteoporosis<\/strong>, possibly cyclical cortisol secretion.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Clinical Features<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Young patients<\/strong> (&lt;30 years).<\/li>\n\n\n\n<li>Central obesity, HTN, glucose intolerance, proximal muscle weakness, menstrual disruption.<\/li>\n\n\n\n<li><strong>Marked osteoporosis<\/strong> out of proportion to mild Cushing\u2019s.<\/li>\n\n\n\n<li>Paradoxical \u2191UFC during dexamethasone suppression.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Adrenal Morphology<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Adrenals often normal size or mildly enlarged (4\u201315 g).<\/li>\n\n\n\n<li><strong>Multiple pigmented nodules<\/strong> (1 mm to 3 cm) with lipofuscin.<\/li>\n\n\n\n<li>Surrounded by atrophic cortex.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Association with Carney Complex<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>~50% have <strong>Carney complex<\/strong>:\n<ul class=\"wp-block-list\">\n<li>Spotty skin pigmentation (lentigines, blue nevi), myxomas (atrial, cutaneous, mammary), testicular large-cell Sertoli tumors, GH-secreting pituitary adenomas, melanotic schwannomas.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li>Familial in ~60% of Carney complex; autosomal dominant inheritance for most.<\/li>\n\n\n\n<li>Genes: <strong>PRKAR1A<\/strong> (MC), <strong>PDE11A<\/strong>, <strong>MYH8<\/strong>, others.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Management<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Bilateral laparoscopic adrenalectomy<\/strong> cures hypercortisolism.<\/li>\n\n\n\n<li>Genetic counseling if Carney complex suspected.<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>CUSHING SYNDROME\u2014CLINICAL FINDINGS Definition Clinical Approach Common Signs and Symptoms Additional Clues TESTS USED IN THE DIAGNOSIS OF CUSHING SYNDROME General Strategy 1. Case-Detection Tests 2. Confirmatory Testing 3. Subtype Testing CUSHING SYNDROME: PATHOPHYSIOLOGY Mechanisms Clinical Variation by Etiology ACTH-Dependent ACTH-Independent PRIMARY PIGMENTED NODULAR ADRENOCORTICAL DISEASE (PPNAD) Overview Clinical Features Adrenal Morphology Association with Carney [&hellip;]<\/p>\n","protected":false},"featured_media":0,"template":"","oen_topic_chapter":[684],"class_list":["post-4422389","oen_topic","type-oen_topic","status-publish","hentry","oen_topic_chapter-adrenal-gland","post-wrapper","thrv_wrapper"],"_links":{"self":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422389","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic"}],"about":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/types\/oen_topic"}],"version-history":[{"count":5,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422389\/revisions"}],"predecessor-version":[{"id":4422820,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422389\/revisions\/4422820"}],"wp:attachment":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/media?parent=4422389"}],"wp:term":[{"taxonomy":"oen_topic_chapter","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic_chapter?post=4422389"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}