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The table below summarizes the findings that differentiate Cushing's disease from other conditions that may cause [[Hypertension|hypertensio]]<nowiki/>n, [[hyperandrogenism]], and [[obesity]]. Facial [[plethora]], [[skin changes]], [[osteoporosis]], [[nephrolithiasis]] and [[neuropsychiatric]] conditions should raise the concern for Cushing's syndrome.<ref name="pmid11253984">{{cite journal |vauthors=Boscaro M, Barzon L, Fallo F, Sonino N |title=Cushing's syndrome |journal=Lancet |volume=357 |issue=9258 |pages=783–91 |year=2001 |pmid=11253984 |doi=10.1016/S0140-6736(00)04172-6 |url=}}</ref><ref name="pmid11571938">{{cite journal |vauthors=Findling JW, Raff H |title=Diagnosis and differential diagnosis of Cushing's syndrome |journal=Endocrinol. Metab. Clin. North Am. |volume=30 |issue=3 |pages=729–47 |year=2001 |pmid=11571938 |doi= |url=}}</ref><ref name="pmid9793762">{{cite journal |vauthors=Newell-Price J, Trainer P, Besser M, Grossman A |title=The diagnosis and differential diagnosis of Cushing's syndrome and pseudo-Cushing's states |journal=Endocr. Rev. |volume=19 |issue=5 |pages=647–72 |year=1998 |pmid=9793762 |doi=10.1210/edrv.19.5.0346 |url=}}</ref><ref name="urlHow Is Metabolic Syndrome Diagnosed? - NHLBI, NIH">{{cite web |url=https://www.nhlbi.nih.gov/health/health-topics/topics/ms/diagnosis |title=How Is Metabolic Syndrome Diagnosed? - NHLBI, NIH |format= |work= |accessdate=}}</ref>
<br>
{| align="center"
|-
|
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! style="background:#4479BA; color: #FFFFFF;" | Conditions
! style="background:#4479BA; color: #FFFFFF;" |Causes
! style="background:#4479BA; color: #FFFFFF;" |Associated features
! style="background:#4479BA; color: #FFFFFF;" |Diagnostic approach   
|-
| style="background:#DCDCDC;" align="center" |[[Cushing's syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Iatrogenic]]
*[[Pituitary adenoma]]
*[[Adrenal tumor]]
*[[Adrenal hyperplasia]]
*[[Ectopic ACTH Syndrome|Ectopic ACTH secretion]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Obesity]]
*[[Hypertension]]
*[[PCOS]]/[[hyperandrogenism]]
*[[Oligomenorrhea]]/[[hypogonadism]]
*[[Osteoporosis]]
*[[Myopathy]]/cutaneous wasting
*[[Neuropsychiatric]] problems
*[[Kidney stone|Kidney stones]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*24-hour urine cortisol
*Midnight salivary cortisol
*[[Dexamethasone Oral|Low dose dexamethasone]] challenge test
*[[CRH]] stimulation
*[[Dexamethasone Oral|High dose dexamethasone]] test
*[[MRI|MRI brain]]
*CT/MRI adrenals
|-
|-
| style="background:#DCDCDC;" align="center" |[[Pseudo-Cushing's syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Obesity]]
*[[Alcoholism]]
*[[Depression]]
*[[HIV]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Obesity]]
*[[Hypertension]]
*[[PCOS]]/[[hyperandrogenism]]
*[[Oligomenorrhea]]/[[hypogonadism]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Urinary free cortisol
*Midnight salivary cortisol
*Low dose dexamethasone challenge test
*[[Glucose tolerance test]]
*Loperamide test
|-
| style="background:#DCDCDC;" align="center" |[[Metabolic syndrome X]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Familial/genetic
*Obesity
*Insulin resistance
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* [[Obesity]]
*[[Hypertension]]
*[[PCOS]]/[[hyperandrogenism]]
*[[Oligomenorrhea]]/[[hypogonadism]]
*[[Dyslipidemia]]
*[[Diabetes mellitus|Diabetes]]/[[Glucose intolerance]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Waist circumference
*[[Lipoproteins|Low-density lipoproteins]]
*[[Lipoproteins|High-density lipoproteins]]
*[[Glucose tolerance test]]
*[[Fasting blood sugar]]
*[[HbA1c]]
|}
===Other differentials===
Cushing's syndrome must be differentiated from diseases that cause [[virilization]] and [[hirsutism]] in female:<ref name="pmid24830586">{{cite journal |vauthors=Hohl A, Ronsoni MF, Oliveira Md |title=Hirsutism: diagnosis and treatment |journal=Arq Bras Endocrinol Metabol |volume=58 |issue=2 |pages=97–107 |year=2014 |pmid=24830586 |doi= |url=}}</ref><ref name="pmid10857554">{{cite journal |vauthors=White PC, Speiser PW |title=Congenital adrenal hyperplasia due to 21-hydroxylase deficiency |journal=Endocr. Rev. |volume=21 |issue=3 |pages=245–91 |year=2000 |pmid=10857554 |doi=10.1210/edrv.21.3.0398 |url=}}</ref><ref name="ISBN:978-0323297387">{{cite book | last = Melmed | first = Shlomo | title = Williams textbook of endocrinology | publisher = Elsevier | location = Philadelphia, PA | year = 2016 | isbn = 978-0323297387 }}=</ref>
{| class="wikitable"
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease name
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Steroid status
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Other laboratory
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Important clinical findings
|-
|[[Cushing's syndrome]]
|
* Increase [[cortisol]] & metabolites
* Variable other [[steroids]]
|
* Variable [[mineralocorticoid]] excess
|
* [[Cushingoid appearance]]
|-
|Non-classic type of [[21-hydroxylase deficiency]]
|Increased:
* [[17-Hydroxyprogesterone|17-hydroxyprogesterone]]
* Exaggerated [[Androstenedione]], [[DHEA]], and [[17-Hydroxyprogesterone|17-hydroxyprogesterone]] in response to [[ACTH]]
|
* Low [[testosterone]] levels
|
* No symptoms in infancy and male
* [[Virilization]] in females
|-
|[[11β-hydroxylase deficiency|11-β hydroxylase deficiency]]
|Increased:
* DOC
* 11-Deoxy-[[Cortisol]]
Decreased:
* [[Cortisol]]
* [[Corticosterone]]
* [[Aldosterone]]
|
* Low [[testosterone]] levels
|
* [[Hypertension]] and [[hypokalemia]]
* [[Virilization]]
|-
|[[3 beta-hydroxysteroid dehydrogenase deficiency]]
|Increased:
* [[DHEA]]
* [[17-hydroxypregnenolone]]
* [[Pregnenolone]]
Decreased:
* [[Cortisol]]
* [[Aldosterone]]
|
* Low [[testosterone]] levels
|
* Salt-wasting [[adrenal crisis]] in infancy
* Mild [[virilization]] of genetically female infants
* [[Undervirilization]] of genetically male infants, making it the only form of [[CAH]] which can cause [[ambiguous genitalia]] in both genetic sexes.
|-
|[[Polycystic ovary syndrome ]]
|
* High [[DHEAS]] and [[androstenedione]] levels
|
* Low [[testosterone]] levels
|
* [[Polycystic ovaries]] in sonography
* [[Obesity]]
* [[PCOS]] is the most common cause of [[hirsutism]] in women
* No evidence another diagnosis
|-
|[[Adrenal tumors]]
|
* Variable levels depends on [[tumor]] type
|
* Low [[testosterone]] level
|
* Older age
* Rapidly progressive symptoms
|-
|Ovarian [[virilizing]] tumor
|
* Variable levels depends on [[tumor]] type
|
* [[Testosterone]] is high
|
* Older age
* Rapidly progressive symptoms
|-
|[[Hyperprolactinemia]]
|
* Normal levels of most of [[steroids]]
|
* Increased [[prolactin]]
|
* [[Infertility]], [[galactorrhea]]
|}


==References==
==References==

Revision as of 15:59, 6 September 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

Overview

Adrenal incidentaloma must be differentiated from other diseases that cause adrenal masses such as adrenal adenoma, adrenocortical carcinoma, Cushing's syndrome, pheochromocytoma, and metastasis.

Differentiating Incidentaloma from other Diseases

Differential Diagnosis Clinical picture Imagings Laboratory tests
Adrenal adenoma
  • Round and homogeneous density, smooth contour and sharp margination [15]
  • Diameter less than 4 cm, unilateral location
  • Low unenhanced CT attenuation values (<10 HU) (image 1)
  • Rapid contrast medium washout (10 minutes after administration of contrast, an absolute contrast medium washout of more than 50 percent)
  • Isointensity with liver on both T1 and T2 weighted MRI sequences
  • Chemical shift evidence of lipid on MRI
Adrenocortical carcinoma
  • Mass effect symptoms; symptoms related to excess glucocorticoid, mineralocorticoid, androgen, or estrogen secretion
  • Irregular shape
  • Inhomogeneous density because of central areas of low attenuation due to tumor necrosis (image 4)
  • Tumor calcification
  • Diameter usually >4 cm
  • Unilateral location
  • High unenhanced CT attenuation values (>20 HU)
  • Inhomogeneous enhancement on CT with intravenous contrast
  • Delay in contrast medium washout (10 minutes after administration of contrast, an absolute contrast medium washout of less than 50 percent)
  • Hypointensity compared with liver on T1 weighted MRI and high to intermediate signal intensity on T2 weighted MRI
  • High standardized uptake value (SUV) on FDG-PET-CT study
  • Evidence of local invasion or metastases
  • Serum DHEAS
  • Measures of clinicallyindicated
  • steroid
Cushing's syndrome
  • Imaging may show adenoma if presents
Pheochromocytoma
  • Increased attenuation on nonenhanced CT (>20 HU)
  • Increased mass vascularity (image 2)
  • Delay in contrast medium washout (10 minutes after administration of contrast, an absolute contrast medium washout of less than 50 percent)
  • High signal intensity on T2 weighted MRI (image 3)
  • Cystic and hemorrhagic changes
  • Variable size and may be bilateral
Adrenal metastasis
    • Symptoms and signs of primary malignancy especially lung cancer.
    • General constitutional symptoms:
    • Fever
    • Fatigue
    • Weight loss
  • Irregular shape and inhomogeneous nature
  • Tendency to be bilateral
  • High unenhanced CT attenuation values (>20 HU) and enhancement with intravenous contrast on CT
  • Delay in contrast medium washout (10 minutes after administration of contrast, an absolute contrast medium washout of less than 50 percent)
  • Isointensity or slightly less intense than the liver on T1 weighted MRI and high to intermediate signal intensity on T2 weighted MRI (representing an increased water content)
  • Elevated standardized uptake value on FDG-PET scan

The table below summarizes the findings that differentiate Cushing's disease from other conditions that may cause hypertension, hyperandrogenism, and obesity. Facial plethora, skin changes, osteoporosis, nephrolithiasis and neuropsychiatric conditions should raise the concern for Cushing's syndrome.[1][2][3][4]

Conditions Causes Associated features Diagnostic approach
Cushing's syndrome
Pseudo-Cushing's syndrome
  • Urinary free cortisol
  • Midnight salivary cortisol
  • Low dose dexamethasone challenge test
  • Glucose tolerance test
  • Loperamide test
Metabolic syndrome X
  • Familial/genetic
  • Obesity
  • Insulin resistance

Other differentials

Cushing's syndrome must be differentiated from diseases that cause virilization and hirsutism in female:[5][6][7]

Disease name Steroid status Other laboratory Important clinical findings
Cushing's syndrome
Non-classic type of 21-hydroxylase deficiency Increased:
  • No symptoms in infancy and male
11-β hydroxylase deficiency Increased:

Decreased:

3 beta-hydroxysteroid dehydrogenase deficiency Increased:

Decreased:

Polycystic ovary syndrome
Adrenal tumors
  • Variable levels depends on tumor type
  • Older age
  • Rapidly progressive symptoms
Ovarian virilizing tumor
  • Variable levels depends on tumor type
  • Older age
  • Rapidly progressive symptoms
Hyperprolactinemia


References

  1. ↑ Boscaro M, Barzon L, Fallo F, Sonino N (2001). "Cushing's syndrome". Lancet. 357 (9258): 783–91. doi:10.1016/S0140-6736(00)04172-6. PMID 11253984.
  2. ↑ Findling JW, Raff H (2001). "Diagnosis and differential diagnosis of Cushing's syndrome". Endocrinol. Metab. Clin. North Am. 30 (3): 729–47. PMID 11571938.
  3. ↑ Newell-Price J, Trainer P, Besser M, Grossman A (1998). "The diagnosis and differential diagnosis of Cushing's syndrome and pseudo-Cushing's states". Endocr. Rev. 19 (5): 647–72. doi:10.1210/edrv.19.5.0346. PMID 9793762.
  4. ↑ "How Is Metabolic Syndrome Diagnosed? - NHLBI, NIH".
  5. ↑ Hohl A, Ronsoni MF, Oliveira M (2014). "Hirsutism: diagnosis and treatment". Arq Bras Endocrinol Metabol. 58 (2): 97–107. PMID 24830586. Vancouver style error: initials (help)
  6. ↑ White PC, Speiser PW (2000). "Congenital adrenal hyperplasia due to 21-hydroxylase deficiency". Endocr. Rev. 21 (3): 245–91. doi:10.1210/edrv.21.3.0398. PMID 10857554.
  7. ↑ Melmed, Shlomo (2016). Williams textbook of endocrinology. Philadelphia, PA: Elsevier. ISBN 978-0323297387.=

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