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362 Laboratory Medicine in Psychiatry and Behavioral Science
Chronic traumatic encephalopathy (CTE) (continued)
Laboratory testing
(continued)
Neuroimaging shows white matter hyperintensities on FLAIR
sequences corresponding to neuropathological changes of white
matter rarefaction, arteriolosclerosis, and phosphorylated tau accu
-
mulation.
Increased CSF phosphorylated tau-231 may prove to be a sensitive
biomarker of CTE.
Bieniek KF, Cairns NJ, Crary JF, et al: The second NINDS/NIBIB consensus meeting to define neuro-
pathological criteria for the diagnosis of chronic traumatic encephalopathy. J Neuropathol Exp Neurol
80(3):210–219, 2021
Katz DI, Bernick C, Dodick DW, et al: National Institute of Neurological Disorders and Stroke consensus
diagnostic criteria for traumatic encephalopathy syndrome. Neurology 96(18):848–863, 2021
Mariani M, Alosco ML, Mez J, Stern RA: Clinical presentation of chronic traumatic encephalopathy.Se-
min Neurol 40(4):370–383, 2020
McKee AC, Stern RA, Nowinski CJ, et al: The spectrum of disease in chronic traumatic encephalop-
athy. Brain 136(Pt 1):43–64, 2013 [published correction appears in Brain 136(Pt 10):e255, 2013]
Mez J, Daneshvar DH, Kiernan PT, et al: Clinicopathological evaluation of chronic traumatic encephalop-
athy in players of American football.JAMA 318(4):360–370, 2017
Mez J, Stern RA, McKee AC: Chronic traumatic encephalopathy.Semin Neurol 40(4):351–352, 2020
Mufson EJ, Kelley C, Perez SE: Chronic traumatic encephalopathy and the nucleus basalis of Mey-
nert.Handb Clin Neurol 182:9–29, 2021
Stein TD, Crary JF: Chronic traumatic encephalopathy and neuropathological comorbidities.Semin Neu-
rol 40(4):384–393, 2020
Turk KW, Geada A, Alvarez VE, et al: A comparison between tau and amyloid-beta cerebrospinal fluid
biomarkers in chronic traumatic encephalopathy and Alzheimer disease.Alzheimers Res Ther
14(1):28, 2022
Uretsky M, Bouix S, Killiany RJ, et al: Association between antemortem FLAIR white matter hyperinten-
sities and neuropathology in brain donors exposed to repetitive head impacts.Neurology 98(1):e27–
e39, 2022
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363 Diseases and Conditions
Cirrhosis
Clinical findings Cirrhosis refers to a pathological state of the liver in which normal
tissue is replaced by fibrous tissue and regenerative nodules after a
prolonged period of inflammation. Initially, the condition is asymp
-
tomatic and in its earliest stages may be reversible. Symptoms emerge
when compensatory processes fail. The most common causes of cirrho
-
sis are viral hepatitis, alcoholic liver disease, and non-alcoholic fatty
liver disease/steatohepatitis. Other causes include storage diseases
such as Wilson’s disease, immune-mediated conditions such as pri
-
mary biliary cholangitis, and cardiovascular disease such as conges-
tive heart failure.
Symptoms seen as compensatory processes begin to fail include
drowsiness, fatigue, cognitive changes, confusion, weakness, sleep
problems, loss of appetite, weight loss, and abdominal discomfort.
With decompensation, jaundice, portal hypertension (with ascites and
peripheral edema), hepatic encephalopathy, and bleeding are seen.
On physical exam, most of the signs of cirrhosis are noted outside the
abdomen. These include fetor hepaticus, parotid gland enlargement,
spider angiomas, icterus, gynecomastia, asterixis, palmar erythema,
Dupuytren contracture, splenomegaly, abdominal venous patterns in
-
dicating portal hypertension, ecchymoses, petechiae, edema, testicular
atrophy, and skin excoriation due to pruritus.
Laboratory testing Initial testing includes the following:
• CBC with platelets
•CMP
•Ferritin
• Transferrin saturation
•GGT
• Total bilirubin
•PT/INR
• Abdominal ultrasound
Testing to determine the
etiology of cirrhosis includes the following:
• Chronic hepatitis B: hepatitis B surface antigen, and hepatitis B
core antibody; if either is positive, hepatitis B virus DNA
• Chronic hepatitis C: anti-hepatitis C antibody; if positive, hepatitis
C virus RNA
• Non-alcoholic fatty liver disease: lipid panel, HbA1c
• Autoimmune hepatitis: antinuclear antibodies, smooth muscle
antibodies
Although liver biopsy has been the gold standard for confirming
and staging fibrosis, less invasive strategies are now routinely used, in-
cluding the estimation of fibrosis based on basic blood tests (e.g., the
Fibrosis-4 Index for Liver Fibrosis and the Non-Alcoholic Fatty Liver
Disease Fibrosis Score, both accessible at www.mdcalc.com). In addi-
tion, more specific blood tests that incorporate direct measures of fibro-
sis include hyaluronic acid and the N-terminal propeptide of type III
collagen.
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364 Laboratory Medicine in Psychiatry and Behavioral Science
Cirrhosis (continued)
Laboratory testing
(continued)
A widely used, noninvasive testing method known as transient
elastography is replacing biopsy for patients with either minimal or
advanced disease. Transient elastography measures liver stiffness
through the abdominal wall using pulse-echo ultrasound acquisition.
The procedure takes 5–10 minutes, and results are available at the point
of care. Liver biopsy may still be needed for patients with intermediate
stages of disease.
Both laboratory and clinical data are used to provide information
about prognosis using the Child-Pugh Score for Cirrhosis Mortality
and for transplant planning using the MELD Score (Model for End-
stage Liver Disease), both accessible at
www.mdcalc.com.
Patients with diagnosed cirrhosis should undergo ultrasound screen-
ing every 6 months for hepatocellular carcinoma.
Ginès P, Krag A, Abraldes JG, et al: Liver cirrhosis. Lancet 398(10308):1359–1376, 2021
Loomba R, Adams LA: Advances in non-invasive assessment of hepatic fibrosis.Gut 69(7):1343–1352,
2020
Smith A, Baumgartner K, Bositis C: Cirrhosis: diagnosis and management. Am Fam Physician 100(12):759–
770, 2019
Stanford Medicine: Stanford Medicine 25: Liver disease, head to foot. Stanford, CA, Stanford Medicine,
2022. Available at:
https://stanfordmedicine25.stanford.edu/the25/liverdisease.html. Accessed Jan-
uary 2022.
https://t.me/med1917
365 Diseases and Conditions
COVID-19
Clinical findings Coronavirus disease 2019 (COVID-19) caused by the severe acute re-
spiratory syndrome coronavirus-2 (SARS-CoV-2) is associated with a
wide range of clinical presentations, from asymptomatic disease to
septic shock and multiorgan failure. Exposure occurs mainly via short-
range airborne transmission and, to a lesser extent, from aerosolized
particles that persist in poorly ventilated indoor settings (long-range
airborne transmission). Contact exposure from touching contaminated
surfaces may also occur. An infected person is contagious for 2 days
before and—in severe cases—up to 20 days after symptoms first ap
-
pear. Mask-wearing, physical distancing, and hand hygiene reduce
transmission rates.
Symptoms of infection occur from 2 to 14 days after exposure and pri-
marily involve the respiratory system. Both direct infection and inflam-
matory responses are implicated. Common symptoms include fever,
cough, shortness of breath, chest tightness, sputum production, hemop-
tysis, fatigue, anosmia, hypogeusia, sore throat, diarrhea, nausea, vom-
iting, anorexia, abdominal pain, and myalgias. Symptoms requiring
urgent intervention include breathing difficulty, persistent chest pain or
pressure, new-onset confusion, inability to awaken or stay awake, and
discoloration of the skin, lips, or nail beds suggestive of hypoxia. Increas
-
ingly, reports have emerged of cardiac, renal, hepatic, endocrine, hema-
tological, and nervous system involvement, resulting in an extremely
wide range of clinical and laboratory abnormalities. In severe cases, per
-
manent injury to the lungs, heart, kidneys, and nervous system are seen.
Nervous system involvement—“neuro-COVID”—includes the cen-
tral, peripheral, and autonomic nervous systems. Signs and symptoms
include the following:
•Headache
• Impaired consciousness
• Delirium
• Generalized myoclonus
• Stroke—ischemic and hemorrhagic
• Venous sinus thrombosis
• Meningitis and encephalitis
• Seizures—secondary to electrolyte derangements, hypoxia, organ
failure, or stroke
• Neurogenic respiratory failure
• Dysautonomia—with orthostasis, hypotension, and vasovagal
syncope
• New-onset myasthenia gravis
• Optic neuritis
• Cranial polyneuropathy
• Sensorineural hearing loss
• Guillain-Barré syndrome
• Transverse myelitis
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366 Laboratory Medicine in Psychiatry and Behavioral Science
COVID-19 (continued)
Clinical findings So-called long-haul COVID may develop weeks to months after initial
(continued) infection, the result of either persistent low-grade inflammation or
neurodegeneration. Prominent symptoms include fatigue, myalgia,
headache, chest pain, tachycardia, cough, shortness of breath, poor
concentration, tremor, muscle twitching, insomnia, and depression. At
6 months, significant disability is seen in >50% of those affected, while
impaired cognition is seen in almost 70%. Long-lasting symptoms in-
clude persistent anosmia/dysgeusia, memory problems, anxiety, and
depression.
Laboratory testing Testing for current COVID-19 infection involves antigen testing, per-
formed either with a rapid test or a laboratory-based test. A swab is
taken from the nose or posterior pharynx to provide the
sample. For
the rapid test, which can be done at home (o
r at a
pharmacy or health
care facility), it is only necessary to follow the package instructions.
Results are available within ~15 minutes. For the laboratory test, the
reverse transcription–PCR method is used, which is the gold standard
of
testing. The results take 1 or more days to return.
Antibody tests are used to determine whether someone was previ-
ously exposed to or infected with COVID-19. Because it takes at least
12 days for the body to generate sufficient antibody levels to be de
-
tected, these tests are not useful to
the person who is concerned about
current infection.
Chest imaging such as chest X-ray, CT scan, and lung ultrasound can
be used to support the diagnosis of COVID-19. The classic finding on
chest CT is that of ground-glass opacities, along with consolidation of
tissue and “crazy paving,” referring to ground-glass opacities with su
-
perimposed intralobular septal thickening. Findings are distributed to
the periphery of both lungs. Chest CT can also reveal lymphadenopa
-
thy, nodules, cystic changes, and pleural effusions. These findings are
not specific to COVID-19 but can also occur with other types of infec
-
tion. These findings may be detectable before
COVID-19 symptoms are
apparent.
As could be expected with such widespread organ involvement, labo-
ratory abnormalities in COVID-19 are frequent and sometimes severe.
Abnormalities include elevated PT, lactate dehydrogenase,
D-dimer,
ALT, CRP, and creatine kinase. Early in the course of the infection, a
large reduction in CD4 and CD8 lymphocytes can be seen. ICU patients
may have high levels of inflammatory mediators, indicators of coagu-
lation activation and cellular immune deficiency, and evidence of myo-
cardial, hepatic, and renal injury. A poor prognosis is heralded by
elevations in serum ferritin,
D-dimer, neutrophil count, BUN, and cre-
atinine.
Aghagoli G, Gallo Marin B, et al: Neurological involvement in COVID-19 and potential mechanisms: a
review. Neurocrit Care 34(3):1062–1071, 2021
Alsharif W, Qurashi A: Effectiveness of COVID-19 diagnosis and management tools: a review. Radiogra-
phy (Lond) 27(2):682–687, 2021
Andalib S, Biller J, Di Napoli M, et al: Peripheral nervous system manifestations associated with COVID-
19. Curr Neurol Neurosci Rep 21(3):9, 2021
Baig AM: Deleterious
outcomes
in long-hauler COVID-19: the effects of SARS-CoV-2 on
the CNS in
chronic COVID syndrome.ACS Chem Neurosci 11(24):4017–4020,
2020
Chaumont H, Meppiel E, Roze E, et al: Long-term outcomes after NeuroCOVID: a 6-month follow-up
study on 60 patients.Rev Neurol (Paris) 178(1–2):137–143, 2022
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367 Diseases and Conditions
COVID-19 (continued)
Divani AA, Andalib S, Biller J, et al: Central nervous system manifestations associated with COVID-
19. Curr Neurol Neurosci Rep 20(12):60, 2020 [published correction appears in Curr Neurol Neurosci
Rep 20(12):66, 2020]
Schroeder ME, Manderski MT, Amro C, et al: Large gathering attendance is associated with increased
odds of contracting COVID-19: a survey based study. J Prev 43(2):157–166, 2022
West R, Kobokovich A, Connell N, Gronvall GK: COVID-19 antibody tests: a valuable public health tool
with limited relevance to individuals.Trends Microbiol 29(3):214–223, 2021
Whittaker A, Anson M, Harky A: Neurological manifestations of COVID-19: a systematic review and cur-
rent update. Acta Neurol Scand 142(1):14–22, 2020
https://t.me/med1917
368 Laboratory Medicine in Psychiatry and Behavioral Science
Creutzfeldt-Jakob disease (CJD)
Clinical findings CJD is a rapidly progressive and fatal neurodegenerative disease
caused by an alteration in a naturally occurring prion protein (PrP
c
) to
an abnormal form termed scrapie prion protein (PrP
Sc
). As with other
prion diseases, most cases of CJD are sporadic, but genetic and acquired
forms also exist. Sporadic CJD (sCJD) is classified into six subcategories
based on the genotype of the prion protein at codon 129 and the molec
-
ular signature of PrP
Sc
on Western blot analysis. Established risk factors
for sCJD include only increasing age and methionine homozygosity at
prion protein codon 129.
The category of acquired CJD includes the variant CJD associated with
ingestion of red meat infected with bovine spongiform encephalopathy
(BSE; “mad cow disease”) and iatrogenic forms. The incidence of vari
-
ant CJD has declined dramatically with measures to eradicate BSE in
animals. Iatrogenic CJD has been associated with corneal transplanta
-
tion, contaminated EEG depth electrodes, contaminated growth hor-
mone preparations, and surgical procedures including dura mater
grafts. With increased awareness and infection control measures, iatro
-
genic cases have also declined, but cases could
still emerge because the
latency for so
me infections is as high as 25
years or longer.
An immune-mediated encephalitis with severe neurological symptoms
closely mimicking sCJD has been reported in COVID-19 infection. This
syndrome was fully reversed with immunotherapy.
The diagnosis of sCJD is made based on clinical and laboratory findings
specified in the CDC guidelines available at
www.cdc.gov/prions/
cjd/diagnostic-criteria.html.
Clinical findings include the following:
• Rapidly progressive dementia
•Myoclonus
• Visual or cerebellar signs
• Motor signs: pyramidal or extrapyramidal
• Akinetic mutism
Cognitive dysfunction primarily involves memory loss but also apha-
sia and frontal/executive dysfunction. Myoclonus is spontaneous or
stimulus-responsive (“startle”). Visual signs may include blurring,
decreased acuity, hemianopia, or cortical blindness. Cerebellar signs in-
clude limb ataxia and wide-based, unsteady, and irregular gait. Motor
signs include weakness, reflex abnormalities, changes in muscle tone,
and abnormal movements. Akinetic mutism is defined by the loss of
movement and speech. Typically, the disease progresses from cognitive
dysfunction to cerebellar signs to myoclonus and akinetic mutism to
death, in rapid sequence.
Laboratory testing Two developments in laboratory testing have significantly improved
early diagnostic capability: real-time quaking-induced conversion (RT-
QuIC) and MRI diffusion-weighted imaging. In RT-QuIC, a sample such
as CSF is subjected to vigorous shaking that breaks up prion protein
aggregates for further incubation and the amplification of misfolded
proteins. Now in its second generation, this test is highly sensitive and
specific for sCJD, and a positive RT-QuIC in combination with character-
istic clinical findings is sufficient for a diagnosis of probable sCJD. The
RT-QuIC test should be performed as soon as prion disease is suspected.
https://t.me/med1917
369 Diseases and Conditions
Creutzfeldt-Jakob disease (CJD) (continued)
Laboratory testing
(continued)
Other tissues that can be used for testing with RT-QuIC include olfac-
tory mucosa and skin samples. An analogous technique, protein mis-
folding cyclic amplification (PMCA), has high diagnostic accuracy for
variant CJD using CSF, blood, or urine samples.
MRI diffusion-weighted imaging has greatly increased the value of
MRI in the early diagnosis of sCJD, when hyperintensities are seen in
the cortex and basal ganglia, with sparing of the perirolandic and hip-
pocampal areas. Depending on the molecular subtype of sCJD, other
patterns may be seen. Usually, these hyperintense lesions do not exhibit
swelling and do not enhance with contrast. The hyperintensities can be
seen to diminish with disease progression, possibly reflecting neuronal
loss. Of note, MRI FLAIR imaging could alternatively be used to meet
the CDC’s diagnostic criteria for positive imaging result.
Other laboratory tests of use in the diagnosis of sCJD include electro-
encephalography and CSF analysis. Although the classic EEG finding
is that of periodic sharp wave complexes, waking EEGs evolve with
disease progression from non-specific patterns of generalized slowing
and frontal intermittent rhythmic delta activity, to paroxysmal patterns
resembling triphasic waves, to this pattern of periodic sharp waves.
Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs)
may be seen in the transition from sleep to wake states.
CSF with a positive 14-3-3 assay may be helpful in diagnosing patients
with a disease duration of <2 years who have a high pretest probability
of sCJD. False-positive results can be seen in acute stroke, encephalitis,
and other dementias.
Atarashi R, Sano K, Satoh K, Nishida N: Real-time quaking-induced conversion: a highly sensitive assay
for prion detection. Prion 5(3):150–153, 2011
Beretta S, Stabile A, Balducci C, et al: COVID-19-associated immune-mediated encephalitis mimicking
acute-onset Creutzfeldt-Jakob disease. Ann Clin Transl Neurol 8(12):2314–2318, 2021
Centers for Disease Control and Prevention: Prion Diseases: CDC’s Diagnostic Criteria for Creutzfeldt-
Jakob Disease (CJD). Atlanta, GA, Centers for Disease Control and Prevention, 2018. Available at:
https://www.cdc.gov/prions/cjd/diagnostic-criteria.html. Accessed January 2022.
Figgie MP Jr, Appleby BS: Clinical use of improved diagnostic testing for detection of prion disease.Vi-
ruses 13(5):789, 2021
Gelisse P, Crespel A, Luigi Gigli G, Kaplan PW: Stimulus-induced rhythmic or periodic intermittent dis-
charges (SIRPIDs) in patients with triphasic waves and Creutzfeldt-Jakob disease.Clin Neurophysiol
132(8):1757–1769, 2021
Nakhleh R, Tessema ST, Mahgoub A: Creutzfeldt-Jakob disease as a cause of dementia.BMJ Case Rep
14(5):e240020, 2021
Park HY, Kim M, Suh CH, et al: Diagnostic value of diffusion-weighted brain magnetic resonance imag-
ing in patients with sporadic Creutzfeldt-Jakob disease: a systematic review and meta-analysis.Eur
Radiol 31(12):9073–9085, 2021
Tokumaru AM, Saito Y, Murayma S: Diffusion-weighted imaging is key to diagnosing specific dis-
eases.Magn Reson Imaging Clin N Am 29(2):163–183, 2021
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370 Laboratory Medicine in Psychiatry and Behavioral Science
Cushing’s syndrome (CS)
Clinical findings CS is characterized by signs and symptoms resulting from excess cir-
culating cortisol levels, most commonly due to the use of glucocorti-
coid drugs (exogenous CS) or the presence of an ACTH-secreting
pituitary tumor. The latter is known as Cushing’s disease (CD). Other
endogenous causes of CS include adrenal tumors and tumors of the
lung, pancreas, ovary, thyroid, or thymus gland. Two forms of endog
-
enous CS are recognized: ACTH-dependent, in which the overproduc-
tion of ACTH drives cortisol production (as in CD and these other
tumors with ectopic ACTH release), and ACTH-independent, in which
the adrenal glands produce cortisol autonomously. Recognition and
early treatment of CS and CD are critical because these conditions are
associated with increased mortality and morbidity, the latter including
hypertension, the metabolic syndrome, osteoporosis with fracture, op
-
portunistic infections, and several important neuropsychiatric disor-
ders.
Presenting signs of CS include the following:
• Central obesity
• Fat deposition in the face and upper back
• Thin skin with wide purple striae
• Hirsutism
•Acne
• Proximal muscle weakness
•Hypertension
• Glucose intolerance, diabetes
• Psychiatric: irritability, emotional lability, fatigue, depression, anx-
iety, mania, psychosis, cognitive deficits, and sleep disturbances
With mild hypercortisolism, physical signs of CS might not be present,
but hypertension, diabetes, and osteoporosis coexisting in a non-
elderly patient might raise the index of suspicion.
Of the psychiatric disorders associated with CS, depression and anxi-
ety are the most common, whereas mania and psychosis are rare. Ma-
nia is most often associated with the use of exogenous steroids. When
depression occurs, cortisol levels tend to be higher and CS symptoms
more severe. When psychotic symptoms develop, they tend to be treat
-
ment resistant. Patients with depression or psychosis may present a
risk of suicide at any time in the course of illness. In general, psychiat-
ric symptoms improve or resolve with treatment of CS that effectively
lowers peripheral cortisol levels, but improvement in cognitive deficits
appears to be more variable. This likely depends on the duration and
the severity of elevated cortisol levels before treatment, among other
factors. Multiple cognitive domains have been found to be affected,
including attention, memory, executive function, verbal fluency, pro-
cessing speed, and social cognition.
In the era of COVID-19, special considerations apply to patients pre-
senting with suspected hypercortisolism. This population is considered
at particular risk for contracting COVID-19 and represents a high-risk
group if infection occurs. Accordingly, diagnostic algorithms have been
streamlined so that cases requiring urgent intervention are flagged.
https://t.me/med1917
371 Diseases and Conditions
Cushing’s syndrome (CS) (continued)
Laboratory testing Laboratory confirmation of endogenous CS involves the following
steps:
1. Confirm elevated peripheral cortisol levels.
2. Distinguish ACTH-dependent from ACTH-independent cases.
3. Distinguish pituitary from ectopic sources of ACTH in ACTH-
dependent cases.
To confirm elevated peripheral cortisol levels, 24-hour urine free cor-
tisol is measured. The reference range will depend on the methods
used in testing, so local laboratory references should be consulted.
If cortisol is elevated, a low-dose dexamethasone suppression test
(DST) is performed to document the lack of feedback inhibition of cor
-
tisol on the HPA axis. Oral dexamethasone 1 mg is given between
11:00
P.M. and midnight, and plasma cortisol is checked at 8:00 A.M. the
next day. If the result is normal or equivocal, a high-dose DST may be
performed over 2 nights using 4 mg of dexamethasone and checking
plasma cortisol at 8:00
A.M. the second morning.
Late-night salivary cortisol level is measured to document the loss of
normal diurnal variation in cortisol.
When the diagnosis of CS has been confirmed, an ACTH level is ob-
tained to determine whether excessive ACTH secretion is the cause. A
normal or high ACTH level suggests ACTH-dependent CS because
high cortisol levels would usually suppress ACTH. A low ACTH level
suggests ACTH-independent CS arising from an adrenal source.
If the diagnosis of ACTH-dependent CS is confirmed, then a high-
resolution pituitary MRI with gadolinium is performed to identify
pituitary lesions such as adenomas. These lesions are usually micro
-
adenomas (<10 mm) and may be difficult to visualize. If the study is
equivocal, it may be necessary to take blood samples from the inferior
petrosal sinuses draining blood from the pituitary to check ACTH
levels for comparison with peripheral blood. Alternatively, a cortico-
tropin-releasing hormone (CRH) stimulation test could be performed.
Pituitary adenomas causing CD will respond to CRH stimulation,
whereas ectopic ACTH-secreting tumors will not.
Neuroimaging studies of CS and CD have shown significant volume
reductions in the hippocampus, anterior cingulate cortex, and medial
frontal gyrus. Although hippocampal volume appears to be at least
partly restored with successful treatment, these reduced cortical vol-
umes may be persistent. In addition, widespread white matter changes
are observed, with some evidence of underlying demyelination.
Barbot M, Zilio M, Scaroni C: Cushing’s syndrome: overview of clinical presentation, diagnostic tools and
complications.Best Pract Res Clin Endocrinol Metab 34(2):101380, 2020
Bauduin SEEC, van der Wee NJA, van der Werff SJA: Structural brain abnormalities in Cushing’s syn-
drome. Curr Opin Endocrinol Diabetes Obes 25(4):285–289, 2018
Berlinska A, Swiatkowska-Stodulska R, Sworczak K: Old problem, new concerns: hypercortisolemia in
the time of COVID-19. Front Endocrinol (Lausanne) 12:711612, 2021
Fujii Y, Mizoguchi Y, Masuoka J, et al: Cushing’s syndrome and psychosis: a case report and literature
review. Prim Care Companion CNS Disord 20(5):18br02279, 2018
Lonser RR, Nieman L, Oldfield EH: Cushing’s disease: pathobiology, diagnosis, and management. J Neu-
rosurg 126(2):404–417, 2017
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