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22 Laboratory Medicine in Psychiatry and Behavioral Science
Angiography, magnetic resonance (cerebrovascular) (continued)
Interfering factors Motion artifact results in unsatisfactory images. Patients
who are agitated or unable to comprehend instructions to
minimize motion from swallowing and breathing cannot be
studied.
Carotid artery overlap (internal with external on each side)
makes it difficult to visualize individual vessels.
Cross-references Angiography, Computed Tomography (Cerebrovascular)
Magnetic Resonance Imaging
American College of Radiology: ACR Appropriateness Criteria: Cerebrovascular Disease. Reston, VA,
American College of Radiology, 1996. Available at: https://acsearch.acr.org/docs/69478/Narrative.
Accessed August 2021.
Bowen BC, Quencer RM, Margosian P, et al: MR angiography of occlusive disease of the arteries in the
head and neck: current concepts. AJR Am J Roentgenol 162:9–18, 1994
Brant-Zawadzki M, Heiserman JE: The roles of MR angiography, CT angiography, and sonography in
vascular imaging of the head and neck. AJNR Am J Neuroradiol 18:1820–1825, 1997
Cure JK: Imaging of vascular lesions of the head and neck. Facial Plast Surg Clin North Am 9:525–549,
2001
Patel MR, Edelman RR: MR angiography of the head and neck. Top Magn Reson Imaging 8:345–365, 1996
Zhang XH, Liang H: Systematic review with network meta-analysis: diagnostic values of ultrasonogra-
phy, computed tomography, and magnetic resonance imaging in patients with ischemic stroke.Med-
icine (Baltimore) 98(30):e16360, 2019
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23 Laboratory Tests
Antidiuretic hormone (ADH)
Type of test Blood
Background and explanation
of test
ADH—also known as arginine vasopressin—is a hormone
secreted by the posterior pituitary gland that controls the
amount and concentration of urine that is produced by the
kidneys.
The concentration of dissolved particles in circulating blood
is termed serum osmolality. When serum osmolality is low
(serum is relatively dilute), ADH secretion is inhibited. In the
absence of ADH, large volumes of dilute urine are excreted.
When serum osmolality is high, more ADH is secreted, and
small volumes of concentrated urine are excreted. These pro
-
cesses help maintain homeostasis. However, recent evidence
suggests that not all actions of ADH are beneficial; high ADH
secretion has been associated with progression of chronic
kidney disease and adverse cardiovascular outcomes.
ADH measurement is used in the diagnosis of conditions
involving large amounts of urine (polyuria) or low serum
sodium (hyponatremia), including diabetes insipidus, psy
-
chogenic polydipsia, SIAD, and syndromes of ectopic ADH
production.
Relevance to psychiatry and
behavioral science
Schizophrenia and other psychotic disorders are associated
with psychogenic polydipsia. Lithium treatment can result
in nephrogenic diabetes insipidus. SSRIs and many other
psychotropic medications can cause SIAD.
Preparation of patient Fasting for 12 hours before the test is preferred. Patients
should refrain from strenuous activity before testing and
should sit calmly for the blood draw.
Indications • Polyuria
•Hyponatremia
Reference range <2.5 pg/mL
Critical value(s) None
Increased levels • Nephrogenic diabetes insipidus
•SIAD
• Acute intermittent porphyria
• Brain lesions: tumor, trauma, neurosurgery
• Guillain-Barré syndrome
• Pulmonary disease (e.g., tuberculosis)
• Ectopic ADH production (cancer)
Decreased levels • Central diabetes insipidus (neurogenic or hypotha-
lamic)
• Psychogenic polydipsia
•Nephrotic syndrome
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24 Laboratory Medicine in Psychiatry and Behavioral Science
Antidiuretic hormone (ADH) (continued)
Interfering factors High platelet values invalidate results.
Drugs associated with increased ADH include lithium, fu-
rosemide, and thiazide diuretics.
Drugs associated with decreased ADH include chlorproma-
zine, clonidine, and guanfacine.
Cross-references Diabetes Insipidus
Hyponatremia
Psychogenic Polydipsia
Syndrome of Inappropriate Antidiuresis
American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com. Ac-
cessed November 2021.
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Kanbay M, Yilmaz S, Dincer N, et al: Antidiuretic hormone and serum osmolarity physiology and related
outcomes: what is old, what is new, and what is unknown? J Clin Endocrinol Metab 104(11):5406–
5420, 2019
Kounin G, Bashir Q: Mechanism and role of antidiuretic hormone. Surg Neurol 53:508–510, 2000
Robertson GL: Antidiuretic hormone: normal and disordered function. Endocrinol Metab Clin North Am
30:671–694, 2001
Robinson AG: Disorders of antidiuretic hormone secretion. Clin Endocrinol Metab 14:55–88, 1985
https://t.me/med1917
25 Laboratory Tests
Antinuclear antibody (ANA) testing
Type of test Blood
Background and explanation
of test
ANA testing screens for systemic rheumatic diseases includ-
ing SLE, rheumatoid arthritis, polymyositis/dermatomyosi-
tis, mixed connective tissue disease, Sjögren’s syndrome,
scleroderma, and CREST syndrome.
In the ANA test performed by indirect fluorescent antibody,
the result is reported as a titer, along with the immunofluo
-
rescence pattern when the titer is high enough to be consid-
ered positive. Different threshold titers are used for
diagnosis; for SLE, an ANA titer of 1:80 or more is accepted
as positive. For other conditions, a titer of 1:160 or more is
considered positive.
When a high titer is obtained with screening, an extractable
nuclear antigen (ENA) antibody panel can help to identify
the specific disease:
• Presence of anti–double-stranded DNA and anti-Smith
antibodies in SLE
• Anti-histone antibodies in drug-induced lupus
• Anti–single-stranded-A antibodies (Ro) and anti–single-
stranded-B antibodies (La) in Sjögren’s syndrome
• Positive anticentromere test, presence of anti–Scl-70 anti-
bodies in scleroderma
The immunofluorescence pattern may also be helpful in iden-
tifying the specific disease:
• Homogeneous (diffuse) pattern: SLE and mixed connec-
tive tissue disease
• Speckled pattern: SLE, Sjögren’s syndrome, scleroderma,
polymyositis, rheumatoid arthritis, and mixed connective
tissue disease
• Nucleolar pattern: scleroderma and polymyositis
• Outline (peripheral) pattern: SLE
The diagnosis of a systemic rheumatic disease is based on
clinical signs and symptoms, and these tests are used only to
confirm the diagnosis and identify the specific disease.
Relevance to psychiatry and
behavioral science
ANA testing is most often used to diagnose SLE (lupus).
Common neuropsychiatric symptoms of lupus include
headaches, anxiety disorders, mood disorders, psychosis,
cognitive dysfunction, and delirium. Seizures, abnormal
movements (chorea, dystonia, hemiballismus), and stroke can
occur. Drug-induced lupus can also cause a positive test and
is important to rule out because this condition will subside
when the offending drug is discontinued. Psychotropic med-
ications associated with drug-induced lupus include carba-
mazepine, oxcarbazepine, phenytoin, and sertraline.
Preparation of patient None needed
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26 Laboratory Medicine in Psychiatry and Behavioral Science
Antinuclear antibody (ANA) testing (continued)
Indications • Symptoms suggestive of autoimmune disease: low-grade
fever, joint pain, fatigue, rash
• Suspicion of a second autoimmune disease in an affected
patient
• Unexplained neuropsychiatric symptoms
Reference range ≥1:160 on immunofluorescence antibody testing
>3 on enzyme-linked immunosorbent assay (ELISA) testing
Critical value(s) None
Positive test • SLE
• Drug-induced lupus
•Sjögren’s syndrome
• Scleroderma
• Rheumatoid arthritis
• Raynaud’s disease
• Dermatomyositis
• Mixed connective tissue disease
Negative test Patient is unlikely to have one of the autoimmune disorders,
although the test may need to be repeated later because of
the intermittent nature of disease activity.
Interfering factors False positives (more likely when titer is ≤1:160) are seen in
3%–5% of
Whites, in 10%–37% of patients older than
65 years, and with certain drugs and infections. False-
positive result can be seen in primary antiphospholipid
syndrome.
Drug-induced lupus can be caused by hydralazine, isonia-
zid, procainamide, and the psychotropic medications noted
above.
Cross-references Systemic Lupus Erythematosus
American Association for Clinical Chemistry: Testing.com Available at: https://www.testing.com. Ac-
cessed June 2021.
Benseler SM, Silverman ED: Neuropsychiatric involvement in pediatric systemic lupus erythematosus.
Lupus 16:564–571, 2007
Hanly JG, Urowitz MB, Siannis F, et al: Autoantibodies and neuropsychiatric events at the time of sys-
temic lupus erythematosus diagnosis: results from an international inception cohort study. Arthritis
Rheum 58:843–853, 2008
Hussain HM, Zakaria M: Drug-induced lupus secondary to sertraline. Aust N Z J Psychiatry 42:1074–
1075, 2008
Katz U, Zandman-Goddard G: Drug-induced lupus: an update. Autoimmun Rev 10:46–50, 2010
Ling M, Murali M: Antinuclear antibody tests. Clin Lab Med 39(4):513–524, 2019
Pisetsky DS: Antinuclear antibody testing: misunderstood or misbegotten? Nat Rev Rheumatol 13(8):495–
502, 2017
https://t.me/med1917
27 Laboratory Tests
Antiphospholipid (aPL) antibodies
Type of test Blood
Background and explanation
of test
The aPL syndrome (APS) is a systemic autoimmune disease
characterized by thrombotic or obstetrical events that occur
in patients with persistent aPL antibodies. The syndrome is
often found in association with other autoimmune diseases
such as SLE but can also be seen in the absence of other au
-
toimmune symptoms. aPL antibodies include lupus antico-
agulant, anticardiolipin, and anti-β-2 glycoprotein 1. Of the
three tests, lupus anticoagulant correlates best with clinical
events, but all three tests are performed to facilitate risk
stratification. Persistence of antibodies is determined by
testing on two or more occasions ≥12 weeks apart. If a pa-
tient with autoimmune symptoms does not test positive, the
test is repeated because antibodies can develop at any time.
Moreover, aPL antibodies are not just diagnostic markers
for APS but also a risk factor for thrombosis and obstetrical
events that are multifactorial. For this reason, non–aPL an
-
tibody risk factors for thrombosis (e.g., smoking, use of birth
control pills or hormone replacement therapy) also must be
considered.
aPL antibodies have been identified in patients with COVID-
19 infection, but it is not known whether they are involved in
thrombotic events. At present, aPL antibodies have no role in
COVID-19 diagnosis or management. Moreover, side effects
of the mRNA vaccines for COVID appear to be well tolerated
in patients with aPL antibodies or aPL syndrome.
Relevance to psychiatry and
behavioral science
Neurological presentations of APS are well recognized. These
include stroke/TIA, cognitive dysfunction, subcortical white
matter changes, dementia, delirium, seizures, headaches,
chorea, transverse myelitis, and motor neuropathy. Stroke oc
-
curring in a child or young adult should raise suspicion for
APS. Headaches are often recurrent and refractory to usual
treatments but may respond well to anticoagulation. In gen
-
eral, psychiatric presentations are not as well recognized, but
psychosis and depression have been reported. Phenothiazine
drugs can cause a transiently positive aPL test.
Preparation of patient None needed
Indications • Evaluation of recurrent thrombotic events
• Thrombotic event in the absence of risk factors
• Evaluation of repeated miscarriage in pregnancy
• Investigation of thrombocytopenia, prolonged PTT, or in-
appropriate clotting
• Confirmation of suspected Sneddon’s syndrome (livedo
reticularis accompanied by stroke/temporary ischemic
event)
Critical value(s) None
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28 Laboratory Medicine in Psychiatry and Behavioral Science
Antiphospholipid (aPL) antibodies (continued)
Positive test The best use of aPL antibodies is for risk stratification, but a
positive test is defined by the following:
• Lupus anticoagulant present in plasma on two or more
occasions ≥12 weeks apart, or
• Anticardiolipin antibody of IgG and/or IgM isotype
in serum or plasma, present in medium to high titer
(>40 GPL or MPL or >99th percentile) on two or more
occasions ≥12 weeks apart, or
•Anti-β-2 glycoprotein 1 antibody of IgG and/or IgM
isotype in serum or plasma (in titer >99th percentile)
on two or more occasions ≥12 weeks apart
The differential diagnosis for a positive test includes the
following:
•APS
• SLE, other autoimmune disorders
•HIV
•Certain cancers
• Advanced age
• Infections (transient)
• Certain drugs (transient): phenothiazines, procain-
amide
• COVID-19 infection
Interfering factors Anticoagulants, current infection, and prior syphilis infec-
tion may yield false-positive results.
Cross-references Antiphospholipid Syndrome
Devreese KMJ: COVID-19-related laboratory coagulation findings. Int J Lab Hematol 43(Suppl 1):36–42,
2021
Favaloro EJ, Henry BM, Lippi G: COVID-19 and antiphospholipid antibodies: time for a reality check?
Semin Thromb Hemost 48(1):72–92, 2022
Garcia D, Erkan D: Diagnosis and management of the antiphospholipid syndrome. N Engl J Med
378(21):2010–2021, 2018
Gezer S: Antiphospholipid syndrome. Dis Mon 49:696–741, 2003
Giannakopoulos B, Passam F, Ioannou Y, et al: How we diagnose the antiphospholipid syndrome. Blood
113:985–994, 2009
Sammaritano LR: Antiphospholipid syndrome. Best Pract Res Clin Rheumatol 34(1):101463, 2020
Sciascia S, Costanzo P, Radin M, et al: Safety and tolerability of mRNA COVID-19 vaccines in people with
antiphospholipid antibodies. Lancet Rheumatol 3(12):e832, 2021
https://t.me/med1917
29 Laboratory Tests
Apolipoprotein E (ApoE) genotyping
Type of test Blood
Background and explanation
of test
ApoE genotype is a major risk determinant of late-onset
Alzheimer’s disease (AD), with the ApoE ε4 allele promot
-
ing amyloid deposition and clinical symptoms of AD about
15 years earlier per ε4 allele. The ApoE ε2 allele confers re
-
duced risk of AD compared to the more common ApoE ε3
allele. In addition to its effect on amyloid-β clearance from
the brain, ApoE genotype is known to significantly influ
-
ence tau pathology and neurodegeneration as well as mi-
croglial activity.
ApoE also is suspected of being pathogenic itself, affecting
critical brain homeostatic processes such as synaptic integ
-
rity and plasticity, lipid efflux and endocytosis, and cerebro-
vascular function. For these reasons, ApoE itself is now
considered an important target of AD therapies, particu
-
larly in young, presymptomatic individuals.
ApoE genotype also is known to influence the odds of at-
taining extreme longevity, with the ε4 allele significantly de-
creasing the odds and the ε2/ε2 and ε2/ε3 genotypes
significantly increasing the odds.
The rare ApoE Christchurch mutation (ApoEch) was found
to greatly delay the onset of AD in a patient with autosomal
dominant AD (presenilin-1 mutation).
Relevance to psychiatry and
behavioral science
ApoE testing can help increase the specificity of diagnosis
in patients who meet clinical criteria for AD, but it does not
predict whether the disease will develop in asymptomatic
individuals. In patients with the clinical diagnosis of AD,
the presence of the ε4/ε4 genotype increases the probability
that AD is the correct diagnosis to about 97%. On the other
hand, ~42% of patients with AD do not have an ε4 allele.
The test, therefore, is used in a specific context and not for
screening or in the early stages of the diagnostic evaluation
for dementia. Although it is possible to obtain ApoE testing
through an online portal such as 23andMe, it is recom-
mended that this testing be done through and in collabora-
tion with a qualified health care provider.
Preparation of patient Patient counseling is mandatory. The patient’s expectations,
the value of a positive or a negative test, out-of-pocket cost,
implications for blood relatives, and the potential for dis-
crimination in employment, insurability, and educational
opportunities should be discussed. A plan for a follow-up
discussion of test results should be made.
Indications • Increasing specificity of diagnosis in a patient who
meets clinical criteria for AD
• Determining eligibility for clinical trials
• Not useful for presymptomatic testing
Reference range No ε4 allele present
Possible genotypes: ε3/ε3; ε3/ε2; ε2/ε2
https://t.me/med1917
30 Laboratory Medicine in Psychiatry and Behavioral Science
Apolipoprotein E (ApoE) genotyping (continued)
Critical value(s) None
Abnormal test Genotypes: ε4/ε4; ε4/ε3; ε4/ε2
Interfering factors None
Cross-references Alzheimer’s Disease
Cerebrospinal Fluid Amyloid β
1–42
Cerebrospinal Fluid Tau Protein
Dementia
Arboleda-Velasquez JF, Lopera F, O’Hare M, et al: Resistance to autosomal dominant Alzheimer’s disease
in an APOE3 Christchurch homozygote: a case report. Nat Med 25(11):1680–1683, 2019
McConnell LM, Sanders GD, Owens DK: Evaluation of genetic tests: APOE genotyping for the diagnosis
of Alzheimer disease. Genet Test 3:47–53, 1999
Petersen RC, Waring SC, Smith GE, et al: Predictive value of APOE genotyping in incipient Alzheimer’s
disease. Ann N Y Acad Sci 802:58–69, 1996
Rebeck GW: The role of APOE on lipid homeostasis and inflammation in normal brains. J Lipid Res 2017
58(8):1493–1499, 2017
Sebastiani P, Gurinovich A, Nygaard M, et al: APOE alleles and extreme human longevity. J Gerontol A
Biol Sci Med Sci 74(1):44–51, 2019
Selkoe DJ, Hardy J: The amyloid hypothesis of Alzheimer’s disease at 25years.EMBO Mol Med 8(6):595–
608, 2016
Yamazaki Y, Zhao N, Caulfield TR, et al: Apolipoprotein E and Alzheimer disease: pathobiology and tar-
geting strategies. Nat Rev Neurol 15(9):501–518, 2019
https://t.me/med1917
31 Laboratory Tests
Aspartate transaminase (AST)
Type of test Blood
Background and explanation
of test
AST is an enzyme found in liver cells and other metaboli-
cally active tissues including the heart, skeletal muscle, kid-
ney, brain, pancreas, lungs, RBCs, and WBCs. AST levels rise
with cellular injury. AST is used with other liver enzyme
tests such as ALT and ALP to evaluate liver function and
detect liver damage. The pattern and degree of abnormality
in each of these tests can be helpful in determining etiology.
Extreme elevations in AST (>10 times the upper limit of nor-
mal [ULN]) are consistent with acute hepatitis, often of viral
origin. As with ALT, the AST level in this condition can re
-
main high for as long as 6 months. In chronic hepatitis, on
the other hand, AST levels may be only minimally elevated
(<4 times the ULN) or even high-normal. In liver disease
such as cirrhosis, cancer, or biliary obstruction, AST levels
may be nearly normal, but they are elevated more often than
ALT. In liver damage due to alcohol, AST is usually signifi-
cantly more elevated than ALT, a pattern unlike that seen in
other causes of liver injury. In severe cirrhosis, the paradox-
ical finding of low AST may be seen, which is attributed to
the loss of hepatocyte mass with a corresponding reduction
of enzyme levels. In extrahepatic biliary obstruction, AST el
-
evation is not as great as ALT elevation. Although AST does
increase in response to muscle or heart injury, troponins are
used instead in the workup of these conditions. The most
common cause of mild AST elevation in the Western hemi
-
sphere is non-alcoholic fatty liver disease.
Relevance to psychiatry and
behavioral science
AST
is one of
the t
ests of
liver health (liver “function”) that
is closely monitored in psychiatric practice, mainly because
of the potential hepatotoxicity of psychotropic drugs.
AST is
also monitored
in patients with alcoholism, substance-
induced liver disease, and hepatitis.
Elevation of AST may be found on routine screening. If the
patient has no clinical symptoms and no risk factors for liver
disease, and AST is <3 times the ULN, a recheck is indicated
after 1–3 months. If the elevation persists, further investiga-
tion is needed. If AST is >3 times the ULN on a single mea-
surement, further investigation is needed. Elevation of AST
may occur with initiation of a new psychotropic medication.
In most cases, this AST increase is benign, and the lab value
will revert to baseline within weeks of dosage stabilization.
Further investigation is needed if the value does not normal-
ize or when ALP or bilirubin is also elevated.
Pathological elevation of AST may occur with alcohol use
disorder, substance-induced liver disease, or hepatitis. It is
important not to be misled by a normal AST value in pa-
tients with established cirrhosis. In patients with cirrhosis
due to hepatitis C who have a normal AST result, active hep-
atitis may be present, such that they would benefit from an-
tiviral therapy, β-blockers to prevent variceal bleeding, and
other treatments.
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