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92 Laboratory Medicine in Psychiatry and Behavioral Science
Creatine kinase (CK)
Type of test Blood
Background and explanation
of test
CK, the enzyme that catalyzes the metabolism of creatine to
creatinine, is found in the heart and skeletal muscles and in
smaller concentrations in brain tissue. Three isoforms exist:
CK-MM, localized mainly to skeletal muscle, CK-MB, local
-
ized mainly to heart muscle, and CK-BB, localized mainly to
brain tissue. CK-BB from the CNS rarely enters the circula
-
tion; CNS injury may be reflected in only a slight elevation of
total CK. CK-MB has been replaced by troponin testing for
the diagnosis of heart attack.
Small amounts of CK-MM in the circulation are normal. Most
cases of el evated CK are either normal variants or the effects
of exercise, particularly when coupled with dehydration.
Persistent elevation of CK warrants investigation as a marker
of muscle injury, which could be caused by endocrine, auto-
immune, genetic, or drug-related factors. Myalgia is muscle
pain in the absence of CK elevation, myopathy is muscle pain
with CK elevation, and rhabdomyolysis is muscle pain, weak
-
ness, or swelling with CK elevation and myoglobinuria.
Statin drugs, macrolide antibiotics (e.g., azithromycin), and
antifungals (e.g., ketoconazole) are common causes of CK
elevation. Among statins, simvastatin and pravastatin are
associated with more muscle-related effects than are atorva
-
statin and rosuvastatin.
COVID-19 infection is associated with a viral myositis (mus-
cle inflammation) that ranges from mild to severe and may or
may not be accompanied by CK elevation.
Relevance to psychiatry and
behavioral science
CK elevation can be seen in patients with NMS, abrupt with-
drawal of clozapine, Parkinsonism-hyperpyrexia syndrome,
seizure, stroke, TBI, delirium tremens, carbon monoxide poi-
soning, or dystonic reactions. CK (and CK-MM) elevation can
be induced by ECT, use of physical restraints, or recent intra
-
muscular injections.
Both typical and atypical antipsychotic drugs can be associ-
ated with an elevation of CK and CK-MM with or without
muscle pathology. In most cases, CK normalizes when the
drug is withdrawn, and renal function is unaffected.
Preparation of patient Patients should avoid strenuous physical activity for
24 hours before testing.
Indications • A patient reporting muscle pain or weakness
• Suspicion of NMS
• Evaluating muscle injury in chronic muscular diseases,
such as muscular dystrophy
• Evaluating muscle injury in acute or subacute condi-
tions, such as myositis
• Detecting muscle injury from statins and other drugs,
including antipsychotic medications
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93 Laboratory Tests
Creatine kinase (CK) (continued)
Reference range Males: 20–200 U/L
Females: 20–180 U/L
Critical value(s) None
Increased levels • NMS
• Parkinson-hyperpyrexia syndrome
• Dystonic reaction
• Seizure
• ECT
• TBI
• Eosinophilia-myalgia syndrome
• Cocaine intoxication with rhabdomyolysis
• Myositis (e.g., with COVID-19)
• Myocarditis
• Stroke
• Delirium tremens
• Acute psychosis or mania
• Recent surgery
• Malignant hyperthermia
• Cardioversion
• Carbon monoxide poisoning
• Recent EMG or electric shock
• Subarachnoid hemorrhage
• Muscular dystrophy
• Hypothyroidism
• Late pregnancy
• Cancer (e.g., prostate, bladder, GI tract)
Decreased levels Small muscle mass
Interfering factors Benign elevations may be
seen in Blacks and those with
large muscle mass.
Heavy or prolonged exercise increases CK levels.
Intramuscular injections and use of physical restraints ele-
vate CK levels.
Cross-references Myocardial Infarction
Neuroleptic Malignant Syndrome
ARUP Laboratories: Creatine kinase, total, serum or plasma, in Lab Test Directory. Salt Lake City, UT,
ARUP Laboratories, 2021. Available at: https://ltd.aruplab.com/Tests/Pub/0020010. Accessed No-
vember 2021.
Belteczki Z, Ujvari J, Dome P: Clozapine withdrawal-induced malignant catatonia or neuroleptic malignant
syndrome: a case report and a brief review of the literature.Clin Neuropharmacol 44(4):148–153, 2021
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94 Laboratory Medicine in Psychiatry and Behavioral Science
Creatine kinase (CK) (continued)
Dos Santos DT, Imthon AK, Strelow MZ, et al: Parkinsonism-hyperpyrexia syndrome after amantadine
withdrawal: case report and review of the literature. Neurologist 26(4):149–152, 2021
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Kim EJ, Wierzbicki AS: Investigating raised creatine kinase.BMJ 373:n1486, 2021
Meltzer HY, Cola PA, Parsa M: Marked elevations of serum creatine kinase activity associated with anti-
psychotic drug treatment. Neuropsychopharmacology 15:395–405, 1996
Saud A, Naveen R, Aggarwal R, Gupta L: COVID-19 and myositis: what we know so far. Curr Rheumatol
Rep 23(8):63, 2021
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95 Laboratory Tests
Creatinine
Type of test Blood, 24-hour urine
Background and explanation
of test
Creatinine is a waste product continually produced in skel-
etal muscle by the breakdown of creatine phosphate, with
the amount produced dependent on the muscle mass of the
individual. All creatinine that is filtered by the kidneys is
eliminated, so the level of creatinine in the blood is inversely
related to the GFR. Serum creatinine is used with BUN to
evaluate kidney function, as both are elevated in kidney dis-
ease.
Traditionally, creatinine clearance (and corresponding GFR)
was estimated by the Cockcroft-Gault formula, but this was
replaced by the more accurate Modification of Diet in Renal
Disease (MDRD) Study formula, which has in turn been re-
placed by the Chronic Kidney Disease Epidemiology Collab-
oration (CKD-EPI) equation. This latest formula takes age,
sex, and serum creatinine into account in a formula that
many find unwieldy to use directly, but these values can be
plugged into an open-access calculator at
www.mdcalc.com/
calc/3939/ckd-epi-equations-glomerular-filtration-rate-gfr.
Importantly, the CKD-EPI formula does not use race or eth-
nicity as a factor. This is in recognition of the fact that the
multiplier used to correct eGFR for Blacks resulted in ineq
-
uitable and delayed care for chronic kidney disease in this
population.
The CKD-EPI formula is now used by many laboratories,
and an eGFR is reported along with serum creatinine. If this
estimate is not provided or if the laboratory used the MDRD
equation, an estimate can be obtained at the website noted
above.
The ratio of BUN to creatinine is sometimes helpful in the
differential diagnosis of the cause of kidney dysfunction. A
normal ratio is between 10:1 and 20:1. An increased ratio
suggests reduced blood flow to the kidney from conditions
such as congestive heart failure or dehydration, or increased
protein (urea nitrogen) from GI bleeding or dietary sources.
A decreased ratio suggests malnourishment or liver disease,
with decreased urea formation.
Relevance to psychiatry and
behavioral science
Delirium is associated with various conditions in which cre-
atinine is elevated. Creatinine is a component of the labora-
tory evaluation for newly hospitalized patients with
suspected eating disorders. The level may be increased, or it
may be normal despite significant renal dysfunction be
-
cause of decreased muscle mass. Lithium may cause true
creatinine elevation, with compromise of renal function and
reduced clearance of other drugs and waste products.
Preparation of patient None needed
Indications • Component of BMP and CMP
• Evaluating general health status
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96 Laboratory Medicine in Psychiatry and Behavioral Science
Creatinine (continued)
Indications (continued) • Suspicion of kidney disease or dysfunction
• Monitoring known kidney disease
• Monitoring renal function on nephrotoxic drugs (e.g.,
lithium, aminoglycosides)
• Preoperative assessment
• Preparing for administration of contrast agents for im-
aging
Reference range Adults 18–60 years
Males: 0.9–1.3 mg/dL
Females: 0.6–1.1 mg/dL
Adults 61–90 years
Males: 0.8–1.3 mg/dL
Females: 0.6–1.2 mg/dL
Adults >90 years
Males: 1.0–1.7 mg/dL
Females: 0.6–1.3 mg/dL
Critical value(s) Planning for dialysis often begins when eGFR by CKD-EPI
(or MDRD) declines to <30 mL/min/1.73m
2
.
Dialysis is usually started when eGFR declines to <15 mL/
min/1.73m
2
Increased levels Kidney diseases
• Glomerulonephritis
• Pyelonephritis
• Acute tubular dysfunction
• Nephrotic syndrome
• Interstitial nephritis
• Amyloidosis
Other conditions
•
Reduced blood flow to kidneys (e.g., atherosclerosis)
• Urinary tract obstruction (e.g., kidney stones or prostate
enlargement)
• Dehydration
• Congestive heart failure
• Shock
• Hemorrhage
• Muscle injury, rhabdomyolysis
• Myasthenia gravis
• Gigantism or acromegaly
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97 Laboratory Tests
Creatinine (continued)
Decreased levels • Liver disease
• Pregnancy
• Small or decreased muscle mass
• Burns
• Carbon monoxide poisoning
Interfering factors Serum creatinine varies with muscle mass. In body builders,
measurement of cystatin C to reflect kidney function may be
more appropriate.
In older persons with declining muscle mass, creatinine
level may remain stable in the face of significantly reduced
renal function. For this population, serial creatinine mea
-
surements should be used.
High-protein foods such as red meat may significantly in-
crease serum creatinine levels.
Creatine supplementation used by athletes slightly in-
creases creatinine levels without apparent harm to kidney
function.
Many drugs falsely elevate creatinine levels, including
ascorbic acid, barbiturates, some cephalosporins, clonidine,
and levodopa.
Cross-references Blood Urea Nitrogen
Lithium
CKD-EPI Equations for Glomerular Filtration Rate (GFR). Available at: https://www.mdcalc.com/calc/
3939/ckd-epi-equations-glomerular-filtration-rate-gfr.
Delanaye P, Cavalier E, Pottel H: Serum creatinine: not so simple!Nephron 136(4):302–308, 2017
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Raman M, Middleton RJ, Kalra PA, Green D: Estimating renal function in old people: an in-depth re-
view. Int Urol Nephrol 49(11):1979–1988, 2017
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98 Laboratory Medicine in Psychiatry and Behavioral Science
Cystatin-C
Type of test Blood
Background and explanation
of test
Cystatin-C is a protein produced by nucleated cells that is
filtered by the kidney and whose concentration rises with
declining GFR, in a manner analogous to that of creatinine.
Cystatin-C is a larger molecule than is creatinine, and its fil
-
tration rate is affected earlier than that of creatinine, so this
protein may provide an earlier warning of renal impair
-
ment. In fact, the relationship of both cystatin-C and creati-
nine with GFR is not linear, such that small initial increases
in either laboratory value may represent a significant de
-
cline in GFR.
Both cystatin-C and creatinine blood values are affected by
factors other than GFR. Unlike creatinine, cystatin-C is not
affected by muscle mass or diet but is affected by age, obe
-
sity, diabetes, and inflammation. Because cystatin-C is also
a prognostic indicator of cardiovascular risk, it may be of
particular use in patients with chronic kidney disease
(CKD). Cystatin-C is thought to be superior to creatinine in
estimating GFR in patients with COVID-19. Specialists who
estimate GFR using both creatinine and cystatin-C report
that those estimates can differ, and when the cystatin-C
-
predicted GFR is lower than the creatinine-predicted GFR,
prognosis tends to be worse.
Cystatin-C testing is not yet universally available. It is also
more costly and has a slower turnaround than creatinine.
Relevance to psychiatry and
behavioral science
This test is superior to creatinine in monitoring early renal
injury in patients undergoing chemotherapy, in renal trans
-
plant recipients, in those treated with lithium, and in those
with cirrhosis, rheumatoid arthritis, or IgA nephropathy. A
developing indication is the prescreening of patients sched
-
uled to undergo imaging with contrast dye, which can be
harmful to marginally functioning kidneys.
Preparation of patient None needed
Indications • Early detection of CKD
• Monitoring known kidney disease
• Prescreening for contrast-enhanced imaging
Reference range 0.5–1.2 mg/L
Critical value(s) None noted
Increased levels • CKD
• Renal injury from toxins such as chemotherapy, lithium,
or aminoglycosides
Decreased levels Not applicable
Interfering factors Hemolyzed or lipemic specimens invalidate results.
Cross-references Creatinine
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99 Laboratory Tests
Cystatin-C (continued)
ARUP Laboratories: Cystatin C, serum with reflex to estimated glomerular filtration rate (eGFR), in Lab
Test Directory. Salt Lake City, UT, ARUP Laboratories, 2021. Available at: https://ltd.aruplab.com/
Tests/Pub/0095229. Accessed November 2021.
Benoit SW, Ciccia EA, Devarajan P: Cystatin C as a biomarker of chronic kidney disease: latest develop-
ments. Expert Rev Mol Diagn 20(10):1019–1026, 2020
Chen S, Li J, Liu Z, et al: Comparing the value of cystatin C and serum creatinine for evaluating the renal
function and predicting the prognosis of COVID-19 patients. Front Pharmacol 12:587816, 2021
Ferguson TW, Komenda P, Tangri N: Cystatin C as a biomarker for estimating glomerular filtration
rate.Curr Opin Nephrol Hypertens 24(3):295–300, 2015
Luo J, Wan g LP, Hu H F, et al: Cystat in C and cardiovascular or all-cause mortality risk in the general pop-
ulation: a meta-analysis.Clin Chim Acta 450:39–45, 2015
Pasala S, Carmody JB: How to use...serum creatinine, cystatin C and GFR. Arch Dis Child Educ Pract Ed
102(1):37–43, 2017
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100 Laboratory Medicine in Psychiatry and Behavioral Science
Cytochrome P450 (CYP450) genotyping
Type of test Genetic
Background and explanation
of test
Many laboratories now offer CYP450 genotyping that in-
cludes the two isoenzymes most involved in psychotropic
drug metabolism: CYP2D6 and CYP2C19. Although the lit
-
erature on the clinical utility of CYP450 genotyping remains
mixed, the FDA has published a Table of Pharmacogenetic
Associations that can be useful to consult regarding testing
for specific drugs. That list is included in the references be
-
low. Whole blood is optimal for testing.
Relevance to psychiatry and
behavioral science
Psychotropic drugs metabolized by CYP2D6 include risper-
idone, venlafaxine, aripiprazole, brexpiprazole, deutetra-
benazine, duloxetine, and atomoxetine, among numerous
others. Poor metabolism resulting in higher drug concentra-
tions is thought to underlie many of the adverse effects of
these drugs. The poor metabolizer
phenotype occurs in 7%
of Whites and 1%–3% of those in other ethnic groups.
Drugs metabolized by CYP2C19 include citalopram, escit-
alopram, diazepam, and doxepin. Poor metabolism result-
ing in higher drug concentrations is thought to underlie
many of the adverse effects of these drugs. The poor metab
-
olizer phenotype at 2C19 is found in 3%–4% of Whites and
14%–21% of Asians.
Preparation of patient None needed
Indications Clinical suspicion of poor metabolizer or ultrarapid metab-
olizer status, based on adverse effects or lack of efficacy
Abnormal test Report returned indicating that the patient’s genotype rep-
resents poor metabolizer or ultrarapid metabolizer status.
Normal test Report returned indicating that the patient’s genotype rep-
resents extensive metabolizer status (two copies of the ac-
tive allele)
Interfering factors None
Cross-references None
ARUP Laboratories: Cytochrome P450 genotyping panel, in Lab Test Directory. Salt Lake City, UT, ARUP
Laboratories, 2021. Available at: https://ltd.aruplab.com/Tests/Pub/3001524. Accessed June 2021.
de Leon J, Armstrong S, Cozza K: Clinical guidelines for psychiatrists for the use of pharmacogenetic test-
ing for CYP450 2D6 and CYP450 2C19. Psychosomatics 47:75–85, 2006
Flockhart DA: Drug interactions and the cytochrome P450 system: the role of cytochrome P450 2C19. Clin
Pharmacokinet 29(Suppl):45–52, 1995
Jessel CD, Mostafa S, Potiriadis M, et al: Use of antidepressants with pharmacogenetic prescribing guide-
lines in a 10-year depression cohort of adult primary care patients.Pharmacogenet Genomics
30(7):145–152, 2020
U.S. Food and Drug Administration: Table of Pharmacogenetic Associations. FDA.gov, 2021. Available
at: https://www.fda.gov/medical-devices/precision-medicine/table-pharmacogenetic-
associations. Accessed June 2021.
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101 Laboratory Tests
Dexamethasone suppression test (DST)
Background and explanation
of test
The DST is used medically to screen for excess cortisol pro-
duction from Cushing’s syndrome and related conditions af-
fecting the HPA axis. Normally, when exogenous cortisol is
administered, the production of cortisol is reduced through
a process of negative feedback to the pituitary gland and hy
-
pothalamus known as HPA axis suppression. In patients
with Cushing’s syndrome, this suppression is reduced or ab
-
sent, and this is known as HPA axis nonsuppression.
There are several protocols for performing the DST, using
different doses of steroid and times of blood draw. A com
-
monly used “low-dose” protocol involves administration of
oral dexamethasone 1 mg between 11:00
P.M. and midnight,
followed by a blood draw for cortisol measurement between
7:00
A.M. and 9:00 A.M. the following day. Normally, the
morning cortisol level will be low or undetectable. In cases
in which the cortisol level exceeds a certain threshold, the
test is said to be positive. A dexamethasone level is drawn
simultaneously to ensure that the dexamethasone was taken
and that its level represents an adequate challenge.
Relevance to psychiatry and
behavioral science
Dysregulation of the HPA axis has been found in patients
with depression, especially melancholic and psychotic de
-
pression, and in PTSD. The DST may be useful in predicting
response to treatment for these conditions and in distin
-
guishing psychotic depression (nonsuppression) from
schizophrenia (suppression). The DST remains an area of ac-
tive research interest.
Preparation of patient Patients should abstain from caffeine and physical activity
and should not fast before the test.
Indications • Screening for Cushing’s syndrome
• Aiding in diagnosis of depression, PTSD, and current
anxiety disorders
• Predicting response to treatment for depression and
PTSD
Reference range Depends on testing protocol; discuss with local laboratory
Critical value(s) Depends on testing protocol
Increased levels Nonsuppression in the following:
• Cushing’s syndrome/disease
• Other adrenal disorders
• Major depression (melancholic, psychotic)
Variable findings in other psychiatric disorders
Decreased levels PTSD
Interfering factors False-positive results can be seen with acute illness, fasting,
caffeine ingestion, dehydration, uncontrolled diabetes, fever,
malnutrition, nausea, obesity, pregnancy, severe stress, and
temporal lobe disease.
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