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232 Laboratory Medicine in Psychiatry and Behavioral Science

Red blood cell (RBC) count (continued)

Interfering factors Blood collection technique significantly affects the results. If

the patient is recumbent during phlebotomy, the cell count is

5% lower. Results are elevated with prolonged venous stasis

during phlebotomy. Lavender tube must be three-fourths full

or the results will be invalid. A clotted sample will yield in

valid results.

Many psychotropic medications can cause spurious reduc-

tions in RBC count, including amitriptyline, amphetamine,

barbiturates, bupropion, carbamazepine, chlordiazepoxide,

chlorpromazine, clomipramine, clonazepam, desipramine,

diphenhydramine, donepezil, fluphenazine, haloperidol,

levodopa, MAOIs, meprobamate, mesoridazine, pemoline,

phenobarbital, phenytoin, thioridazine, thiothixene, trazo

done, and trifluoperazine.

Cross-references Anemia

Complete Blood Count

Hematocrit

Mean Corpuscular Volume

American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com. Ac-

cessed September 2021.

Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,

PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018

https://t.me/med1917

233 Laboratory Tests

Renal function panel

Type of test Blood

Background and explanation

of test

The renal or kidney function panel consists of the following

tests: albumin, BUN, calcium, total carbon dioxide, chloride,

creatinine, glucose, phosphate, potassium, and sodium. A

calculated anion gap value is often inclu ded.

Risk factors for acute renal disease include a history of

trauma, sepsis, hypotension, and reaction to contrast dye.

Risk factors for chronic renal disease include hypertension,

diabetes, atherosclerosis, familial kidney disease, polycystic

kidneys, and use of nephrotoxic medications such as

NSAIDs.

Relevance to psychiatry and

behavioral science

Impaired renal function is associated with a range of neuro-

psychiatric symptoms, from fatigue and lethargy to delirium

and coma. Cognitive impairment, sleep and appetite distur

bances, and sexual dysfunction have also been reported.

Because most psychotropic drugs are excreted at least partly

by the kidneys, changes in renal function have definite phar-

macokinetic effects. Lithium is eliminated only through the

kidneys, such that the serum level is directly proportional to

the GFR. Lithium and other drugs, such as gabapentin, can

in turn affect kidney function. Lithium is associated with di

abetes insipidus and, with long-term use, can cause tubu-

lointerstitial disease. Use of lithium necessitates renal

function monitoring, as described in the Psychotropic Med

ications chapter.

Preparation of patient None needed

Indications • Workup for a patient with risk factors for acute or

chronic kidney disease

•

Monitoring a patient with diabetes for early renal dys

function

Reference range See entries for individual tests.

Critical value(s) See entries for individual tests.

Increased levels See entries for individual tests.

Decreased levels See entries for individual tests.

Interfering factors See entries for individual tests.

Cross-references Diabetes Insipidus

Lithium

Uremic Syndrome

See entries for component tests.

American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com. Ac-

cessed September 2021.

ARUP Laboratories: Renal function panel, in Lab Test Directory. Salt Lake City, UT, ARUP Laboratories,

2021. Available at: https://ltd.aruplab.com/Tests/Pub/0020144. Accessed September 2021.

https://t.me/med1917

234 Laboratory Medicine in Psychiatry and Behavioral Science

Reticulocyte count

Type of test Blood

Background and explanation

of test

Reticulocytes are immature RBCs formed in bone marrow

that mature in the circulation, usually within 1–2 days. These

cells provide one measure of the effectiveness of RBC pro

duction (erythropoiesis). The reticulocyte count is expressed

as a percentage of the total RBC count.

A better index of RBC production is the reticulocyte produc-

tion index (RPI), which corrects for anemia and the prema-

ture shift of more immature reticulocytes from bone marrow

to blood. The RPI is calculated using the following equation:

RPI = % reticulocytes × (patient’s hematocrit/45) ×

(1/maturation time)

The maturation time varies with hematocrit; 45%=1 day,

35% =1.5 days, 25% =2.0 days, 15%= 2.5 days. The RPI should

increase with anemia; failure to increase suggests an inade

quate bone marrow response.

Relevance to psychiatry and

behavioral science

Reticulocyte count is decreased in alcohol use disorder and

megaloblastic anemia (e.g., with vitamin B

or folate defi-

ciency).

Preparation of patient None needed

Indications • Diagnosing cause of anemia: bone marrow failure vs.

bleeding or hemolysis

•

Monitoring effectiveness of

treatment for anemia (perni-

cious anemia, folate

deficiency,

or iron deficiency)

• Evaluating bone marrow recovery in aplastic anemia

• Determining effects of radiation on bone marrow

Reference range In the presence of anemia, an RPI >2 suggests effective bone

marrow response.

Critical value(s) None

Increased levels • Posthemorrhage

• Hemolytic anemia

• After treatment of anemia

Decreased levels • Iron deficiency anemia

• Aplastic anemia

• Pernicious anemia

• Anemia of chronic disease

• Radiation therapy

• Bone marrow failure (e.g., from cancer)

• Myelodysplastic syndromes

• Alcohol use disorder

https://t.me/med1917

235 Laboratory Tests

Reticulocyte count (continued)

Interfering factors Improper specimen collection or handling may invalidate

the results; this includes drawing blood after a recent trans

fusion or proximal to an IV catheter, or a hemolyzed sample.

Drugs causing spurious elevations include antipyretics,

chloroquine, levodopa, quinine, and sulfonamides.

Drugs causing spurious reductions include several chemo-

therapeutic agents and sulfonamides.

Cross-references Anemia

Red Blood Cell Count

American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com. Ac-

cessed September 2021.

Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,

PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018

https://t.me/med1917

236 Laboratory Medicine in Psychiatry and Behavioral Science

Serotonin transporter polymorphism

Type of test Genetic

Background and explanation

of test

The serotonin transporter terminates the actions of sero-

tonin in the synaptic cleft by reuptake of this neurotransmit-

ter into the presynaptic terminal where serotonin is

recycled. The gene encoding the serotonin transporter is

member 4 of solute carrier family 6, known by the short

hand SLC6A4. In humans, this gene is located on chromo-

some 17 (17q11). Among polymorphisms identified for this

gene is a 44-base-pair insertion/deletion sequence in the

promoter region known as 5-HTTLPR. Individuals with a

deletion (the short or S allele) have a lower rate of serotonin

transporter transcription than those with an insertion (the

long or L allele). One clinical consequence of this difference

is that individuals with the S allele, having lower trans

porter density on the presynaptic neuron, have fewer sites

for drugs such as SSRIs to bind and would likely have a re

duced response to treatment with these drugs.

At this writing, SLC6A4 5-HTTLPR has been established as

cost-effective in predicting efficacy and adverse effects with

SSRI treatment, as noted below. Other polymorphisms in

the serotonin transporter (e.g., rs25531 SNP) are under in

vestigation to determine their clinical utility.

Relevance to psychiatry and

behavioral science

The short or S allele confers an elevated risk of developing

a major depressive episode after exposure to an adverse life

event. This effect may be most pronounced early in the life

time course of the illness. The S allele may also predict a

poor outcome with antidepressant medication treatment,

including delayed response, increased adverse effects, and/

or induction of mania or rapid cycling in a patient with bi

polar disease. It appears that these effects are seen mostly

with purely serotonergic drugs such as SSRIs, so affected

patients may be better treated with non-SSRI antidepressant

drugs such as SNRIs or TCAs. The S allele is most common

among Asians and Whites of European descent and least

common among sub-Saharan Africans.

Preparation of patient None needed

Indications • Depression in a young patient of high-risk ethnicity

• Depression in a patient with history of childhood abuse

or neglect

• Depression in a patient with serious recent life adversity

• Question of bipolarity in a depressed patient awaiting

treatment

• Treatment-resistant depression

Positive test Deletion identified (one or two S alleles)

Negative test No deletion identified (two L alleles)

Interfering factors None known

Cross-references Major Depressive Disorder

https://t.me/med1917

237 Laboratory Tests

Serotonin transporter polymorphism (continued)

Bradley P, Shiekh M, Mehra V, et al: Improved efficacy with targeted pharmacogenetic-guided treatment

of patients with depression and anxiety: a randomized clinical trial demonstrating clinical

utility. J Psychiatr Res 96:100–107, 2018

Le-Niculescu H, Roseberry K, Gill SS, et al: Precision medicine for mood disorders: objective a ssessment,

risk prediction, pharmacogenomics, and repurposed drugs.Mol Psychiatry 26(7):2776–2804, 2021

Luddington NS, Mandadapu A, Husk M, et al: Clinical implications of genetic variation in the serotonin

transporter promoter region: a review. Prim Care Companion J Clin Psychiatry 11(3):93–102, 2009

Oz MD, Baskak B, Uckun Z,et al: Association between serotonin 2A receptor (HTR2A), serotonin trans-

porter (SLC6A4) and brain-derived neurotrophic factor (BDNF) gene polymorphisms and citalo-

pram/sertraline induced sexual dysfunction in MDD patients. Pharmacogenomics J 20:443–450, 2020

Plenge P, Yang D, Salomon K, et al: The antidepressant drug vilazodone is an allosteric inhibitor of the

serotonin transporter.Nat Commun 12(1):5063, 2021

Svensson JE, Svanborg C, Plavén-Sigray P, et al: Serotonin transporter availability increases in patients

recovering from a depressive episode.Transl Psychiatry 11(1):264, 2021

https://t.me/med1917

238 Laboratory Medicine in Psychiatry and Behavioral Science

Single-photon emission computed tomography

Typeoftest Nuclearmedicine

Background and explana-

tionof test

SPECTbrain scanning is a nuclear medicine procedure that

evaluates cerebral blood flow, which is understood to reflect

neuronal activity. A lipophilic radiopharmaceutical such as

technetium-labeledhexamethylpropyleneamineoxime

(99mTc-HMPAO) or ethylene cysteine diethylester(99mTc

ECD) is injected intravenously, and the labeled compound

crosses the blood-brain barrier while continuing to emit

gamma rays. An array of gamma-detecting cameras captures

cerebral perfusion patternsin three dimensions. Molecular

imaging is also made possible by injection of radiopharma

ceuticals such as ioflupane

123

I, whichbinds to dopamine

transporters and aids in the differential diagnosis of Parkin

son’s disease (PD).

TheSPECTprocedure is like PET scanning, althoughthe re-

sultingcontrast and spatial resolutionhave in the past been

inferiorto PET. Improvements in SPECT technology involv

ingmultiheaded gamma detectors have pushed the limits of

resolution into thesame range as PET.Moreover, SPECT is

much less costly than PET, and the equipment is more readily

available in clinical settings. SPECT is also less problematic

for claustrophobic patients because theequipmentis less con

fining. As with PET, SPECT is often performed in tandem

with structural imaging such as CT or MRI.

Relevance to psychiatry and Indications for SPECT are like those for PET, although SPECT

behavioral science has been less studied and less validated than PET for psychi-

atric applications. Use of SPECT was constrained in the past

because of its inability to investigate brain structures smaller

than 1 cm.Despite this limitation, numerous studies haveal

readydemonstrated the utility of SPECT in distinguishing

psychogenic nonepileptic seizures from epileptic seizures, in

the differential diagnosis of dementia, in the evaluation of

TBI, and in other neuropsychiatric conditions. It may be that

the radiological tradition of reporting only hypoperfusion

will have to be revisited for psychiatric applications, because

several conditions have been found to involve increased re

gionalblood flow.

Preparationofpatient Patientsshould eat beforethe procedure and take medica-

tions as usual but should avoid caffeine, nicotine, and alcohol.

In addition, they should avoid drinking large amounts of liq-

uid because of the need to remain still while the scan takes

place. Ifsedation is needed,administer after tracer is injected.

Indications • Distinguishing seizure from psychogenic nonepileptic

seizure

• Localizing epileptic foci before surgery

• Diagnosing encephalitis

• Detecting toxic encephalopathy (with global perfusion

deficit)

• Informing differential diagnosis of dementia subtypes

https://t.me/med1917

239 Laboratory Tests

Single-photon emission computed tomography (continued)

Indications (continued) • Detecting and evaluating cerebrovascular disease

• Evaluating suspected TBI

• Distinguishing PD from other movement disorders

• Informing differential diagnosis of ADHD (controver-

sial)

Normal result Normal blood flow patterns

Abnormal result • Globally reduced blood flow

• Regionally or focally reduced blood flow

• Focally increased blood flow

Interfering factors Clinical value of SPECT scanning depends to a large extent

on interpreter expertise.

A commonly seen false-positive finding is crossed cerebellar

diaschisis, in which reduced cerebellar blood flow is seen

contralateral to supratentorial lesion, such as an infarct.

Cross-references Positron Emission Tomography, Brain

Amen DG, Trujillo M, Newberg A, et al: Brain SPECT imaging in complex psychiatric cases: an evidence-

based, underutilized tool.Open Neuroimag J 5:40–48, 2011

Fond G, Garosi A, Faugere M, et al: Peripheral inflammation is associated with brain SPECT perfusion

changes in schizophrenia. Eur J Nucl Med Mol Imaging 49(3):905–912, 2022

Gallucci-Neto J, Brunoni AR, Ono CR, et al: Ictal SPECT in psychogenic nonepileptic and epileptic sei-

zures. J Acad Consult Liaison Psychiatry 62(1):29–37, 2021

Henderson TA, Cohen P, van Lierop M, et al: A reckoning to keep doing what we are already doing with

PET and SPECT functional neuroimaging. Am J Psychiatry 177(7):637–638, 2020

Miyagawa T, Przybelski SA, Maltais D, et al: The value of multimodal imaging with

123

I-FP-CIT SPECT

in differential diagnosis of dementia with Lewy bodies and Alzheimer’s disease dementia. Neurobiol

Aging 99:11–18, 2021

Pagani M, Carletto S, Ostacoli L: PET and SPECT in psychiatry: the past and the future.Eur J Nucl Med

Mol Imaging 46(10):1985–1987, 2019

Peitl V, Badžim VA, Šiško Markoš I, et al: Improvements of frontotemporal cerebral blood flow and cog-

nitive functioning in patients with first episode of schizophrenia treated with long-acting aripipra-

zole. J Clin Psychopharmacol 41(6):638–643, 2021

Richieri R, Boyer L, Faget-Agius C, et al: Determinants of brain SPECT perfusion and connectivity in

treatment-resistant depression. Psychiatry Res 231(2):134–140, 2015

https://t.me/med1917

240 Laboratory Medicine in Psychiatry and Behavioral Science

Sodium

Type of test Blood

Background and explanation

of test

Sodium is the most abundant positively charged ion in the

blood and has critical roles in neurotransmission, mainte

nance of osmotic pressure, and maintenance of acid-base bal-

ance. The sodium level reflects dietary intake less renal

excretion, and a normal level is maintained through the ac

tions of several hormones: aldosterone, which decreases re-

nal sodium loss, natriuretic hormone, which increases renal

sodium loss, and antidiuretic hormone (ADH), which in

creases resorption of water. As free body water increases or

decreases, these hormones stimulate the kidney to compen

sate to restore sodium balance. In clinical practice, sodium

levels are obtained to evaluate electrolytes, acid-base bal

ance, water balance, water intoxication, and dehydration.

Relevance to psychiatry and

behavioral science

Serum sodium abnormalities are found in several conditions

seen in psychiatric practice, including polydipsia, lithium-

induced diabetes insipidus, SIAD, beer potomania, and hy

popituitarism. Drugs of abuse (e.g., amphetamines, Ecstasy,

bath salts) can cause a life-threatening hyponatremia from

increased ADH secretion, diaphoresis, and polydipsia. Psy

chotropic drugs associated with sodium derangements in-

clude antidepressants (e.g., SSRIs, TCAs), second-generation

antipsychotics (e.g., aripiprazole, clozapine, olanzapine,

risperidone, ziprasidone), carbamazepine, oxcarbazepine,

lithium, phenothiazines, and opioids. Geriatric practitioners

should be aware that age is a significant risk factor for hypo-

natremia, which is often associated with medications, SIAD,

or endocrinopathy.

Preparation of patient None needed

Indications • Standard component of metabolic panels (BMP and

CMP) and element of electrolyte panel

• Admission workup and evaluation of delirium, seizure,

and SIAD

• Evaluating and monitoring electrolyte and acid-base

disturbances, dehydration, and fluid overload

• Evaluating and monitoring medication-induced effects

Reference range ≤90 years: 136–145 mEq/L

>90 years: 132–146 mEq/L

Critical value(s) < 120 mEq/L or >160 mEq/L

Increased levels • Dehydration with inadequate water intake

• Excessive free water loss: excessive sweating, extensive

thermal burns, diabetes insipidus, osmotic diuresis

• Increased sodium intake in IV fluids (isotonic saline)

• Decreased sodium loss: hyperaldosteronism (Cushing’s

syndrome, Conn’s syndrome)

• Tracheobronchitis

https://t.me/med1917

241 Laboratory Tests

Sodium (continued)

Decreased levels • Water intoxication, psychogenic polydipsia

• SIAD

• Treatment with thiazide diuretics and other drugs listed

above

• Third-space loss of sodium: ascites, peripheral edema,

pleural effusion, loss through bowel lumen in ileus or

obstruction

• Increased free body water: excessive sodium-free oral,

IV, or irrigant administration

• Congestive heart failure

• Increased sodium loss: Addison’s disease, diarrhea,

vomiting, sweating, burns, nasogastric suction, diuretic

therapy, chronic renal insufficiency

• Hyperlipidemia

• Sodium-deficient diet

• Hypothyroidism

• Hyperglycemia: sodium decreases by 1.5–3.0 mEq/L for

each 100 mg/dL increase in blood glucose

Interfering factors Recent trauma, shock, or surgery can affect sodium values.

A spurious reduction of sodium (pseudohyponatremia) can

occur with certain assays in the presence of hyperprotein-

emia and hyperlipidemia due to decreased water content.

Numerous non-psychotropic drugs affect sodium levels.

Cross-references Diabetes Insipidus

Hypernatremia

Hyponatremia

Psychogenic Polydipsia

Syndrome of Inappropriate Antidiuresis

Adrogue HJ, Madias NE: Hyponatremia. N Engl J Med 342:1581–1589, 2000

Ali SN, Bazzano LA. Hyponatremia in association with second-generation antipsychotics: a systematic

review of case reports. Ochsner J 18(3):230–235, 2018

Faria AC, Carmo H, Carvalho F, et al: Drinking to death: hyponatraemia induced by synthetic phenethyl-

amines. Drug Alcohol Depend 212:108045, 2020

Filippatos TD, Makri A, Elisaf MS, Liamis G: Hyponatremia in the elderly: challenges and solutions.Clin

Interv Aging 12:1957–1965, 2017

Lien YH, Shapiro JI: Hyponatremia: clinical diagnosis and management. Am J Med 120:653–658, 2007

Liu BA, Mittmann N, Knowles SR, et al: Hyponatremia and the syndrome of inappropriate secretion of

antidiuretic hormone associated with the use of selective serotonin reuptake inhibitors: a review of

spontaneous reports. CMAJ 155:519–527, 1996

Reynolds RM, Padfield PL, Seckl JR: Disorders of sodium balance. BMJ 332:702–705, 2006

https://t.me/med1917

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