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392 Laboratory Medicine in Psychiatry and Behavioral Science
Drug abuse (continued)
Clinical findings Withdrawal symptoms include yawning, lacrimation, diaphoresis, rhi-
(continued) norrhea, dysphoria, irritability, insomnia, nausea, vomiting, diarrhea,
abdominal cramping, piloerection (“gooseflesh”), intense muscle and
bone pain, myoclonus, mydriasis, tachycardia, and hypertension. Med
-
ical complications are numerous with long-standing abuse.
Sedative-hypnotics
Symptoms of mild to moderate intoxication include euphoria, emo-
tional lability, impaired judgment, impulsivity, slowed reaction time,
drowsiness, lethargy, dysarthria, nystagmus, incoordination, ataxia,
and blackouts. With more severe
intoxication, particularly with alcohol
co-ingestion, stupor, coma, respiratory depression, and death may
occur.
Withdrawal symptoms include anxiety, irritability, tachycardia, hyper-
tension, tremor, diaphoresis, subjective weakness, nausea and vomit-
ing, insomnia, and seizures. With prolonged high-dose use, withdrawal
delirium may be seen, with fever, visual and tactile hallucinations, de
-
lusions, catatonia, and severe agitation. Other complications of sedative
abuse include falls with fracture and motor vehicle accidents.
Laboratory testing See Urine Drug Screen in the Laboratory Tests chapter for detailed
information about
testing.
Screening for drug use first involves an immunoassay, which is inex-
pensive and available at the point of care but provides only qualitative
information and is subject to false-positive and false-negative results. A
positive result is considered provisional until confirmed in the labora-
tory by methods such as gas or liquid chromatography–tandem mass
spectrometry.
The most common means of tampering with urine drug specimens in
the workplace and forensic settings is dilution of the sample. Validity
checks performed in the laboratory—including measurement of urine
creatinine and specific gravity—can determine whether dilution has oc-
curred. Urine pH and other assays can be used to determine whether
the specimen has been adulterated. False-positives on urine drug test-
ing in a c
ommercial laboratory do not result from eating poppy seeds
(for opiates) or passive smoke inhalation (for cannabis).
When opioids are prescribed long-term for pain syndromes, misuse can
be flagged by aberrant behaviors such as lost prescriptions, repeated
requests for early refills, or unauthorized dose escalations. Although
prescription drug monitoring programs help considerably with misuse
issues, frequent drug testing may be needed based on risk level. Testing
is recommended every 1–3 months for patients at high risk because of
a known substance abuse problem, mental health condition, aberrant
behaviors, or use of high opioid dosage (>120 morphine mg equiva-
lent). For patients without such risk factors, testing may be scheduled
every 6–12 months.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Dadiomov D: Laboratory testing for substance use disorders, in Absolute Addiction Psychiatry Review.
Edited by Marienfeld C. Cham, Switzerland, Springer, 2020
Lin SY, Lee HH, Lee JF, Chen BH: Urine specimen validity test for drug abuse testing in workplace and
court settings. J Food Drug Anal 26(1):380–384, 2018
Moeller KE, Kissack JC, Atayee RS, Lee KC: Clinical interpretation of urine drug tests: what clinicians
need to know about urine drug screens. Mayo Clin Proc 92(5):774–796, 2017
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393 Diseases and Conditions
Drug abuse (continued)
Niles JK, Gudin J, Radcliff J, Kaufman HW: The opioid epidemic within the COVID-19 pandemic: drug
testing in 2020.Popul Health Manag 24(S1):S43–S51, 2021
Sazegar P: Cannabis essentials: tools for clinical practice.Am Fam Physician 104(6):598–608, 2021
Vogel EA, Chieng A, Robinson A, et al: Associations between substance use problems and stress during
COVID-19. J Stud Alcohol Drugs 82(6):776–781, 2021
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394 Laboratory Medicine in Psychiatry and Behavioral Science
Drug-induced liver injury (DILI)
Clinical findings Prescribed and over-the-counter drugs, herbal drugs, and dietary sup-
plements are all known to have adverse effects on the liver, with
asymptomatic elevation of liver enzymes being the most common
manifestation and liver failure resulting in either transplant or death
being the most serious. DILI is the most frequent cause of acute liver
failure in the United States and other developed countries.
Liver effects can be intrinsic to the drug, as with acetaminophen; these
effects are dose-related and predictable and usually occur early, within
1–5 days. Idiosyncratic reactions, on the other hand, occur unpredict
-
ably with a wide range of drugs at therapeutic as well as toxic drug
levels. Usual onset of idiosyncratic reactions is in 5–90 days (sooner
with prior drug exposure). DILI comprises both intrinsic and idiosyn
-
cratic forms. The patterns of liver involvement in DILI can be hepato-
cellular, cholestatic, or mixed.
The class of drugs most often implicated in DILI is the antibiotics,
although herbal drugs and dietary supplements are increasingly
recognized as causative. Of psychotropic drugs, all classes of anti
-
depressants, many antipsychotics, several mood stabilizers/anticon-
vulsants, and other drugs are implicated. Among the antidepressants,
fatal hepatotoxicity has been reported with nefazodone, trazodone,
duloxetine, bupropion, and sertraline. SSRI antidepressants have the
least potential toxicity. Among the antipsychotics, clozapine and
olanzapine are associated with the most severe hepatotoxicity. The
National Library of Medicine maintains an online database known as
LiverTox (available at
www.ncbi.nlm.nih.gov/books/NBK547852)
that provides information on liver injury with reference to specific
drugs.
Known risk factors for DILI include older age, female sex, and race,
with Asians at greater risk than Blacks, who are at greater risk than
Whites. It is still controversial as to whether preexisting liver disease
is a risk factor, but regular alcohol use and chronic hepatitis are noted
as factors in some studies. In the United States, DILI presents with
jaundice in 70% of cases. Most patients recover with drug discon-
tinuation, but 17% develop chronic DILI and 10% require transplant
and/or die from the disease.
DILI should be suspected in any patient with a new elevation of liver
enzymes. All drugs consumed in the prior 3 months should be
reviewed, including herbals, over-the-counter drugs, and time-limited
drugs that have run their course. The temporal association of symp-
toms with the use of the suspected drug(s) should be confirmed.
Additional information can be inferred from the improvement seen
with drug discontinuation. A positive response to corticosteroids and
recurrence when steroids are withdrawn help to diagnose autoim-
mune hepatitis rather than DILI. Liver enzymes usually fall within
days to weeks, with <10% of patients developing chronic disease.
Laboratory testing • The most useful tests in the diagnosis and monitoring of DILI are
ALT, AST, ALP, and total bilirubin.
• At the initial visit, classify liver injury by calculating the R value
(ALT divided by ALP). If the R value is ≥5, the pattern is hepato-
cellular. If the R value is ≤2, the pattern is cholestatic. If the R value
is <5 and >2, the pattern is mixed.
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395 Diseases and Conditions
Drug-induced liver injury (DILI) (continued)
Laboratory testing
(continued)
• A hepatocellular pattern can also be identified by an isolated ele-
vation of ALT ≥5 times the upper limit of normal (ULN).
• A cholestatic pattern can also be identified by an isolated elevation
of ALP ≥2 times the ULN.
• If AST or ALT is >3 times the ULN, ALP is normal on initial testing,
and patient is jaundiced, the mortality rate is 10%.
• In hepatocellular DILI, a serum bilirubin ≥ 3 times the ULN in the
absence of biliary obstruction or Gilbert’s syndrome carries a 5%–
50% mortality rate.
• Further testing for patients with the hepatocellular pattern in-
cludes hepatitis C virus RNA and IgM anti–hepatitis E virus in ad-
dition to hepatitis A virus and hepatitis B virus and autoimmune
serology.
• Further testing for patients with the cholestatic or mixed pattern
includes ultrasound and cholangiography.
• Tests used to distinguish DILI from autoimmune hepatitis include
antibodies (e.g., antinuclear antibody testing) for autoimmune
hepatitis and HLA genotyping for DILI.
• Although liver imaging in DILI typically is normal, abdominal ul-
trasound is recommended to exclude biliary obstruction and any
focal liver abnormalities.
• Elastography may be used to exclude other causes of liver disease
such as fatty liver disease.
• Liver biopsy may be needed in exceptional cases.
Chalasani NP, Maddur H, Russo MW, et al: ACG clinical guideline: diagnosis and management of idio-
syncratic drug-induced liver injury.Am J Gastroenterol 116(5):878–898, 2021
Dias CL, Fonseca L, Gadelha A, Noto C: Clozapine-induced hepatotoxicity: a life threatening situa-
tion.Schizophr Res 235:3–4, 2021
Druschky K, Toto S, Bleich S, et al: Severe drug-induced liver injury in patients under treatment with an-
tipsychotic drugs: data from the AMSP study. World J Biol Psychiatry 22(5):373–386, 2021
European Association for the Study of the Liver: EASL clinical practice guidelines: drug-induced liver
injury. J Hepatol 70(6):1222–1261, 2019
Katarey D, Verma S: Drug-induced liver injury. Clin Med (Lond) 16(Suppl 6):s104–s109, 2016
Kumachev A, Wu PE: Drug-induced liver injury. CMAJ 193(9):E310, 2021
Lee BT, Odin JA, Grewal P: An approach to drug-induced liver injury from the geriatric perspective.Curr
Gastroenterol Rep 23(4):6, 2021
McGill MR, Jaeschke H: Biomarkers of drug-induced liver injury. Adv Pharmacol 85:221–239, 2019
National Library of Medicine: National Center for Biotechnology Information: LiverTox. Available at:
https://www.ncbi.nlm.nih.gov/books/NBK547852. Accessed April 2022.
Nikogosyan G, Orias D, Goebert D, et al: Acute aripiprazole-associated liver injury.J Clin Psychophar-
macol 41(3):344–346, 2021
Park SH, Ishino R: Liver injury associated with antidepressants.Curr Drug Saf 8(3):207–223, 2013
Voican CS, Corruble E, Naveau S, Perlemuter G: Antidepressant-induced liver injury: a review for clini-
cians. Am J Psychiatry 171(4):404–415, 2014
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396 Laboratory Medicine in Psychiatry and Behavioral Science
Dysphagia
Clinical findings Swallowing is a complex motor function involving nuclei of the brain-
stem, cranial nerves, striated muscles of the tongue, and smooth muscles
of the pharynx and esophagus. The three phases of swallowing—oral,
pharyngeal, and esophageal—must be coordinated for efficient swal-
lowing to occur. The workup of dysphagia is performed to distinguish
oropharyngeal from esophageal origins.
Oropharyngeal dysphagia is characterized by difficulty initiating
swallowing, with coughing and choking and risk of aspiration. This
type of dysphagia is most often associated with neurogenic causes in
-
cluding stroke, dementia, and Parkinson’s disease. Esophageal dys-
phagia is characterized by the subjective report that food feels “stuck”
in the chest, pain with swallowing (odynophagia), regurgitation of
food, wheezing, hoarseness, drooling, coughing, and choking. This
type of dysphagia is most often associated with gastroesophageal re
-
flux disease and functional esophageal disorders. Chronic opioid use
can also cause this type of dysphagia. Dysphagia for solid food indi
-
cates mechanical obstruction at the level of
the esophagus or the base
of
the tongue. Dysphagia for liquids indicates neurogenic dysphagia,
but this type can progress to include dysphagia for solid food.
Bedside evaluation for dysphagia includes a cranial nerve exam and
auscultation of the lungs. An informal first-pass water test can be per
-
formed in which 50 mL of water is swallowed in 5-mL aliquots. With
this test, oropharyngeal symptoms may become immediately apparent.
An evaluation by a speech-language pathologist could then provide
sufficient information to determine which of several instrumented tests
might be indicated.
Laboratory testing Commonly used instrumented tests for dysphagia include the modi-
fied barium swallow (MBS) and fiberoptic endoscopic evaluation of
swallowing (FEES). High-resolution manometry is used to evaluate
the function of pharyngeal muscles and the upper esophageal sphinc
-
ter in patients with suspected oropharyngeal dysphagia. Upper GI en-
doscopy is the first test used for patients with suspected esophageal
dysphagia. Manometry can also be used to evaluate the competence of
the lower esophageal sphincter in these patients.
Babaei A, Szabo A, Shad S, Massey BT: Chronic daily opioid exposure is associated with dysphagia, esoph-
ageal outflow obstruction, and disordered peristalsis. Neurogastroenterol Motil 31(7):e13601, 2019
Jones CA, Colletti CM, Ding MC: Post-stroke dysphagia: recent insights and unanswered questions.Curr
Neurol Neurosci Rep 20(12):61, 2020
Rommel N, Hamdy S: Oropharyngeal dysphagia: manifestations and diagnosis.Nat Rev Gastroenterol
Hepatol 13(1):49–59, 2016
Suttrup I, Warnecke T: Dysphagia in Parkinson’s disease.Dysphagia 31(1):24–32, 2016
Wilkinson JM, Codipilly DC, Wilfahrt RP: Dysphagia: evaluation and collaborative management.Am
Fam Physician 103(2):97–106, 2021
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397 Diseases and Conditions
Encephalitis, viral
Clinical findings Encephalitis refers to brain inflammation caused by infection or auto-
immunity with consequent neurological dysfunction. The clinical di-
agnosis requires the presence of altered mental status (decreased level
of consciousness, lethargy, or personality change) for ≥ 24 hours with
-
out an identified alternative cause, in conjunction with two or more of
the following criteria:
• Fever ≥ 100.4°F within the 72 hours before or after presentation
• Seizures (generalized or partial) not explained by a preexisting sei-
zure disorder
• New focal neurological signs (e.g., aphasia, ataxia, cranial nerve
palsies)
•CSF WBC count ≥ 5/mm
3
• Neuroimaging evidence of an abnormality of brain parenchyma
(new or acute)
• EEG abnormalities consistent with encephalitis and not attribut-
able to another cause
Meningitis commonly accompanies encephalitis, with additional
symptoms including nuchal rigidity, vomiting, and photophobia. Psy-
chotic symptoms (e.g., hallucinations and agitation) can be seen with
the mental status alterations of encephalitis, which is consistent with a
delirium syndrome. Dysregulation of the HPA axis can lead to diabetes
insipidus, SIAD, and other problems.
In half of encephalitis cases, no cause is identified. Of the identified
causes, viruses are the most commonly implicated. In the United
States, most cases of viral encephalitis are caused by herpes simplex
virus (HSV) type 1 or 2, varicella zoster virus, enteroviruses, or arbo
-
viruses transmitted from infected animals to humans by tick or mos-
quito bites. Rabies is a very rare cause of encephalitis in humans.
Because HSV is the most common cause of sporadic fatal encephalitis
in the Western world, the first step in the differential diagnosis is to
distinguish HSV from other viral causes. This is done by laboratory
testing, as discussed below. Clinical features favoring HSV include
older age, acute presentation, fever, and GI symptoms. HSV encepha-
litis occurs across the age spectrum and lacks a seasonal or geograph-
ical pattern.
Enterovirus-related encephalitis occurs sporadically or in outbreaks
that typically occur during the summer months. Presenting symptoms
include diarrhea, vomiting, and viral exanthems such as herpangina
and hand-foot-and-mouth disease.
Arthropod-borne viruses—arboviruses—causing encephalitis in hu-
mans in North America include the mosquito-borne eastern equine,
western equine, Venezuelan equine, Chikungunya, Jamestown, Cali-
fornia, St. Louis, La Crosse, and West Nile viruses, as well as the tick-
borne Powassan. Arbovirus encephalitis occurs seasonally, with the
incidence dependent on geographical region. Zika virus was once a
concern for pregnant females because of associated birth defects such
as microcephaly in offspring, but Zika has not been transmitted by
mosquitoes in the continental United States since 2018.
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398 Laboratory Medicine in Psychiatry and Behavioral Science
Encephalitis, viral (continued)
Laboratory testing In 2013, the International Encephalitis Consortium published guide-
lines for the laboratory workup of encephalitis in adults. Recommen-
dations for routine studies are as follows:
1. CSF:
• Collect ≥ 20 mL if possible and freeze ≥5–10 mL if possible
• Check opening pressure, WBC count with differential, RBC count,
protein, and glucose
• Gram stain and bacterial culture
• HSV 1/2 PCR (consider HSV CSF IgG and IgM also, if available)
• Varicella zoster virus (VZV) PCR (consider VZV IgG and IgM also
if available)
•Enterovirus PCR
• Cryptococcal antigen and/or India ink staining
• Oligoclonal bands and IgG index
• VDRL for syphilis
2. Serum:
• Blood cultures
• HIV serology (consider RNA)
• Treponemal testing (RPR, specific treponemal test)
• Hold acute serum and collect convalescent serum 10–14 days later
for paired antibody testing
3. Imaging:
• Brain imaging (MRI preferred to CT)
• Chest imaging (X-ray and/or CT)
4. Neurophysiology:
• EEG
Other tissues/fluids (e.g., stool culture, biopsy of skin lesions) are
tested if there is extra-CNS involvement.
Conditional studies are recommended based on host factors, geo-
graphical factors, season and exposure, and the presence of specific
signs and symptoms. See Venkatesan et al. (2013) reference cited below
for complete guidelines.
Kennedy PGE, Quan PL, Lipkin WI: Viral encephalitis of unknown cause: current perspective and recent
advances. Viruses 9(6):138, 2017
Tyler KL: Acute viral encephalitis.N Engl J Med 379(6):557–566, 2018
Venkatesan A, Tunkel AR, Bloch KC, et al: Case definitions, diagnostic algorithms, and priorities in en-
cephalitis: consensus statement of the International Encephalitis Consortium.Clin Infect Dis
57(8):1114–1128, 2013
Wright WF, Pinto CN, Palisoc K, Baghli S: Viral (aseptic) meningitis: a review. J Neurol Sci 398:176–183,
2019
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399 Diseases and Conditions
Ethylene glycol poisoning
Clinical findings
Laboratory testing
Ethylene glycol is an odorless, sweet-tasting substance that is found in
certain detergents, paints, de-icing products, brake fluid, and anti
-
freeze. It can be accidentally ingested by children, intentionally taken
in overdose, or abused as a substance in place of ethanol. The lethal
dose varies according to the dilution of ethylene glycol ingested,
whether alcohol is also ingested, whether vomiting occurs, and the
adequacy of renal excretion. Ingestion of as little as 4 fl oz of ethylene
glycol has been found to be fatal for an average-sized adult. Even so, if
the patient presents to the emergency room without delay and is rap
-
idly diagnosed and treated, a good outcome is possible even with a
large ingestion.
Three stages of ethylene glycol toxicity are recognized:
Stage 1: Predominately CNS manifestations (30 minutes–12 hours after
ingestion)
In this stage, the patient may report epigastric pain and nausea, and
soon appears to be inebriated. Symptoms such as lethargy, weakness,
incoordination, slurred speech, dizziness, headache, euphoria, or un
-
usual behavior may be observed. These effects are caused by unmetab-
olized ethylene glycol in the circulation. Over time, CNS symptoms can
worsen to include seizures (status epilepticus), myoclonus, stupor,
coma, cranial nerve deficits, quadriplegia, and brain death.
Stage 2: Cardiopulmonary manifestations (12–24 hours after ingestion)
As ethylene glycol is metabolized to its toxic metabolites, cardiopulmo-
nary failure can develop. Rapid deep breathing is often seen, a compen-
sation for the developing metabolic acidosis. CNS depression may be
extreme, such that airway protection by intubation is required. Pulmo
-
nary edema and respiratory failure may occur. Heart rate and blood
pressure abnormalities as well as congestive heart failure can develop.
These effects are caused by direct effects of toxic metabolites or by
deposition of oxalate crystals in the cardiovascular and pulmonary sys
-
tems. This is the stage at which death occurs in fatal cases.
Stage 3: Renal manifestations (24–72 hours after ingestion)
Patients who survive the first two stages often develop acute renal fail-
ure, which can be oliguric, anuric, or non-oliguric. Microscopic or gross
hematuria can be seen, and hemodialysis may be indicated. These ef
-
fects are caused by obstructive nephropathy or acute tubular necrosis
(ATN) due to calcium oxalate, ATN due to other causes, direct toxicity
of ethylene glycol metabolites, focal hemorrhagic cortical necrosis, and
interstitial nephritis.
A fourth stage of delayed-onset neuropathy develops in some patients,
with cranial nerve deficits that are most marked in the facial and audi
-
tory nerves, gait problems, dysmetria, ankle clonus, extensor plantar
reflexes, and an ascending motor/sensory neuropathy.
An ethylene glycol level >20 mg/dL confirms toxicity, but the turn-
around time for test is usually 1–4 days.
Classic laboratory abnormalities in ethylene glycol poisoning include
metabolic acidosis, increased anion gap, and increased osmolar gap,
but specific findings depend on time of blood draw.
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400 Laboratory Medicine in Psychiatry and Behavioral Science
Ethylene glycol poisoning (continued)
Laboratory testing
(continued)
Ethylene glycol itself has low molecular weight and little intrinsic tox-
icity such that large molar concentrations can develop in the circulation
in the hours immediately after ingestion. Initially, plasma osmolality
increases in proportion to its concentration. At this stage, an increased
osmolar gap with a normal anion gap and the absence of metabolic ac-
idosis would be found. Subsequently, the osmolar gap returns to nor-
mal as metabolic acidosis progresses and the anion gap increases,
indicating the presence of toxic metabolites.
Other laboratory findings that may assist in the diagnosis of toxicity
include falsely elevated lactate levels and calcium oxalate monohydrate
crystals in urine. In addition, hypocalcemia and thrombocytopenia can
be seen. If antifreeze ingestion is suspected, urine could be subjected to
ultraviolet illumination to see if it fluoresces; this is due to the presence
of sodium fluorescein being added to antifreeze formulations, presum-
ably to help identify automotive fluid leaks.
Brain imaging abnormalities in ethylene glycol poisoning involve the
basal ganglia, thalamus, brainstem, and white matter. In stage 1, diffuse
cerebral edema is seen, and subsequently on CT scan hypodensities are
noted in the basal ganglia, thalamus, and brainstem. MRI is more sen-
sitive to these changes, showing hyperintensities on T2-weighted im-
ages in these same areas as well as the amygdala and hippocampus.
Restricted diffusion in deep white matter is consistent with cytotoxic
edema.
ARUP Laboratories: Ethylene glycol, in Laboratory Test Directory. Salt Lake City, UT, ARUP Laborato-
ries, 2021. Available at:
https://www.aruplab.com/Tests/Pub/0090110. Accessed June 2021.
Esumi R, Suzuki K, Ishikura K, Imai H: Challenges in diagnosing comatose patients with ethylene glycol
poisoning. Am J Med 134(2):e127–e128, 2021
Malhotra A, Mongelluzzo G, Wu X, et al: Ethylene glycol toxicity: MRI brain findings.Clin Neuroradiol
27(1):109–113, 2017
Poirier-Blanchette L, Simard C, Schwartz BC: Spurious point-of-care lactate elevation in ethylene glycol
intoxication: rediscovering a clinical pearl.BMJ Case Rep 14(2):e239936, 2021
Sheta HM, Al-Najami I, Christensen HD, Madsen JS: Rapid diagnosis of ethylene glycol poisoning by
urine microscopy. Am J Case Rep 19:689–693, 2018
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401 Diseases and Conditions
Fatty liver disease
Clinical findings
Laboratory testing
Two types of fatty liver disease are recognized: alcoholic fatty liver
disease and non-alcoholic fatty liver disease (NAFLD; also known as
metabolic-associated fatty liver disease). Alcoholic fatty liver disease
develops in heavy alcohol users because the metabolism of alcohol
generates intermediates such as acetaldehyde that are injurious to liver
cells. Without intervention, alcoholic fatty liver disease is likely to
progress to hepatitis and cirrhosis.
NAFLD refers to the accumulation of fat in liver cells among patients
with risk factors for the metabolic syndrome and insulin resistance, in
-
cluding obesity, type 2 diabetes, hypertension, and hyperlipidemia.
This type of fatty liver disease can also progress to steatohepatitis (non
-
alcoholic steatohepatitis, or NASH), with inflammation and liver cell
injury leading to fibrosis, cirrhosis, and cancer. NAFLD has become a
major public health problem in the United States, with almost 25% of
adults affected.
Most cases of fatty liver disease are clinically silent until later stages.
Early symptoms are nonspecific and include only fatigue and right
upper quadrant discomfort. Alcoholic fatty liver disease might be
suspected based on history or physical exam findings such as labile
hypertension. NAFLD might be suspected because features of the met-
abolic syndrome are present. Detection of fatty liver often involves the
finding of elevated liver enzymes on routine blood testing, and diag-
nosis of fatty liver requires further laboratory studies as discussed
below.
Tests used to diagnose fatty liver disease include LFTs, abdominal im-
aging, and elastography. In NAFLD, mild elevation in AST and ALT is
seen in conjunction with GGT up to 3 times the upper limit of normal.
In alcoholic liver disease, AST elevation is greater than ALT elevation
in a ratio of more than 2:1. Abdominal imaging—ultrasound, CT, and
MRI—yields information about liver anatomy, including fatty content
and nodularity.
Elastography is a noninvasive testing method that measures liver
stiffness through the abdominal wall using ultrasound (vibration-
controlled transient elastography, or VCTE) or MRI (magnetic reso-
nance elastography, or MRE). These techniques are useful for patients
with either minimal or advanced fibrotic disease.
Estimation of degree of fibrosis can be obtained noninvasively using
published formulas based on results of blood tests. The Fibrosis-4
Index for Liver Fibrosis usesAST, ALT, platelet count, and age, whereas
the Non-Alcoholic Fatty Liver Disease Fibrosis Score uses AST, ALT,
platelet count, albumin, abnormal fasting glucose, BMI, and age. Both
instruments are
accessible at www.mdcalc.com. Another formula for
predicting moderate fibrosis and cirrhosis is the Enhanced Liver Fibro-
sis Score, obtained from measured values of tissue inhibitor of metal-
loproteinase-1 (TIMP-1), amino-terminal propeptide of type III
procollagen (PIIINP), and hyaluronic acid (HA). These formulas can be
used in combination to determine the presence of advanced fibrosis,
which is associated with hepatic decompensation including ascites,
variceal bleeding, and encephalopathy, as well as hepatocellular car-
cinoma.
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