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332 Laboratory Medicine in Psychiatry and Behavioral Science
Alcohol use disorder (AUD)
Clinical findings The patient and/or informant reports a pattern of excessive drinking:
• For males, 4+ drinks daily or 15 drinks weekly
• For females and older males: 3+ drinks daily or 8 drinks weekly
• For pregnant individuals: any drinking
• Binge drinking: 5+ drinks for males and 4+ drinks for females
within 2 hours
A patient may admit to wanting to stop drinking but being unable to
do so. They are secretive about drinking and engage in risky behaviors,
such as drunk driving. The patient and/or informant reports problems
in relationships, at school, or at work because of the patient’s drinking,
and the patient may have become dangerous or violent while drunk.
They may be in denial about the seriousness of the problem. The patient
may have a history of alcohol withdrawal when drinking was stopped,
with symptoms ranging from mild shaking and anxiety to delirium tre-
mens, with fever , unstable vital signs, and confusion.
On examination, patients may be in a disheveled and agitated state
with unstable vital signs or may have a normal appearance. Alcohol on
the breath may be covered up by mouthwash or aftershave. In a long
-
time heavy drinker, examination may reveal tremor, slurring of speech,
hyperactive deep tendon reflexes, incoordination, gait instability, mus-
cle wasting, peripheral neuropathy, or cognitive impairment affecting
memory and executive functions. With the onset of liver disease, fetor
hepaticus, asterixis, gynecomastia, hepatosplenomegaly, ascites, testic
-
ular atrophy, and skin changes become prominent. The latter include
jaundice, spider telangiectasia, palmar erythema, caput medusa, ecchy
-
moses, nail changes such as clubbing, hyperpigmentation, porphyria
cutanea tarda, exacerbation of rosacea (with rhinophyma), psoriasis,
seborrhea, skin infections, and excoriation due to pruritus.
Laboratory testing Laboratory abnormalities supporting a diagnosis of AUD suspected on
clinical grounds include the following:
• Elevated GGT (> 47 U/L in males or >25 U/L in females) consistent with
4+ drinks daily for 4 weeks or more. It takes 2–3 weeks of abstinence
to normalize the GGT level. Elevation of GGT has high sensitivity
for liver disease but low specificity in the evaluation of etiology.
Specificity improves through patient selection; although GGT as
-
say would have little use in screening for alcoholic liver disease, it
would be highly useful in confirming recent drinking in a chronic
drinker who is in treatment and is supposedly abstinent. In males,
GGT is used alone for this indication. In females, it is best used in
tandem with CDT. Specificity also improves when elevated GGT is
found in combination with an AST-to-ALT ratio >2, which is con-
sistent with alcoholic liver disease.
• Elevated CDT
≥
2.6%. Test is positive in people drinking 50–80 g of
ethanol daily for a minimum of several weeks. In general, the spec-
ificity of the test is high (97%), but the sensitivity is variable (65%–
95%). Sensitivity can be improved without loss of specificity when
GGT is measured in conjunction with CDT because the combined
test is positive in people drinking ≥40 g of ethanol daily. With 2–
4 weeks of abstinence, CDT value normalizes.
• Ratio of AST to ALT >2:1
• Elevated MCV (>101 fL, although age- and sex-dependent)
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333 Diseases and Conditions
Alcohol use disorder (AUD) (continued)
Laboratory testing
(continued)
• Elevated uric acid level (≥7 mg/dL, although this is age- and sex-
dependent).
• Elevated total homocysteine level (> 15 μmol/L).
• Elevated phosphatidylethanol (PEth). This refers to a group of
phospholipids formed in the presence of ethanol and incorporated
into membranes of RBCs. PEth has a half-life of 4–10 days and a
window of detection of 2–4 weeks (longer in chronic, heavy drink-
ers). Serial PEth testing is useful in monitoring abstinence in known
drinkers over time. Although a reference range is not yet estab-
lished, a level >20 ng/mL is considered evidence of moderate to
heavy drinking. False elevations can be seen in patients with ad
-
vanced liver disease.
Recent drinking can be confirmed using breath analysis, saliva ethanol,
urine ethanol, or blood alcohol level (BAL). Urine ethylglucuronide
could also be measured; this metabolite of ethanol remains positive in
urine for 2–3 days, longer than ethanol itself. GGT and/or CDT can
often be useful, as noted above.
In patients with known alcohol dependence or abuse, the BAL can be
useful in diagnosing intoxication or withdrawal (the latter when BAL
is zero in the presence of relevant signs and symptoms). Other common
blood lab abnormalities in patients with AUD include hypomagnese-
mia, hypophosphatemia, hypoglycemia, anemia, thrombocytopenia,
and hypoprothrombinemia.
In patients with alcohol-related dementia, CT or MRI may show gener-
alized atrophy (both cortical and central atrophy, the latter evidenced
by ventricular enlargement). Atrophy may decrease to some extent
with abstinence. In patients with cerebellar signs, CT or MRI may show
atrophy of cerebellar cortex, most often in the anterior and superior seg-
ments of the vermis. Radiologists should be alerted to clinical findings
suggestive of cerebellar involvement.
Clinical diagnosis of alcohol-related polyneuropathy can be confirmed
by EMG, with single-fiber study complementing conventional needle
EMG. In acute alcoholic myopathy, AST and creatine kinase can be ele
-
vated in the presence of painful muscle weakness. Chronic alcohol-
related myopathy, which is progressive with continued drinking, can
be diagnosed by EMG or NCT. Patients with recurrent seizures or who
are “found down” may develop rhabdomyolysis with myoglobinuria
and acute renal failure.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Andresen-Streichert H, Müller A, Glahn A, et al: Alcohol biomarkers in clinical and forensic con-
texts. Dtsch Arztebl Int 115(18):309–315, 2018
Brust JC: A 74-year-old man with memory loss and neuropathy who enjoys alcoholic beverages. JAMA
299:1046–1054, 2008
Chrostek L, Cylwik B, Szmitkowski M, et al: The diagnostic accuracy of carbohydrate-deficient transfer-
rin, sialic acid and commonly used markers of alcohol abuse during abstinence. Clin Chim Acta
364:167–171, 2006
Helander A, Böttcher M, Dahmen N, Beck O: Elimination characteristics of the alcohol biomarker phos-
phatidylethanol (PEth) in blood during alcohol detoxification.Alcohol Alcohol 54(3):251–257, 2019
Neumann J, Beck O, Helander A, Böttcher M: Performance of PEth compared with other alcohol biomark-
ers in subjects presenting for occupational and pre-employment medical examination.Alcohol Alco-
hol 55(4):401–408, 2020
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334 Laboratory Medicine in Psychiatry and Behavioral Science
Alcohol use disorder (AUD) (continued)
Nguyen VL, Haber PS, Seth D: Applications and challenges for the use of phosphatidylethanol testing in
liver disease patients (mini review).Alcohol Clin Exp Res 42(2):238–243, 2018
Rinck D, Frieling H, Freitag A, et al: Combinations of carbohydrate-deficient transferrin, mean corpuscu-
lar erythrocyte volume, gamma-glutamyltransferase, homocysteine and folate increase the signifi-
cance of biological markers in alcohol dependent patients. Drug Alcohol Depend 89:60–65, 2007
Sillanaukee P: Laboratory markers of alcohol abuse. Alcohol Alcohol 31:613–616, 1996
Ulwelling W, Smith K: The PEth blood test in the security environment: what it is; why it is important;
and interpretative guidelines. J Forensic Sci 63(6):1634–1640, 2018
https://t.me/med1917
335 Diseases and Conditions
Aluminum toxicity
Clinical findings Because aluminum is found everywhere in the environment, exposure
occurs naturally through ingestion of food, drinking water, or certain
over-the-counter drugs such as antacids; use of aluminum-containing
cookware; food packaging; cosmetics such as antiperspirants, sun
creams, and toothpaste; and some vaccines. Under normal circum
-
stances, these sources pose little health risk because only a small frac-
tion of aluminum is absorbed through the GI tract and skin. Thus,
although the tolerable weekly intake set by the European Food Safety
Authority of 1 mg of aluminum per kilogram of body weight can easily
be exceeded by food intake alone, this fact is of little clinical signifi-
cance; internal exposure measured by aluminum levels in the urine or
blood provides a better measure of toxicity.
Potentially toxic exposure to aluminum occurs in occupations such as
aluminum welding and processing. Historically, this level of exposure
was also found among renal dialysis patients treated with aluminum-
containing dialysis fluids, but this exposure has been mitigated since
the year 2000 by a change in dialysate constituents and is now rare.
Environmental exposure from industrial emissions, hazardous waste
sites, and contaminated well water still occurs. Worth noting is the fact
that reverse osmosis water filters remove almost 100% of aluminum
from drinking water. In addition, exposure from vaccine adjuvants is
minimal; aluminum levels in blood and urine from vaccinated patients
are the same as those from unvaccinated patients. COVID-19 vaccines
approved in the United States do not contain aluminum.
Neurotoxic effects of significant aluminum exposure were identified in
a cohort of dialysis patients studied before 2000. At the molecular
level, aluminum induces oxidative stress, modifies calcium signaling
pathways in the hippocampus, and reduces synthesis of acetylcholine.
Clinical symptoms include disorientation, memory impairment,
apraxia, speech impairment, seizures, and dementia. Neuropathologi
-
cal study shows neuronal loss and vascular changes, all of which are
minimal. Amyloid plaques and neurofibrillary tangles are not evident.
In those who survive, neurotoxic effects are at least partially reversed
with elimination of exposure.
With industrial exposure associated with toxic urine and blood levels,
neuropsychological changes in concentration, learning, and memory
have been found. In addition, industrial exposure to aluminum can
give rise to metal fume fever, a flu-like illness with headache, fever/
chills, myalgias, cough, chest tightness, and a metallic taste in the
mouth. Onset of this syndrome can be delayed for several hours, and
symptoms can last for 1–2 days. Chronic exposure to fine aluminum
dust can cause pulmonary fibrosis.
Elevated aluminum concentrations have been found in the brain tissue
of patients with Alzheimer’s disease (AD), autism spectrum disorder,
and epilepsy. This does not necessarily imply causation; aluminum has
a high affinity for proteins, which it is able to cross-link. Numerous
studies have failed to establish a connection between aluminum levels
and AD, and other potential disease links to aluminum have been less
well studied. One case of adult-onset epilepsy was reported from a
1988 water poisoning event in the Cornish town of Camelford, but in
that fatal case, both exposure and aluminum levels in the brain tissue
were extremely high.
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336 Laboratory Medicine in Psychiatry and Behavioral Science
Aluminum toxicity (continued)
Clinical findings A critical reading of the literature would suggest there is currently no
(continued) convincing evidence that aluminum accumulation causes AD. The spe-
cific encephalopathy caused by aluminum toxicity is distinct from AD.
Concern has also arisen in relation to aluminum exposure and breast
cancer. Although aluminum levels tend to be higher in cancerous tis
-
sue, the metal does not appear to trigger tumor formation but instead
is stored to a greater degree in cancerous tissue. More research is
needed to resolve remaining questions regarding metal exposure and
breast cancer.
Laboratory testing Aluminum is found in the blood (serum) and urine of all individuals.
The upper limit of normal (ULN) for the general population is <5 μg/L
in serum and <15 μg/L in urine. Some sources use <7 μg/L as the ULN
for urine. For routine screening and testing of dialysis patients using
phosphate binders, serum is the specimen of choice. For chronic expo-
sure and monitoring, urine is the specimen of choice. Elevated levels
should be confirmed on a second specimen because the sample is very
susceptible to environmental contamination during collection. In ad
-
dition, medications and nutritional supplements may interfere with
the test and should be discontinued if possible before sampling. With
occupational exposure, early changes found on neuropsychological
testing corresponded to serum aluminum levels of ≥13 μg/L and urine
levels of ≥120 μg/L. For aluminum workers, testing before employ
-
ment and annually thereafter is recommended.
ARUP Laboratories: Aluminum, serum, in Laboratory Test Directory. Salt Lake City, UT, ARUP Labora-
tories, 2021. Available at: https://ltd.aruplab.com/Tests/Pub/0099266. Accessed December 2021.
Goullé JP, Grangeot-Keros L: Aluminum and vaccines: Current state of knowledge.Med Mal Infect
50(1):16–21, 2020
Klotz K, Weistenhöfer W, Neff F, et al: The health effects of aluminum exposure.Dtsch Arztebl Int
114(39):653–659, 2017
Principi N, Esposito S: Aluminum in vaccines: does it create a safety problem?Vaccine 36(39):5825–5831,
2018
Schifman RB, Luevano DR: Aluminum toxicity: evaluation of 16-year trend among 14,919 patients and
45,480 results. Arch Pathol Lab Med 142(6):742–746, 2018
https://t.me/med1917
337 Diseases and Conditions
Alzheimer’s disease (AD)
Clinical findings AD is a neurodegenerative disorder with an insidious onset and gradual
progression from a preclinical stage, in which only neuropathological
abnormalities are identified, to late-stage dementia, in which the person
has lost the ability to function independently. Long before cognitive
symptoms are noticed, the affected individual may exhibit apat
hy,
changes in mood,
heightened anxiety,
or sleep problems. Although the
earliest cognitive changes
are commonly seen in day-to-day memory
functions (with distant memories preserved while recent memories are
lost), non-amnestic presentations with first symptoms in language,
visuospatial function, or executive functions are al
so recognized.
Criteria for the diagnosis of dementia formulated by the National Insti-
tute on Aging–Alzheimer’s Association (NIA-AA) include the following:
• The presence of cognitive or neuropsychiatric symptoms that inter-
fere with function, represent a decline, and are not explained by de-
lirium or major psychiatric disorder.
• Cognitive impairment detected through history and testing (bedside
mental status exam or neuropsychological testing).
• Impairment involving two or more of the following domains:
• Ability to acquire and remember new information
• Reasoning, handling of complex tasks, judgment
• Visuospatial abilities
• Language functions (speaking, reading, writing)
• Personality, behavior, comportment
Criteria for probable
AD formulated b
y the
NIA-AA include the
following:
• Meets the above criteria for dementia, with insidious onset and
gradual progression.
• Prominent cognitive deficits in one of the following domains along
with at least one other cognitive domain: memory, language, visuo-
spatial function, or executive function.
• No evidence of substantial cerebrovascular disease, core features of
dementia with Lewy bodies, prominent features of behavioral vari
-
ant FTD, prominent features of non-AD primary progressive apha-
sia, or another disease or medication that substantially affects
cognition.
Laboratory testing Standard laboratory testing for patients undergoing workup for demen-
tia includes the following blood tests: TSH, vitamin B
12
, homocysteine,
CBC with differential, CMP, ESR, and CRP. Abnormal findings in any of
these tests could reveal conditions that might contribute to cognitive
changes. In addition, brain MRI without gadolinium is performed to
evaluate atrophy, infarcts, white matter changes, microhemorrhages,
and conditions such as hydrocephalus or mass lesions. If MRI is not
available, noncontrast head CT is recommended. Atrophy in AD
involves the hippocampal areas and temporoparietal cortices.
Depending on patient demographics or other findings from history or
physical exam, further testing may be indicated, such as the following:
antinuclear antibody testing, HbA1c, lipid profile, folate, ammonia,
lead, Lyme antibodies, RPR, HIV, serum protein electrophoresis, MMA,
PT, and PTT. Chest X-ray or sleep study may be needed.
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338 Laboratory Medicine in Psychiatry and Behavioral Science
Alzheimer’s disease (AD) (continued)
Laboratory testing
(continued)
If the evaluation is inconclusive as to the cause of dementia or the pre-
sentation is atypical, early onset, or rapidly progressive, more compre-
hensive testing may be needed. This would include blood tests for
TPOAb, antithyroglobulin antibodies, and apoliprotein E testing. CSF
would be tested for AD biomarkers (low amyloid-β
42
, elevated tau,
elevated phospho-tau, and amyloid-tau index <1). Some labs might
now test for soluble triggering receptor expressed on myeloid cells 2
(TREM2) in CSF, which is a proxy of microglial activity and associated
with the rate of AD progression. FDG-PET or SPECT imaging showing
bilateral temporoparietal hypometabolism would be helpful in sup-
porting an AD diagnosis and distinguishing AD from frontotemporal
degeneration. Amyloid and tau PET imaging showing excessive and
widespread binding would also increase diagnostic certainty.
Familial autosomal dominant AD is a rare, early onset (before age
65 years) condition caused by mutations in the amyloid precursor pro-
tein, presenilin 1, or presenilin 2 genes. In cases in which these muta-
tions have been inherited, AD is certain to develop. Much more
common is sporadic, late-onset AD, for which scores of susceptibility
genes have been recognized. The most important genetic risk for late-
onset disease is the ε4 allele of APOE, which is strongly associated with
accelerated amyloid-β deposition in the brain and a higher risk of de
-
veloping AD.
Altuna-Azkargorta M, Mendioroz-Iriarte M: Blood biomarkers in Alzheimer’s disease.Neurologia (Engl
Ed) 36(9):704–710, 2021
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Atri A: The Alzheimer’s disease clinical spectrum: diagnosis and management.Med Clin North Am
103(2):263–293, 2019
de Leon MJ, DeSanti S, Zinkowski R, et al: MRI and CSF studies in the early diagnosis of Alzheimer’s
disease. J Intern Med 256:205–223, 2004
Edwin TH, Henjum K, Nilsson LNG, et al: A high cerebrospinal fluid soluble TREM2 level is associated
with slow clinical progression of Alzheimer’s disease.Alzheimers Dement (Amst) 12(1):e12128, 2020
McKhann GM, Knopman DS, Chertkow H, et al: The diagnosis of dementia due to Alzheimer’s disease:
recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on di
-
agnostic guidelines for Alzheimer’s disease.Alzheimers Dement 7(3):263–269, 2011
Waldemar G, Dubois B, Emre M, et al: Recommendations for the diagnosis and management of Alzheimer’s
disease and other disorders associated with dementia: EFNS guideline. Eur J Neurol 14:e1–e26, 2007
https://t.me/med1917
339 Diseases and Conditions
Anemia
Clinical findings Anemia refers to a deficiency of RBCs in the body, reflected by a low
hemoglobin level. It can arise acutely (e.g., with hemorrhage) or de
-
velop slowly (e.g., with chronic kidney disease). Three mechanisms
account for most cases: inadequate RBC production, blood loss, and
RBC destruction (hemolysis).
Iron deficiency is the most common cause of anemia. Chronic iron
deficiency anemia can be associated with symptoms such as burning
paresthesias of the tongue, smooth tongue, sores at the angles of the
mouth, spoon-shaped nails, and cognitive dysfunction. Of interest to
behavioral health professionals, these findings may occur in patients
with pica (i.e., ingestion of dirt, clay, or other substances). Other causes
of anemia include vitamin B
12
deficiency, folate deficiency, anemia
associated with inflammation, aplastic anemia, bone marrow disease
such as leukemia, hemolytic anemia, and sickle cell anemia. Psycho
-
tropic medications such as quetiapine have been associated with he-
molytic anemia.
The classic symptoms of anemia are fatigue, weakness, and pallor. A
robust association with depression has been noted. Sleep disorders are
often reported, including restless legs syndrome and periodic limb
movements of sleep. A slowly developing anemia that is still mild may
be asymptomatic, but as anemia becomes more severe, symptoms such
as headache, dizziness, palpitations, chest pain, shortness of breath,
and exercise intolerance may be seen. With acute blood loss, volume
depletion and hypoperfusion become evident. With acute intravascu
-
lar hemolysis, signs and symptoms also include jaundice, back pain,
and free hemoglobin in the plasma and urine. In these cases, renal
failure may ensue. Particular attention should be paid to pregnant
patients during their first 30 weeks of pregnancy, when anemia is
associated with an increased risk of neurodevelopmental disorders in
the offspring. In elderly patients, anemia increases the risk of cardio
-
vascular disease, cognitive impairment, falls with fracture, and re-
duced quality of life.
A useful physical sign can be elicited by asking patients to hyperex-
tend their hand; if the palmar creases are lighter than the surrounding
skin, the hemoglobin level usually is <8 g/dL.
Laboratory testing Reference hemoglobin ranges are as follows:
• Adult females: 12.1–15.1 g/dL
• Adult males: 13.8–17.2 g/dL
Panic hemoglobin values include the following:
• <5.0 g/dL associated with heart failure and death
• >20 g/dL associated with capillary clogging
Diagnostic algorithm for anemia:
1. Check CBC with platelets and differential (including RBC indices
and morphology on manual differential), and check reticulocytes
(number and percentage).
2. If anemia is present on CBC (hemoglobin <13 g/dL in males or
<12 g/dL in females), check reticulocyte index (also called reticu-
locyte production index).
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340 Laboratory Medicine in Psychiatry and Behavioral Science
Anemia (continued)
Laboratory testing
(continued)
3. If reticulocyte index is normal, classify anemia by RBC indices
(MCV, mean corpuscular hemoglobin concentration [MCHC]):
• Microcytic, hypochromic: iron deficiency anemia, sideroblastic ane-
mia, or thalassemia
• Normocytic, normochromic: inflammation, autoimmune disease,
chronic kidney disease, endocrine disease, critical illness, or bone
marrow disease
• Macrocytic: vitamin B
12
deficiency, folate deficiency, alcohol use dis-
order, drug effects, hypothyroidism, myelodysplasia
4. If reticulocyte index is ≥ 2.5, look at peripheral smear for frag-
mented cells.
• If not present: acute blood loss (hemorrhage)
• If present: intravascular hemolysis, autoimmune destruction, sickle
cell disease, or other hemolytic anemias
5. To distinguish among causes of normocytic, normochromic ane-
mia, check serum iron, total iron-binding capacity (TIBC), and fer-
ritin levels.
6. To distinguish among causes of microcytic, hypochromic anemia,
look at peripheral smear.
• If smear is abnormal, consider thalassemia, sideroblastic anemia,
or bone marrow disease
• If smear is normal, check serum iron, TIBC, and ferritin levels.
• Low/normal TIBC and iron, normal/high ferritin = inflamma-
tion or chronic disease.
• High TIBC, low iron, low ferritin = iron deficiency. Serum
ferritin <15 ng/mL confirms diagnosis of iron deficiency, and
>100 ng/mL excludes diagnosis.
To monitor recovery with iron supplementation in iron deficiency
anemia, the patient’s hemoglobin is checked after 3 weeks to confirm
response and after 9 weeks to confirm recovery when the source of iron
deficiency has been identified and corrected. With iron supplementa
-
tion, the hemoglobin level should rise by ~2 g/dL every 3 weeks.
To ensure iron stores have been replenished, iron supplementation
should continue for 3–6 months from the time hemoglobin normalizes.
Gafter-Gvili A, Schechter A, Rozen-Zvi B: Iron deficiency anemia in chronic kidney disease.Acta Haema-
tol 142(1):44–50, 2019
Hidese S, Saito K, Asano S, Kunugi H: Association between iron-deficiency anemia and depression: a
web-based Japanese investigation.Psychiatry Clin Neurosci 72(7):513–521, 2018
Leung W, Singh I, McWilliams S, et al: Iron deficiency and sleep: a scoping review.Sleep Med Rev
51:101274, 2020
Phillips J, Henderson AC: Hemolytic anemia: evaluation and differential diagnosis. Am Fam Physician
98(6):354–361, 2018
Stauder R, Valent P, Theurl I: Anemia at older age: etiologies, clinical implications, and manage-
ment.Blood 131(5):505–514, 2018
Vulser H, Wiernik E, Hoertel N, et al: Association between depression and anemia in otherwise healthy
adults. Acta Psychiatr Scand 134(2):150–160, 2016
Wiegersma AM, Dalman C, Lee BK, et al: Association of prenatal maternal anemia with neurodevelop-
mental disorders.JAMA Psychiatry 76(12):1294–1304, 2019
https://t.me/med1917
341 Diseases and Conditions
Anorexia nervosa (AN)
Clinical findings AN is characterized by a self-imposed restriction of food intake with
significantly low body weight, fear of gaining weight, and body image
distortion. High morbidity and mortality rates in this condition arise
from malnutrition and its various medical complications, as well as
coexisting psychiatric disorders, including suicide. The disorder pre
-
dominantly affects women, with a mean age at onset of 18 years, but is
typically resistant to treatment so that recovery occurs only gradually,
over years to decades. Genetic and psychosocial factors underlie the
condition, which may be sustained by changes in neural architecture.
Two types of AN are recognized: the restricting type and the binge
eating/purging type, with the latter including either binge-eating or
purging behaviors such as self-induced vomiting or misuse of laxatives,
diuretics, or enemas. Crossover between types is common in the course
of the illness, so type is determined by current symptoms rather than
symptom history. The binge-eating/purging type is distinguished from
bulimia nervosa by the maintenance of normal weight in the latter con
-
dition.
Physical findings among adults presenting with AN include low body
weight (BMI ≤17.5), bradycardia, orthostatic hypotension, dehydration,
muscle wasting, and lanugo. Dental erosion, hand calluses, and sali
-
vary gland hypertrophy may be seen in those with purging behaviors.
Psychiatric comorbidities include major depression, anxiety disorders,
OCD, trauma-related disorders, and substance misuse. The suicide rate
is among individuals with AN is 18 times that of control subjects.
Medical complications of AN affect all organ systems. Cardiac signs
include serious bradycardia during sleep, prolonged QT, heart muscle
wasting with dysrhythmias and sudden death, changes in left ventric
-
ular function, pericardial and valvular pathology, and dysregulation of
peripheral vascular contractility. Injury to hepatocytes can lead to acute
liver failure associated with encephalopathy and coagulation problems.
Other potential complications include a decline in the GFR, bone mar-
row atrophy, difficulty standing because of loss of muscle mass, osteo-
porosis, and cerebral atrophy. The latter finding usually improves with
weight restoration.
Laboratory testing For all patients with AN, consider the following:
• Urinalysis: On presentation, check urine sample before the patient
is weighed to determine specific gravity (reflecting hydration sta-
tus), pH, presence of ketones, and evidence of kidney injury.
• CBC with differential: low cell counts due to bone marrow atrophy,
with relative lymphocytosis. Rarely, platelet count is also low.
• Chemistries: high bicarbonate, normal calcium, and low values for
sodium, potassium, chloride, phosphorus, magnesium, glucose,
and albumin. High BUN and creatinine reflect prerenal azotemia.
For malnourished and severely symptomatic
patients:
• ECG: bradycardia, prolongation of QT interval, nonspecific ST-
segment changes, U waves, and, in severe cases, dysrhythmias,
including ventricular fibrillation and asystole. In presence of severe
sinus bradycardia or junctional rhythm, marked prolongation of
corrected QT interval, or syncope, admission to telemetry unit is
recommended.
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