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452 Laboratory Medicine in Psychiatry and Behavioral Science
Hypoparathyroidism
Clinical findings Hypoparathyroidism is a rare condition characterized by low calcium
levels and inappropriately low or undetectable levels of PTH. It occurs
most often in older females with parathyroid injury or accidental re
-
moval as complications of thyroid surgery. Other causes include ge-
netic and autoimmune diseases. PTH regulates calcium and phosphate
levels through its actions on the bones, kidneys, and intestines, and
some of the clinical symptoms of hypoparathyroidism stem from the
absence of physiological actions of PTH on the skeleton and kidneys.
The skeleton adds bone, but bone turnover is low so that bone mass
increases. The kidneys are unable to conserve calcium and thus excrete
a greater amount in urine. Other biochemical abnormalities of hypo
-
parathyroidism include elevated phosphate levels and low levels of
1,25-dihydroxy vitamin D.
The most prominent symptoms of hypoparathyroidism are related to
neuromuscular irritability and include paresthesias, muscle cramps,
carpopedal spasm, seizures, and laryngospasm. Calcifications in the
kidneys, basal ganglia, and soft tissues are common. The incidence of
depression is increased, and there is some evidence of cognitive im
-
pairment referred to as “brain fog” that is proportional to calcium con-
centration and duration of disease. Cardiac signs include prolongation
of the corrected QT interval and cardiac arrhythmias. Cataracts, dental
abnormalities, increased rates of infection, and skin changes are seen,
the latter including dry, scaly skin; brittle nails; and coarse or thin hair.
Laboratory testing Laboratory tests used in the workup of suspected hypoparathyroidism
include the following:
•
Ionized (free) calcium level or albumin-corrected total calcium
level (low)
•
PTH level (inappropriately low or undetectable)
• Phosphate (high)
Bilezikian JP: Hypoparathyroidism. J Clin Endocrinol Metab 105(6):1722–1736, 2020
Clarke BL, Brown EM, Collins MT, et al: Epidemiology and diagnosis of hypoparathyroidism.J Clin En-
docrinol Metab 101(6):2284–2299, 2016
Gafni RI, Collins MT: Hypoparathyroidism. N Engl J Med 380(18):1738–1747, 2019
Mannstadt M, Bilezikian JP, Thakker RV, et al: Hypoparathyroidism.Nat Rev Dis Primers 3:17055, 2017
[published correction appears in Nat Rev Dis Primers 3:17080, 2017]
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453 Diseases and Conditions
Hypothyroidism
Clinical findings In areas of the world where iodine intake is sufficient, the most common
cause of hypothyroidism is autoimmune disease. The prevalence of this
condition increases with age and is more common in females. Certain
medications are also associated with hypothyroidism through various
mechanisms, including amiodarone, gonadal steroid hormones, gluco
-
corticoids, furosemide, lithium, levodopa, antipsychotics, phenytoin,
and propranolol, among others.
The onset of hypothyroidism can be insidious. Signs and symptoms
include the following:
• Bradycardia
• Weight gain
• Fatigue
• Cold intolerance
• Dry skin
• Alopecia
• Myxedema (skin thickening) often apparent on face, legs, and dor-
sum of hands and feet
•
Carpal tunnel syndrome
• Menstrual irregularities
• Depression
• Psychosis (“myxedema madness”)
• Cognitive impairment: poor concentration, memory difficulties,
dullness
•
Coma when severe and untreated
Hypothyroidism disrupts all aspects of metabolism and contributes to
hypertension, dyslipidemia, infertility, and neuromuscular dysfunc-
tion. Importantly, it increases the risk of cardiovascular disease even in
treated patients when treatment is inadequate. The effects in pregnancy
can be serious, including bradycardia, goiter, inappropriate weight
gain, and adverse effects on the fetus.
Although the management of subclinical hypothyroidism (high TSH,
normal free T4 [FT4]) has been controversial in the past, it is now rec
-
ognized that patients with a TSH level >10 mIU/L with or without an
elevated TPOAb are at risk of dyslipidemia and cardiovascular disease,
and treatment is recommended. Treatment-refractory depression may
also be related to subclinical thyroid disease. Even among patients with
TSH values in the high-normal range, there is a higher frequency of
depressive episodes, symptoms are more severe, and antidepressant
treatment response can be suboptimal. Thyroid replacement with target
TSH levels <2.5 mIU/L may be required to achieve remission, and this
is true for patients with bipolar as well as unipolar disease. In fact, pa-
tients with treatment-resistant depression may benefit from thyroid
supplementation titrated to a target TSH level as low as <2.0 mIU/L.
Laboratory testing The testing laboratory’s reference range should be consulted for deter-
mining the upper limit of normal for TSH, which varies with age.
For screening purposes, TSH alone is considered sufficient testing.
FT4 is needed in addition to TSH to diagnose subclinical thyroid dys-
function, central hypothyroidism (due to hypothalamic or pituitary
disease), and drug effects and to monitor treatment.
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454 Laboratory Medicine in Psychiatry and Behavioral Science
Hypothyroidism (continued)
Laboratory testing
(continued)
The FT4 level is measured in preference to the total T4 because its mea-
surement is not affected by serum protein levels.
TSH and FT4 together suggest the following diagnoses:
• TSH high, FT4 low: hypothyroidism
• TSH high, FT4 normal: subclinical hypothyroidism
If the FT4 is normal in the context of high TSH, further workup should
include thyroid antibodies to diagnose possible autoimmune disease.
Recent reviews suggest that subclinical hypothyroidism in non-elderly
patients should be treated when the TSH level is >4.0 mIU/L.
Because subclinical hyperthyroidism is more injurious to elderly pa-
tients than subclinical hypothyroidism, treatment for these patients is
individualized and based on symptoms. The treatment threshold in this
population is a TSH level ≥10 mIU/L.
The schedule for checking TSH in patients treated with thyroid hor-
mone replacement is as follows:
• 4–8 weeks after initiating treatment
• 4–8 weeks after a change in dosage
• 6 months after adequate replacement dosage is achieved
• Every 12 months thereafter or as dictated by clinical situation
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Barbesino G: Thyroid function changes in the elderly and their relationship to cardiovascular health: a
mini-review.Gerontology 65(1):1–8, 2019
Calissendorff J, Falhammar H: To treat or not to treat subclinical hypothyroidism, what is the evi-
dence?Medicina (Kaunas) 56(1):40, 2020
Chiovato L, Magri F, Carlé A: Hypothyroidism in context: where we’ve been and where we’re going.Adv
Ther 36(Suppl 2):47–58, 2019
Chrysant SG: The current debate over treatment of subclinical hypothyroidism to prevent cardiovascular
complications.Int J Clin Pract 74(7):e13499, 2020
Cohen BM, Sommer BR, Vuckovic A: Antidepressant-resistant depression in patients with comorbid sub-
clinical hypothyroidism or high-normal TSH levels.Am J Psychiatry 175(7):598–604, 2018
Duntas LH, Yen PM: Diagnosis and treatment of hypothyroidism in the elderly. Endocrine 66(1):63–69,
2019
Garber JR, Cobin RH, Gharib H, et al: Clinical practice guidelines for hypothyroidism in adults: cospon-
sored by the American Association of Clinical Endocrinologists and the American Thyroid Associa-
tion.Endocr Pract 18(6):988–1028, 2012 [published correction appears in Endocr Pract 19(1):175, 2013]
Redford C, Vaidya B: Subclinical hypothyroidism: should we treat? Post Reprod Health 23(2):55–62, 2017
Treister-Goltzman Y, Yarza S, Peleg R: Lipid profile in mild subclinical hypothyroidism: systematic re-
view and meta-analysis. Minerva Endocrinol (Torino) 46(4):428–440, 2021
https://t.me/med1917
455 Diseases and Conditions
Infectious mononucleosis (IM)
Clinical findings IM is a viral syndrome caused in most cases by the Epstein-Barr virus
(EBV), a herpesvirus spr
mostly in adolescents and young adults, it also can occur in older
adults
Like other herpesviruses, EBV establishes an asymptomatic, lifelong
latent infection of immune system B cells with occasional reactivation.
The acute IM syndrome is characterized by fever, malaise, fatigue,
headache, sore throat, pharyngeal inflammation with exudates, palatal
petechiae, tonsillar enlargement, periorbital and eyelid edema, and
symmetrical lymphadenopathy (especially cervical and postauricular,
but also axial and inguinal). Splenomegaly and hepatomegaly may be
observed, and an erythematous maculopapular rash may develop
with or without the use of antimicrobials.
Early complications include splenic rupture and hepatitis. Splenic rup-
ture is uncommon but can occur spontaneously; this risk is increased
by abdominal trauma, which is why athletes in contact sports are ad-
vised to refrain from playing for a period of ~3 weeks from the time
symptoms resolve. Hepatitis is common and usually self-limiting.
Importantly, IM has well-established associations with later develop-
ment of multiple sclerosis, Hodgkin’s lymphoma, nasopharyngeal
carcinoma, and gastric cancer. There is also evidence that the risk of a
depressive episode is increased in the 1- to 4-year period after IM is
diagnosed. A tentative link has been established to later development
of chronic fatigue syndrome, at least in a subset of patients.
Laboratory testing Testing of blood for EBV-specific antibodies is the gold standard of
diagnosis for IM, but turnaround time for this testing may be unac
-
ceptably long. For this reason, many clinicians use the rapid hetero-
phile
within 5–10 minutes. Specificity of this test is high, but sensitivity is
low,
In these cases, testing by EBV-specific serology can be used.
EBV-specific antibody testing for IgM and IgG antibodies to viral cap-
sid antigen (VCA) and Epstein-Barr nuclear antigen (EBNA) can be
used to follow up on Monospot testing, whether positive or negative.
These tests have higher sensitivity than Monospot.
Lymphocytosis (>5×10
9
/L) is seen in peripheral blood, and atypical
lymphocytes are seen on blood smear. A combination of lymphocytes
>50% and atypical lymphocytes >10% is useful in confirming the di
-
agnosis.
Akiyama Y, Ishikane M, Ohmagari N: Epstein-Barr vi rus induced skin rash in infectious mononucleo-
sis. IDCases 26:e01298, 2021
Cai X, Ebell MH, Haines L: Accuracy of signs, symptoms, and hematologic parameters for the diagnosis
of infectious mononucleosis: a systematic review and meta-analysis.J Am Board Fam Med 34(6):1141–
1156, 2021
Fevang B, Wyller VBB, Mollnes TE, et al: Lasting immunological imprint of primary Epstein-Barr virus in-
fection with associations to chronic low-grade inflammation and fatigue.Front Immunol 12:715102, 2021
Murata T, Sugimoto A, Inagaki T, et al: Molecular basis of Epstein-Barr virus latency establishment and
lytic reactivation. Viruses 13(12):2344, 2021
Vindegaard N, Petersen LV, Lyng-Rasmussen BI, et al: Infectious mononucleosis as a risk factor for de-
pression: a nationwide cohort study. Brain Behav Immun 94:259–265, 2021
Womack J, Jimenez M: Common questions about infectious mononucleosis.Am Fam Physician 91(6):372–
376, 2015
https://t.me/med1917
456 Laboratory Medicine in Psychiatry and Behavioral Science
Insomnia disorder
Clinical findings
Laboratory testing
Insomnia disorder is diagnosed when the patient reports dissatisfaction
with sleep quality or quantity associated with difficulty initiating or
maintaining sleep or early morning awakening. The sleep disturbance
causes significant impairment or distress and occurs at least 3 nights
per week for at least 3 months. The problem can be isolated or can be
associated with another mental disorder or medical condition. Risk
factors for insomnia disorder include female sex, advancing age, being
unmarried, and habits such as smoking, alcohol use, and sedentary life
-
style, although these factors by no means identify all individuals at risk.
Precipitants include stressful events, worsening medical conditions
such as cardiac or pulmonary disease or chronic pain, new-onset de
-
pression or anxiety disorder, or treatment with medications such as β-
blockers, steroids, NSAIDs, decongestants, and antiandrogens. When a
poor sleep pattern emerges, it can become chronic because of behav-
ioral factors such as spending too much time in bed or taking too many
naps, or due to classical conditioning in which the bed and bedroom
have become feared stimuli because of past sleeplessness.
About half of those reporting insomnia meet criteria for a psychiatric
disorder, and this risk is heightened in both directions; psychiatric
disorders increase the risk of insomnia, and insomnia increases the risk
of psychiatric disorders. Insomnia may also be a risk factor for suicide,
independent of depression. Insomnia is associated with cognitive
deficits in working memory and attentional switching. Furthermore,
chronic insomnia increases the risk of medical conditions such as
hypertension, diabetes, coronary heart disease, heart failure, acute MI,
and death. Although insomnia was once dismissed as a nuisance com-
plaint among patients, it is now considered a serious problem requiring
attention.
Recent research has implicated brain circuits regulating arousal and
emotion in the pathophysiology of insomnia, rather than circuits in
-
volved in circadian rhythms. Insomnia is increasingly understood as a
state of constant hyperarousal during wake and sleep cycles in which
metabolic rate is increased. During sleep, cortisol and ACTH are ele
-
vated (in the first part of the sleep cycle) and the normal relationship
between parasympathetic tone and heart rate variability is disrupted.
In most cases, the diagnosis of insomnia disorder is made clinically. The
most important diagnostic tool is a complete history detailing medical
and psychiatric problems, medications, and specific sleep issues. A sleep
diary is highly recommended to capture data regarding the nature of
sleep disruption. Various published insomnia scales can be used to de-
termine the severity of insomnia and monitor the effects of treatment.
Polysomnography is indicated in the workup for insomnia only if sleep
apnea, periodic limb movements, or parasomnias such as REM sleep
behavior disorder are suspected.
Wrist actigraphy is a noninvasive, low-cost means to obtain informa-
tion about day-night cycles and to monitor the effects of treatment for
insomnia.
Although neuroimaging is not required for the diagnosis of insomnia
disorder, if it is obtained for another indication in a patient with
chronic insomnia, it may show reduced hippocampal volume and re-
duced gray matter in the frontal lobes.
https://t.me/med1917
457 Diseases and Conditions
Insomnia disorder (continued)
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Burman D: Sleep disorders: insomnia.FP Essent 460:22–28, 2017
Buysse DJ: Insomnia.JAMA 309(7):706–716, 2013
Patel D, Steinberg J, Patel P: Insomnia in the elderly: a review.J Clin Sleep Med 14(6):1017–1024, 2018
Perez MN, Salas RME: Insomnia. Continuum (Minneap Minn) 26(4):1003–1015, 2020
Riemann D, Nissen C, Palagini L, et al: The neurobiology, investigation, and treatment of chronic insom-
nia. Lancet Neurol 14(5):547–558, 2015
Sutton EL: Insomnia. Ann Intern Med 174(3):ITC33–ITC48, 2021
Van Someren EJW: Brain mechanisms of insomnia: new perspectives on causes and conse-
quences. Physiol Rev 101(3):995–1046, 2021
Winkelman JW: Clinical practice: insomnia disorder. N Engl J Med 373(15):1437–1444, 2015
https://t.me/med1917
458 Laboratory Medicine in Psychiatry and Behavioral Science
Klinefelter’s syndrome
Clinical findings Klinefelter’s syndrome is a genetic disorder found in males that results
from sex chromosome nondisjunction leading in most cases to a
47,XXY karyotype. In this classic form, the extra X chromosome gives
rise to characteristic features of small testes, hypergonadotropic hypo-
gonadism, and language processing difficulties. A wide range of clin-
ical phenotypes is seen because of mosaic forms (e.g., 47,XXY/46,XY)
and higher-grade forms (e.g., 48,XXXY or 48,XXYY) as well as varia
-
tion in downstream effects, severity of hypogonadism, and duration of
untreated disease. Only about 25%
those mostly in adulthood because symptoms worsen with age. The
condition is not heritable.
In its fully developed form, 47,XXY Klinefelter’s syndrome may in-
clude any of the following signs and symptoms: small, firm testes, gy-
necomastia, broad hips, decreased facial and axillary hair, tall stature
with long legs, underdeveloped musculature, incoordination, infertil-
ity, erectile dysfunction, decreased libido in some cases, speech and
language impairment, and susceptibility to anxiety, depression, bipo
-
lar disorder, autism spectrum disorder, and schizophrenia, as well as
various social and behavioral problems.
In most cases, boys with this phenotype enter puberty as usual so that
secondary sex characteristics are relatively unaffected. Serum testos
-
terone levels then begin to decline in young adulthood. Infertility be-
comes an issue, and metabolic abnormalities develop, including
obesity, insulin resistance, dyslipidemia, and hypertension. The risk of
cardiovascular disease, autoimmune disease (e.g., lupus, Hashimoto’s
thyroiditis), osteoporosis, certain cancers (e.g., breast cancer, germ cell
tumors), and dental caries is elevated and continues to increase with
age.
Psychological consequences of Klinefelter’s syndrome are relatively
under-researched and not well understood. The possibility of gender
incongruence should be addressed as early as possible and appropri-
ate referrals made. In addition, screening for psychiatric disorders
should be undertaken routinely throughout life.
Laboratory testing Chromosomal analysis (karyotyping) of peripheral blood cells is used
to diagnose Klinefelter’s syndrome.
Karyotyping is recommended:
• In males with primary hypogonadism (low serum testosterone lev-
els and elevated gonadotropins [LH and FSH] along with small
testicular volumes (<5 mL per testis)
• In males with nonobstructive azoospermia or severe oligozoosper-
mia (total sperm count <10× 10
6
/ejaculate or sperm concentration
<5×10
6
/mL)
Other laboratory testing is recommended for patients diagnosed with
Klinefelter’s syndrome, as follows:
• Metabolic profile at least annually
• Testosterone and LH at least annually
• Vitamin D and calcium levels at first visit and then as indicated
• ECG to evaluate QTc at first visit and then as indicated
• Bone mineral density (DEXA) scan at first visit and then as indicated
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459 Diseases and Conditions
Klinefelter’s syndrome (continued)
Bearelly P, Oates R: Recent advances in managing and understanding Klinefelter syndrome.F1000Res
8:F1000 Faculty Rev-112, 2019
Bonomi M, Rochira V, Pasquali D, et al: Klinefelter syndrome (KS): genetics, clinical phenotype and hy-
pogonadism. J Endocrinol Invest 40(2):123–134, 2017
Giagulli VA, Campone B, Castellana M, et al: Neuropsychiatric aspects in men with Klinefelter’s syn-
drome. Endocr Metab Immune Disord Drug Targets 19(2):109–115, 2019
Gravholt CH, Chang S, Wallentin M, et al: Klinefelter’s syndrome: integrating genetics, neuropsychology,
and endocrinology.Endocr Rev 39(4):389–423, 2018
Groth KA, Skakkebæk A, Høst C, et al: Clinical review—Klinefelter’s syndrome: a clinical update.J Clin
Endocrinol Metab 98(1):20–30, 2013
Kanakis GA, Nieschlag E: Klinefelter’s syndrome: more than hypogonadism.Metabolism 86:135–144,
2018
Skakkebæk A, Wallentin M, Gravholt CH: Klinefelter’s syndrome or testicular dysgenesis: genetics, en-
docrinology, and neuropsychology. Handb Clin Neurol 181:445–462, 2021
Zitzmann M, Aksglaede L, Corona G, et al: European Academy of Andrology guidelines on Klinefelter’s
syndrome. Andrology 9(1):145–167, 2021
https://t.me/med1917
460 Laboratory Medicine in Psychiatry and Behavioral Science
Lead poisoning
Clinical findings Lead poisoning is a well-recognized problem in children but can also
affect adults, either acutely or from chronic exposure. In addition, there
is evidence that childhood exposure can lead to neurodegenerative
changes later in life consistent with Alzheimer’s disease and Parkin-
son’s disease. Lead is a neurotoxin that competes with calcium at bind-
ing sites, with serious nervous system, kidney, and bone effects. Until
the early 1990s, lead was ubiquitous in the world, including the United
States and other developed countries. Exposure from paints, pipes, gas
-
oline additives, and a broad array of everyday products resulted in very
high blood lead levels in the world’s populations. In the United States,
children born from the 1960s to the early 1980s are known to have had
the highest exposure, and it is expected that this cohort will demon
-
strate the lasting effects of lead exposure when its members reach the
age at which neurodegenerative disease usually appears.
Lead mitigation efforts have had demonstrable effects on lead levels in
developed countries, but risk remains for those in developing coun
-
tries, those living near airports (within 1 km), consumers of Ayurvedic
and other folk medicines, those who frequent firing ranges, those liv-
ing in older homes with lead pipes,
and those with PVC children’s toys i
sources of exposure in the United States are gunshot wounds and
Ayurvedic and folk medicines.
Acute ingestion of a large amount of lead (e.g., a patient with pica eat-
ing lead chips) is associated with colicky abdominal pain, a metallic
taste, and a florid delirium termed lead encephalopathy. Acute lead poi-
soning can be fatal. Those who survive acute poisoning are usually left
with cognitive and motor deficits.
Adults with chronic low-level lead exposure may be asymptomatic or
may present with mild cognitive impairment and a peripheral motor
neuropathy with wrist and foot drop. Affected patients may or may
not report abdominal pain or metallic taste. Chronic low-level expo-
sure has cumulative effects and may go unnoticed until the patient
presents with dementia, clear motor deficits, or kidney failure. All or
-
gan systems can be affected.
With either acute or chronic toxicity, signs/symptoms may include
anemia, fatigue, weakness, dyspnea, hypertension, hearing loss, osteo-
penia/osteoporosis, cognitive deficits, infertility, miscarriage, im-
mune dysfunction, vitamin D deficiency, mood and personality
changes, headaches, paresthesias, tremors, seizures, coma, weight loss,
poor appetite, nausea and vomiting, and constipation or diarrhea.
Laboratory testing The lead level can be measured in blood or 24-hour urine, but blood is
the specimen of choice. In 2021, the CDC revised the reference levels
for children as follows:
• 0–5 years: ≤3.4 μg/dL
• 6 years and older: ≤4.9 μg/dL
Because even lower levels have been found to be associated with cog-
nitive impairment and maladaptive behaviors, some experts maintain
that no measurable lead level is safe. These values should be inter-
preted with this fact in mind.
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461 Diseases and Conditions
Lead poisoning (continued)
Laboratory testing
(continued)
Critical values of lead in blood:
• Pregnant females: ≥ 10 μg/dL
• Children: >20 μg/dL
• Adults: >45 μg/dL
• Medical emergency (any age): >70 μg/dL
Reference interval for 24-hour urine lead: 0–31 μg/dL
Other laboratory tests useful in the workup of suspected lead poison-
ing include the following:
• CBC with platelets
• Serum iron studies
• Electrolytes
• LFTs
• ESR
• Blood sugar
• EMG/Nerve conduction studies (focused on extensor muscles of
the wrist and fingers and abductor muscle of the thumb)
ARUP Laboratories: Lead, blood (venous), in Laboratory Test Directory. Salt Lake City, UT, ARUP Labo-
ratories, 2022. Available at: https://ltd.aruplab.com/Tests/Pub/0020098. Accessed February 2022.
Ciocan C, Mansour I, Beneduce A, et al: Lead poisoning from Ayurvedic treatment: a further case.Med
Lav 112(2):162–167, 2021
Hung DZ, Yang KW, Wu CC, Hung YH: Lead poisoning due to incense burning: an outbreak in a fam-
ily. Clin Toxicol (Phila) 59(8):756–759, 2021
Mitra P, Sharma S, Purohit P, Sharma P: Clinical and molecular aspects of lead toxicity: an update.Crit
Rev Clin Lab Sci 54(7–8):506–528, 2017
Nicolli A, Mina GG, De Nuzzo D, et al: Unusual domestic source of lead poisoning.Int J Environ Res Pub-
lic Health 17(12):4374, 2020
Njati SY, Maguta MM: Lead-based paints and children’s PVC toys are potential sources of domestic lead
poisoning: a review. Environ Pollut 249:1091–1105, 2019
Reuben A: Childhood lead exposure and adult neurodegenerative disease.J Alzheimers Dis 64(1):17–42,
2018
Rocha A, Trujillo KA: Neurotoxicity of low-level lead exposure: histor y, mechanisms of action, and be-
havioral effects in humans and preclinical models. Neurotoxicology 73:58–80, 2019
Samarghandian S, Shirazi FM, Saeedi F, et al: A system atic review of clinical and laboratory findings of
lead poisoning: lessons from case reports.Toxicol Appl Pharmacol 429:115681, 2021
Shabani M, Hadeiy SK, Parhizgar P, et al: Lead poisoning; a neglected potential diagnosis in abdominal
pain. BMC Gastroenterol 20(1):134, 2020 [published correction appears in BMC Gastroenterol
21(1):411, 2021]
Štepánek L, Nakládalová M, Klementa V, Ferencíková V: Acute lead poisoning in an indoor firing
range. Med Pr 71(3):375–379, 2020
https://t.me/med1917
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