Clinical Chemistry 65:1

51–56 (2019) Clinical Case Study

An Unusual Case of Decompensated Heart Failure

in a Young Man
Christopher W. Farnsworth1* and Thomas J. Baranski2

CASE
QUESTIONS TO CONSIDER
A 21-year-old man presented to the emergency department
(ED)3 with chest pain, worsening shortness of breath, 1. What are some causes of decompensated heart failure
lethargy, nausea, vomiting, and palpitations. He pre- in otherwise healthy, young individuals?

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sented to another ED the previous day with similar symp- 2. What are the indications for thyroid testing in acutely ill
toms and was sent home with a diagnosis of anxiety and patients?
panic attack. His only relevant past medical history was
repaired Chiari malformation. There was no family his- 3. What are some common causes of acute thyrotoxicosis?
tory of ischemic heart disease. His lipid concentrations
were as follows: total cholesterol, 79 mg/dL [2.05
roid stimulating hormone (TSH) ⬍0.04 mcIU/mL, free
mmol/L; reference interval (ref), ⬍200], HDL choles-
thyroxine (FT4) of 0.6 ng/dL (7.7 pmol/L) (ref, 0.7–1.3),
terol, 26 mg/dL (0.67 mmol/L; ref, 40 –199), LDL cho-
and free triiodothyronine (FT3) ⬎20.0 pg/mL (30.8
lesterol, 22 mg/dL (1.14 mmol/L; ref, 0 –129), triglycer-
pmol/L; ref, 2.4 – 4.2).
ides, 43 mg/dL (0.49 mmol/L; ref, 0 –150), and he had a
Twenty-four hours after admission, bedside ECG
BMI (body mass index) of 29. The patient was otherwise
demonstrated evidence of acute decompensated heart fail-
in normal health.
ure (HF) with worsening left ventricular dysfunction and an
On arrival, his troponin I was 47.94 ng/mL
ejection fraction of 21%. Therefore, the ␤ blocker was
(Siemens Dimension; ref, ⬍0.24). Electrocardiography
stopped and dobutamine was started despite tachycardia.
(ECG) was performed that revealed sinus tachycardia
The patient’s heart rate soon improved to 110, his urine
(140 beats/min) without elevation of ST-segments. As
a result, a ␤ blocker was administered for non-ST- output improved, and troponins trended down. Three days
following admission, his symptoms improved dramatically,
elevation myocardial infarction. The patient also devel-
and extubation was performed; no further complaints of
oped severe hypoxic respiratory failure with an arterial
dyspnea or chest pain were received.
PO2 of 62 mmHg (ref, 80 –100), which required oxygen
by nonrebreathing mask at 25 L/min. He was later intu-
DISCUSSION
bated due to increased respiratory fatigue (respirations
26/min), hypotension (blood pressure 85/57), and in-
The differential diagnosis for a young patient presenting
creased oxygen requirements. The patient also became
with acute coronary syndrome and HF is broad. High on
oliguric with creatinine increasing to 1.9 mg/dL. He was
the differential is an inherited cardiac condition. Although
acidotic, hyperkalemic, and his liver function test results
this could not definitively be ruled out, it was unlikely in this
were high (Table 1). There was clinical concern for infec-
patient owing to lack of family history of acute coronary
tion, but all cultures were negative. Furthermore, a urine
syndrome. Cardiac infection and sepsis could also cause HF,
drug screen, antinuclear antibody, antineutrophil cyto-
but blood cultures were negative. Illicit drug use, particu-
plasmic antibody, and coagulation testing were all nor-
larly cocaine, is frequently associated with myocardial in-
mal. Thyroid testing was performed that revealed a thy-
farctions and HF in young patients. However, a urine drug
screen was negative, making illicit drug use as the precipitat-
ing event of acute coronary syndrome and HF less likely.
Given suppressed TSH and increased free T3, thyroid storm
1
Department of Pathology and Immunology and 2 Department of Medicine, Washington as a result of thyrotoxicosis seemed the most likely diagnosis.
University in St. Louis. St. Louis, MO.
* Address correspondence to this author at: Washington University School of Medicine,
However, antithyroid drugs were not administered owing to
425 S Euclid Ave., Campus Box 8118, St. Louis, MO 63110. Fax 314-362-1461; e-mail high suspicion for exogenous T3 hyperthyroidism.
cwfarnsworth@wustl.edu. Clinically, acute thyrotoxicosis is associated with
Received May 1, 2018; accepted July 11, 2018.
DOI: 10.1373/clinchem.2018.291559
sweating, dyspnea, psychosis, vomiting, and increased car-
© 2018 American Association for Clinical Chemistry diac output. Many of these symptoms can be seen in panic
3
Nonstandard abbreviations: ED, emergency department; ref, reference interval; ECG, attack, and it is not surprising that this was the original
electrocardiogram; TSH, thyroid stimulating hormone; FT4, free thyroxine; FT3, free trii-
odothyronine; HF, heart failure; SARM, selective androgen receptor modulator; LVEF, left diagnosis. However, a diagnosis of hyperthyroidism was
ventricular ejection fraction. made by clinical symptoms and TSH concentration. Thy-

51
52
Table 1. Selected laboratory results.a

Reference interval Admission Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Discharge

Clinical Chemistry 65:1 (2019)

Troponin I <0.24 ng/mL 47.94 32.13 19.52 0.29
Creatine kinase 30–200 Units/L 1760 1634 1291
Clinical Case Study

Triglycerides 0–150 mg/dL (0–1.70 mmol/L) 43 (0.49)

HDL cholesterol 40–199 mg/dL (1.04–5.15 mmol/L) 26 (0.67)
LDL cholesterol 0–129 mg/dL (0–3.34 mmol/L) 44 (1.14)
Total cholesterol <200 mg/dL (<5.18 mmol/L) 79 (2.046)
TSH 0.35–5.50 mcIU/mL <0.04 0.04 2.94
FT4 0.7–1.3 ng/dL (9.0–16.7 pmol/L) 0.6 (7.7) 0.83 (10.68)
FT3 2.3–4.2 pg/mL (3.5–6.5 pmol/L) >20.0 (3.08) 8.4 (12.9) 5.4 (8.3)
Aspartate transaminase 11–47 Units/L 95 204 211 156 954 527 252 106
Alanine transaminase 7–53 Units/L 144 147 187 1605 1523 1111 642 587
Creatinine 0.7–1.3 mg/dL (61.9–114.9 μmol/L) 1.27 (112.3) 1.21 (107.0) 0.91 (80.4) 1.9 (168.0) 1.63 (144.1) 1.4 (123.8) 1.3 (114.9) 1.11 (98.1)
Sodium 135–145 mmol/L 138 141 142 141 143 143 140 139
Potassium 3.3–4.9 mmol/L 4.5 4.3 4.4 6.6 5.2 4.6 4.4 4.2
a
Results listed as conventional units (SI units).

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roid hormone testing is not usually indicated in critically ill
patients because sick euthyroid syndrome, a phenomenon
of abnormal thyroid hormone concentrations, can occur as
a result of acute illness in otherwise clinically euthyroid pa-
tients (1 ). Assessment of thyroid function was warranted in
this patient given suspicion for thyrotoxicosis. This diagno-
sis was confirmed by the patient’s clinical symptoms and
laboratory TSH ⬍0.04 ng/mL. There are many potential
causes of hyperthyroidism including Graves disease, multi-
nodular goiter, adenoma, and thyroid hormone ingestion.
In patients with suppressed TSH, measurement of FT4 and
FT3 can help to establish the underlying cause of hyperthy-
roidism. Although Graves disease is the most likely cause of
hyperthyroidism, it was unlikely in this patient given low
FT4 and high FT3. Moreover, Graves disease is unlikely to
spontaneously resolve without medical interventions such as
antithyroid medication or thyroidectomy. In contrast, T3
thyrotoxicosis is often a result of exogenous thyroid hor-
mone ingestion and presents clinically with similar symp-
toms to increased FT4 thyrotoxicosis. T3 thyrotoxicosis is
identified by laboratory findings of increased FT3 concen-
trations, FT4 concentrations that are low or within the ref-
erence interval, and suppressed TSH concentrations. Inter-
estingly, there have been cases of thyrotoxicosis from so
called “hamburger hyperthyroidism,” in which affected in-
dividuals have eaten ground beef that was tainted with bo-
vine thyroid tissue. Toxic nodular goiter can also cause T3 thy-
rotoxicosis; however, this was ruled out during the patient’s
physical exam and is unlikely in iodine replete populations.
The finding of increased FT3 and low FT4 raised
suspicion of an exogenous cause of cardiotoxicity second-
ary to thyrotoxicosis. This was confirmed by monitoring
of FT3, which steadily decreased during the course of the
patient’s stay (with concurrent increases in TSH). Impor-
tantly, antithyroid medications are not useful in patients
with exogenous T3 hyperthyroidism because these drugs
will only block the production of T4 and T3 and the
conversion of T4 to T3. The diagnosis of exogenous T3
thyrotoxicosis was confirmed by the patient’s own ac-
count upon extubation. He claimed to be taking several
supplements that had been purchased online for muscle
building and weight loss, one of which was called “Liquid
T3.” Further toxicological analysis of the patient’s urine
revealed the presence of androgen precursors and prest-
eroids that also may have played a role in the develop-
ment of heart and respiratory failure in this patient. Be-
cause of the use of these substances, a psychological
evaluation was performed and the patient was diagnosed
with body dysmorphic disorder.
BODY DYSMORPHIC DISORDER
Over the past several decades there has been an increasing
prevalence of body dysmorphia in men known as muscle
dysmorphia (2 ). Whereas in women, body dysmorphia
generally presents with anorexia, men with muscle dysmor-
Clinical Case Study
phia have dissatisfaction with the shape and size of their
body and believe that their bodies are insufficiently muscu-
lar. The estimated prevalence of muscle dysmorphia in the
US is 100000 men, but this figure is debated (3 ). Generally,
men with this disorder are characterized by compulsive
weight lifting, strict dietary regimens, and the use of dietary
supplements. Although supplement use is usually limited to
those purchased over the counter at health stores, it can also
include anabolic steroids, human growth hormone, selective
androgen receptor modulators (SARMs), insulin, and thy-
roid hormones (4 ).
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Before the 1980s, supplements and performance
enhancing drugs were largely confined to athletes.
More recently, these substances have found their way
into the general public; primarily in nonathlete weight
lifters desiring a leaner and more muscular physique
(5 ). Although their emergence in this population is
likely multifactorial, one major cause has been the rise
of the internet. One recent study observing anabolic-
androgenic steroid searches using Google found hun-
dreds of thousands of results and websites (6 ). Al-
though many of the searches were general (“Steroids
bodybuilding”), other searches were far more specific
(“Steroids for Sale”) and seem to indicate intent to
purchase anabolic steroids over the internet. The US
Government Accountability Office performed a study
in 2005 in which 22 orders for anabolic steroids were
placed to various websites. Of these, 14 orders were
fulfilled; 10 of which contained anabolic steroids ar-
riving from other countries (7 ). A more recent study
examined nonsteroidal SARMs, an anabolic steroid
ligand that binds to the androgen receptor and exerts
androgenic effects such as muscle growth. This non-
FDA (US Food and Drug Administration) approved
product could be obtained from over 21 suppliers
when ordered from the internet (8 ). More disturbing,
one quarter of the tested substances contained other active
compounds not listed, such as tamoxifen (estrogen receptor
antagonist), androstatrienedione (aromatase inhibitor), and
ibutamoren (growth hormone secretagogue). Another con-
founding factor is the lack of regulation of dietary supple-
ments. A study performed in 2013 found multiple herbs
and dietary supplements marketed for thyroid support con-
tained T4 or T3 (9 ). These thyroid supplements are often
used by body builders to achieve a leaner, more muscular
physique. Together, these studies indicate that nonpre-
scribed or nonapproved anabolic substances are relatively
easy for consumers to obtain. Moreover, these compounds
are not regulated, so their content may vary significantly
from what is advertised to the consumer.
Given the emergence of muscle dysmorphia and ease
of access to nonregulated drugs and supplements, physi-
cians must be alert to the signs and symptoms associated
with ingestion of these substances. Owing to the covert
nature of substance abuse and because clinical trials can-
Clinical Chemistry 65:1 (2019) 53
Clinical Case Study
POINTS TO REMEMBER
• Causes of HF among young patients include cardiomyop-
athy, myocarditis, drug-related myocardial lesions,
and thyrotoxicosis.
• Thyroid function tests can be abnormal in acutely ill
patients. Therefore, thyroid testing should only be
performed in patients with a high index of suspicion
for hyper- or hypothyroidism.
• Causes of thyrotoxicosis include Graves disease, multinod-
ular goiter, adenoma, and thyroid hormone ingestion.
• Patients with muscle dysmorphia, a subset of body
dysmorphia, believe that they are insufficiently muscu-
lar. Many of these patients are characterized by com-
pulsive weight lifting and supplement intake.
• Abuse of nonregulated supplements and anabolic steroids
is exacerbated by ease of purchase and lack of regulation.
Physicians must be alert to the signs and symptoms asso-
ciated with ingestion of nonprescribed compounds such as
anabolic steroids, SARMs, and thyroid hormones.
not ethically replicate the large doses of substances that
are generally taken, data on treating the acute or long-
term effects of many of these drugs is limited. Random-
ized trials are needed to assess the effectiveness of thera-
peutic interventions for dealing with the myriad of
potential abused substances among this population (10 ).
CASE RESOLUTION
The patient’s symptoms improved considerably over the
course of his stay. Troponin I concentrations trended
down from 47.94 ng/mL to 0.49 ng/mL on discharge.
The increase in troponin I was attributed to demand
ischemia from tachycardia and thyroid toxicity. The pa-
tient was diagnosed with exogenous thyrotoxicosis insti-
gating acute HF and was discharged with a left ventricu-
Commentary
Jim D. Faix*
Sudden exaggerated symptoms of thyrotoxicosis are
rarely seen today because patients with hyperthyroidism
Montefiore Medical Center, Bronx, NY.
* Address correspondence to the author at: Montefiore Medical Center, Pathology, Core
Laboratory Administrative Office, 111 East 210th St., Foreman 8 - Silver Zone, Bronx, NY
10467. E-mail jfaix@montefiore.org.
54 Clinical Chemistry 65:1 (2019)
lar ejection fraction (LVEF) volume of 44% without
further medications. The patient followed up with a car-
diologist 1 month later with no further symptoms; his
troponin I levels returned to baseline (⬍0.03 ng/mL),
and his LVEF volume was 66%.
Author Contributions: All authors confirmed they have contributed to
the intellectual content of this paper and have met the following 4 require-
ments: (a) significant contributions to the conception and design, acquisi-
tion of data, or analysis and interpretation of data; (b) drafting or revising
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the article for intellectual content; (c) final approval of the published article;
and (d) agreement to be accountable for all aspects of the article thus
ensuring that questions related to the accuracy or integrity of any part of the
article are appropriately investigated and resolved.
T.J. Baranski, provision of study material or patients.
Authors’ Disclosures or Potential Conflicts of Interest: No authors
declared any potential conflicts of interest.
References
1. Farwell AP. Thyroid hormone therapy is not indicated in the majority of patients with
the sick euthyroid syndrome. Endocr Pract 2008;14:1180 –7.
2. Pope HG Jr, Gruber AJ, Choi P, Olivardia R, Phillips KA. Muscle dysmorphia. An under-
recognized form of body dysmorphic disorder. Psychosomatics 1997;38:548 –57.
3. Tod D, Edwards C, Cranswick I. Muscle dysmorphia: current insights. Psychol Res Be-
hav Manag 2016;9:179 – 88.
4. Cafri G, Olivardia R, Thompson JK. Symptom characteristics and psychiatric comorbid-
ity among males with muscle dysmorphia. Compr Psychiatry 2008;49:374 –9.
5. Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health conse-
quences of performance-enhancing drugs: an Endocrine Society Scientific Statement.
Endocr Rev 2014;35:341–75.
6. Brennan BP, Kanayama G, Pope HG Jr. Performance-enhancing drugs on the web: a
growing public-health issue. Am J Addict 2013;22:158 – 61.
7. US Government Accountability Office. Anabolic steroids are easily purchased
without a prescription and present significant challenges to law enforcement
officials. Washington (DC): US Government Accountability Office; 2005. Docu-
ment No. GAO-06-243R.
8. Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical composition
and labeling of substances marketed as selective androgen receptor modulators and
sold via the internet. JAMA 2017;318:2004 –10.
9. Kang GY, Parks JR, Fileta B, Chang A, Abdel-Rahim MM, Burch HB, Bernet VJ. Thyrox-
ine and triiodothyronine content in commercially available thyroid health supple-
ments. Thyroid 2013;23:1233–7.
10. Pope HG Jr, Khalsa JH, Bhasin S. Body image disorders and abuse of anabolic-
androgenic steroids among men. JAMA 2017;317:23– 4.
are identified and treated earlier. Although not a classic
case of “thyroid storm,” this patient’s presentation was
suggestive and the diagnosis of hyperthyroidism was
Received August 31, 2018; accepted September 5, 2018.
DOI: 10.1373/clinchem.2018.295188
姝 2018 American Association for Clinical Chemistry