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A Descriptive Study of Adverse Events from Clenbuterol

Misuse and Abuse for Weight Loss and Bodybuilding
a b c
Henry A. Spiller MS, DABAT, FAACT , Kyla J. James PharmD , Steven Scholzen BS &
c
Douglas J. Borys PharmD, DABAT
a
Central Ohio Poison Center, Columbus, Ohio, USA; and Department of Pediatrics, College of
Medicine , Ohio State University , Columbus , Ohio , USA
b
School of Pharmacy , Sullivan University , Louisville , Kentucky , USA
c
School of Pharmacy , Concordia University Wisconsin , Mequon , Wisconsin , USA
Accepted author version posted online: 12 Feb 2013.Published online: 11 Jul 2013.

To cite this article: Henry A. Spiller MS, DABAT, FAACT , Kyla J. James PharmD , Steven Scholzen BS & Douglas J. Borys
PharmD, DABAT (2013) A Descriptive Study of Adverse Events from Clenbuterol Misuse and Abuse for Weight Loss and
Bodybuilding, Substance Abuse, 34:3, 306-312, DOI: 10.1080/08897077.2013.772083

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 SUBSTANCE ABUSE, 34: 306–312, 2013
Copyright 
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ISSN: 0889-7077 print / 1547-0164 online
DOI: 10.1080/08897077.2013.772083

CASE STUDY

A Descriptive Study of Adverse Events

from Clenbuterol Misuse and Abuse for Weight Loss
and Bodybuilding
Henry A. Spiller, MS, DABAT, FAACT
Central Ohio Poison Center, Columbus, Ohio, USA; and Department of Pediatrics, College of Medicine,
Ohio State University, Columbus, Ohio, USA
Downloaded by [134.117.10.200] at 11:16 18 September 2013

Kyla J. James, PharmD

School of Pharmacy, Sullivan University, Louisville, Kentucky, USA

Steven Scholzen, BS and Douglas J. Borys, PharmD, DABAT

School of Pharmacy, Concordia University Wisconsin, Mequon, Wisconsin, USA

ABSTRACT. Background: Clenbuterol is a β 2 -agonist approved in the United States for vet-
erinary use in nonfood animals. Clenbuterol use is emerging among bodybuilders and fitness
enthusiasts attracted to the hypertrophic and lipolytic effects. Cases: This was a retrospective
chart review of clenbuterol exposures reported to 2 poison control centers. Misuse of clen-
buterol for weight loss and bodybuilding was reported in 11 of 13 clenbuterol users. Reported
clinical effects included tachycardia, widened pulse pressure, tachypnea, hypokalemia, hy-
perglycemia, ST changes on electrocardiogram (ECG), elevated troponin, elevated creatine
phosphokinase (CPK), palpitations, chest pain, and tremor. Measured serum clenbuterol con-
centration was 2983 pg/mL post 4.5 mg ingestion. Coingestants included T3 and anabolic
steroids. Treatments included activated charcoal, benzodiazepines, β-blockers, potassium re-
placement, and intravenous (IV) fluid. Conclusions: There is an increasing use of the Internet
for illicit drug use for bodybuilding and weight loss purposes. These patients may not present
as the stereotype of illicit drug abusers, but as healthy athletic low-risk patients. Clinical effects
persisted greater than 24 hours with evidence of myocardial injury in 2 patients. Clenbuterol
is increasingly being abused within the bodybuilding subculture. These cases illustrate the
hidden dangers of clenbuterol abuse among bodybuilders and fitness enthusiasts.

Keywords: Clenbuterol, abuse, bodybuilding, weight loss

INTRODUCTION

Clenbuterol hydrochloride is a β 2 -adrenergic agonist with

Research conception and design HS, KJ. Collection of data HS, KJ,
Analysis HS, KJ, SS and DB, Interpretation of results HS, KJ, SS and DB,
Writing HS, KJ, DB, SS, Revision HS, KJ.
Correspondence should be addressed to Henry A. Spiller, MS, DABAT,
FAACT, Director, Central Ohio Poison Center, Nationwide Children’s
Hospital, 700 Children’s Drive, Columbus, OH 43205, USA. E-mail:
henry.spiller@nationwidechildrens.org
sympathomimetic properties consistent with those found
within its pharmacological class. Compared with other β-
adrenergic agonists, clenbuterol has greater potency, an
extended half-life (25–40 hours), and is more readily ab-
sorbed (70–80%) from the gastrointestinal tract (1, 2). Sym-
pathomimetic effects from β 2 -receptor stimulation include
tachycardia, supraventricular tachycardia, atrial fibrillation,

palpitations, hypotension, vomiting, hyperglycemia, and hy-
pokalemia (3, 4). The approved use of clenbuterol in the
United States is limited to equine use as a bronchodilator
(Ventipulmin) (5, 6). Clenbuterol is available in Europe and
Latin America as a bronchodilator in humans, with a recom-
mended dose of 20 to 40 μg orally, twice daily. However,
clenbuterol has been a popular performance-enhancing sub-
stance due to its anthropometric altering effects and has sub-
sequently been banned by the World Anti-Doping Agency
and the International Olympic Committee (7). Animal and
human studies have demonstrated that clenbuterol enhances
lipolysis, glycolytic capacity, and minimizes protein degra-
dation (8, 9). β 3 -Receptors within skeletal muscle fibers are
thought to account for the anabolic properties of clenbuterol
(10). Additionally, clenbuterol is readily available through In-
ternet commerce and has proliferated a trend of abuse among
bodybuilders, for weight loss, and by fitness enthusiasts at-
Downloaded by [134.117.10.200] at 11:16 18 September 2013
tracted to the hypertrophic and lipolytic effects (5, 11, 12).
The risks associated with these behaviors are compounded
by supratherapeutic dosing and coingestion of additional
agents such as anabolic steroids and nonprescription sup-
plements. Significant cardiotoxic effects after misuse/abuse
of clenbuterol for bodybuilding and sports-related purposes
have been reported, including myocardial ischemia, evidence
of myocardial injury and/or infarction, coronary artery va-
sospasm, and ventricular dysrhythmias (4, 13, 20, 29, 30).
We conducted a retrospective chart review of clenbuterol
exposures in humans reported to 2 regional poison control
centers between October 2006 and January 2012.
METHODS
This was a retrospective review of poison center databases
from 2 regional poison centers for human exposures to clen-
buterol. Data collected after individual chart review, includ-
ing review of individual case notes fields, included demo-
graphics, substances involved including coingestatants if
known, reason for exposure/use of clenbuterol, dose, clin-
ical effects and laboratory results reported, and medical out-
come. Case notes were reviewed for source of purchase of
clenbuterol if noted in the history.
Additionally the National Poison Data System (NPDS)
was queried for number of cases reported by year from Jan-
uary 2007 through November 2012. NPDS represents all
cases reported to US poison control centers. NPDS does not
provide case notes so these data were used to track annual
trends, if any. The American Association of Poison Con-
trol Centers (AAPCC) maintains the national database of
information logged by the country’s poison control centers
(PCCs). Case records in this database are from self-reported
calls: they reflect only information provided when the public
or health care professionals report an actual or potential expo-
sure to a substance (e.g., an ingestion, inhalation, or topical
exposure, etc.), or request information/educational materi-
als. Exposures do not necessarily represent a poisoning or
CASE STUDY 307
overdose. The AAPCC is not able to completely verify the
accuracy of every report made to member centers. Additional
exposures may go unreported to PCCs and data referenced
from the AAPCC should not be construed to represent the
complete incidence of national exposures to any substance(s).
CASE PRESENTATION
Thirteen cases of clenbuterol were located at the 2 regional
poison centers. All cases are summarized in Table 1. The
mean and median age was 29 and 25 years, respectively.
Eleven patients (85%) were male. Six of 13 adult patients pro-
vided a quantifiable dose estimate. The ingested dose ranged
from 300 to 4500 μg (mean = 2600 μg). The single child
patient ingested his mother’s clenbuterol, who had obtained
the drug via the Internet for weight loss. Eight patients were
treated and released from the emergency department, with 3
patients admitted to the hospital (cases 3, 5, 6) and 2 lost to
follow-up (cases 4, 13). In 12 of the patients, the clenbuterol
was purchased via the Internet for “bodybuilding” or “weight
loss.” In one patient (a 46-year-old veterinary worker), an
unintentional exposure occurred to an equine bronchodilator
Ventipulmin syrup (75 μg/mL) while he was at work.
Reported clinical effects in the thirteen cases included
tachycardia (n = 10; maximum heart rate [HR] = 118–170),
widened pulse pressure (n = 6; 65–90 mm Hg), tachypnea
(n = 3; 20–44 respirations per minute), hypokalemia (n =
3; 2.7–3.1 mEq/L), hyperglycemia (n = 3; maximum blood
glucose 159–334 mg/dL), ST changes on electrocardiogram
(ECG; n = 2), elevated troponin (n = 2; 0.86–36.3 mcg/L),
elevated creatine phosphokinase (CPK; n = 2; 256–1549
IU/L), palpitations (n = 2), chest pain (n = 3), tremor (n =
4), nausea (n = 4), and vomiting (n = 2). Coingestants are
listed in Table 1.
NPDS
From January 2007 through November 2012, a total of 426
human exposure cases of clenbuterol exposure were reported
to NPDS. However, 58 of these 462 cases involved contami-
nated heroin, 19 contaminated cocaine, and 9 cases of other
street drugs. These reported cases of drugs of abuse contam-
inated with clenbuterol primarily occurred in 2007 to 2009
and in these cases the use of clenbuterol was not intended by
the individual but was a contaminant of the heroin or cocaine.
There were 341 clenbuterol cases unrelated to drugs of abuse
(80%), reported by year in Figure 1.
Case 3
A 30-year-old male presented with tremor and tinnitus and
complains of feeling “shaky and fluttery” after ingesting
3000 μg of clenbuterol (15 mL of 200 μg/mL syrup). He
reported obtaining clenbuterol “over-the-counter” for weight
 308 SUBSTANCE ABUSE

TABLE 1
Case Summary

Ingested Peak Peak Nadir Pulse Duration of

Case Age M/F dose (μg) HR SBP DBP pressure Management effect (hours) Coingestants Other

1 46 M Drop 72 153 88 65 Observation <8 n/a

2 25 M Unknown 118 — — — Observation <8 n/a
3 30 M 3000 170 143 53 90 Fluids >24, <72 n/a
β-BlockersPotassium
replacement
4 21 M Unknown — — — — Lost to follow-up n/a n/a
5 25 M 4500 160 140 33 75 AC Fluids β-Blockers >24, <72 Proanabolic boladrol Serum
Benzodiazepines Clomiphene citrate clenbuterol:
Phreak 2.983 ng/mL
6 25 M Unknown 140 114 49 65 β-Blockers >72, <90 Liothyronine Serum T3 :
Benzodiazepines Beastdrol 7.5 pg/mL
7 19 M 1000 130 170 90 80 Odansetron <8 Levothyronine
8 2 M 100–200 165 128 57 70 Ibuprofen 24 n/a Temp: 102◦ F
9 37 M 1000 108 Observation <8 n/a
10 21 M 4000 139 Benzodiazepine <8 n/a
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11 36 M Unknown 140 Potassium <12 n/a

supplementation
Benzodiazepine
12 37 F Unknown 140 Potassium <12 n/a
supplementation
Benzodiazepine
13 28 F Unknown — — — — Lost to follow-up n/a Liothyronine

M/F = male or female; HR = heart rate; bpm = beats per minute; SBP = systolic blood pressure (mm Hg); DBP = diastolic blood pressure (mm Hg);
PP = pulse pressure (mm Hg); AC = activated charcoal; n/a = not available—no coingestants were mentioned in the history or no information available on
duration of effects in patient lost to follow-up.

loss purposes. In the emergency department 5 hours post in-
gestion, vital signs were blood pressure 126/53 mm Hg, vari-
able heart rate ranging from 126 to 170 bpm, and respiratory
rate 18 breaths per minute. He was admitted to the critical
care unit where tachycardia persisted at 127 bpm, with peak
systolic blood pressure 143 mm Hg, widened pulse pres-
sure 90 mm Hg, and maximum respiratory rate 20 breaths
per minute. Pertinent laboratory measures included potas-
sium 2.7 mEq/L and glucose 334 mg/dL. Telemetry yielded
nonspecific inferolateral ST changes; however, correspond-
ing troponin measures were insignificant (<0.03 ng/mL) ap-
proximately 8 hours after ingestion. The patient was treated

FIGURE 1 Clenbuterol exposures reported to US poison centers by year (Color figure available online).

supportively with intravenous fluids and β-blockers, and
potassium replacement. He remained tachycardic for approx-
imately 24 hours in the range of 100 bpm, but normal sinus
rhythm had been restored. Follow-up laboratory measures
included potassium 3.9 mEq/L and glucose 107 mg/dL.
Case 5
A 25-year-old male arrived in the emergency department with
a history of ingesting 4500 μg of clenbuterol (22.5 mL of
200 μg/mL syrup) approximately 45 minutes prior to arrival.
The patient admitted to “chronic use” of clenbuterol that he
obtained from the Internet. Additionally, he reported use of
proanabolic boladrol within last 2 weeks, use of a supplement
known as Phreak (Phantom Laboratories), and had recently
begun using clomiphene citrate—all of which were obtained
from the Internet. The patient was agitated, anxious with a
heart rate of 160 bpm and complained of headache. The pa-
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tient was administered a single dose of activated charcoal
and admitted to critical care services. Pertinent laboratory
measures on arrival included potassium, 2.7 mEq/L; glu-
cose, 247 mg/dL; creatine phosphokinase, 247 ng/mL; and
troponin, <0.01 ng/mL, with no evidence of abnormal cor-
responding telemetry measures. Tachycardia was managed
with an esmolol intravenous infusion titrated to maintain
systolic blood pressure (SBP) levels above 90 mm Hg. Addi-
tional therapies included potassium replacement, intravenous
fluids, benzodiazepines for agitation, and acetaminophen for
headache. Follow-up laboratory measures after 4 hours in-
cluded potassium, 3.1 mEq/L, glucose, 262 mg/dL, CPK,
195 ng/mL. Troponin levels increased to 0.02 ng/mL with
a peak of 0.86 ng/mL at 22 hours post exposure. Measured
serum clenbuterol concentration was 2.983 ng/mL. Within
3 hours of admission, SBP and heart rate (HR) decreased to
140 mm Hg and 134 bpm, respectively. Despite normaliza-
tion of SBP and HR, diastolic blood pressure continued to
decrease, rendering a peak pulse pressure of 75 mm Hg. Es-
molol infusion was continued until approximately 36 hours
post exposure and patient’s vital signs were stable within
48 hours.
Case 6
A 25-year-old male presented to emergency services with
chest pain and palpitations after ingesting an unknown quan-
tity of clenbuterol, liothyronine sodium (50 μg), and an an-
abolic agent “beastdrol” within the last 12 hours. He reported
a 4-day history of using liothyronine sodium (25 μg × 3 days,
50 μg × 1 day), but clenbuterol was recently added to his
regimen for “weight loss and fat burning.” His mother gave
additional history of a 100-pound weight loss in the patient
over the last few months due to “working out.” Upon arrival,
he was agitated with a heart rate of 140 bpm; pulse pressure
64 mm Hg; troponin 5 ng/mL; and creatine kinase 700 ng/mL.
Telemetry revealed “diffuse ST-segment changes,” but was
not deemed to be a myocardial infarction. The patient contin-
CASE STUDY 309
ued to deteriorate and had acute respiratory distress syndrome
and myocarditis within 10 hours of admission. The patient
received steroids and mechanical ventilation for adult respi-
ratory distress syndrome (ARDS). Follow-up troponin levels
were 36.3 ng/mL at 14 hours and 5.87 ng/dL at 72 hours
after initial presentation. The serum T3 measurement,
7.5 pg/mL, was consistent with use of concomitant liothyro-
nine. The patient was discharged on hospital day 4.
Case 8
A mother reported finding her normally healthy, 2-year-old
son with a “bottle of pills” she had purchased from the In-
ternet for weight loss. She reported having stopped taking
the clenbuterol after losing a pregnancy while using them
for weight loss. The dose ingested by the child was un-
known. The bottle initially contained 80 × 20-μg tablets,
with 61 tablets remaining plus a few “crushed or wet.” Based
upon the information reported, ingestion was in the range
of 100 to 200 μg (5 to 10 tablets). The child was seen in
the local emergency department and transferred to a tertiary
children’s health care facility for observation. Clinical ef-
fects reported were vomiting, fever, agitation hypokalemia
(K = 3.3 mEq/L), and tachycardia. Effects resolved by 18 to
20 hours post ingestion.
DISCUSSION
Clenbuterol is available in Europe and Latin America as
bronchodilator in humans, with a recommended dose of 20
to 40 μg orally, twice daily. In the United States, clenbuterol
is available for veterinary use only (6). However, it is the
unique β 3 -adrenergic effects of clenbuterol, unrelated to its
brochodialating effects, that has brought this drug to the at-
tention of illicit users. Research in humans and animals has
shown increased skeletal and cardiac muscle growth. In hu-
mans, doses of 60 μg, twice daily (2 μg/kg/day), were effec-
tive in producing muscle hypertrophy and increased muscle
strength (9, 13). Ranchers have abused clenbuterol in cattle
to increase lean muscle mass in their herds (14, 15). Clen-
buterol abuse in humans for muscle growth has been docu-
mented in bodybuilding and professional sports (4, 16–19).
Additionally, clenbuterol is being marketed on the Internet
as a slimming agent and has been abused/misused for weight
loss purposes (12, 18).
Intentional illicit use was the reason in 11 of the 13 re-
ported cases of clenbuterol exposure. However, these cases
represent a different paradigm to previous reports related to
clenbuterol-tainted heroin use (20–23). The Internet has fur-
ther enabled this subculture with additional routes of access
to illicit drugs in the pursuit of their bodybuilding ideals.
This population distinguishes themselves from other drug-
using populations and uses terms such as “supplements” or
“medicines” in attempt to normalize abnormal behavior (24).

310
Reference
Daubert et al., J Med
Toxicol, 2007 (4)
Hutchins et al., J Emerg
Med, 2012 (13)
Hutchins et al., J Emerg
Med, 2012 (13)
Goldstein et al, South Med
J, 1998 (29)
Kierzkowska et al., Circ J,
2005 (30)
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Summary of Published Case Reports of Clenbuterol Abuse/Misuse
Age/Gender
31/M bodybuilder
18/M bodybuilder with
history of asthma; no identified
risk factors for coronary heart
disease; nonsmoker
22/M bodybuilder with
unremarkable past medical
history; nonsmoker
26/M nonremarkable past medical
history; nonsmoker
17/M bodybuilder with
nonremarkable past medical
history
TABLE 2
Clenbuterol ingestion/coingestants
108 μg Ventipulmin syrup (72.5 μg/mL)
acquired veterinary source.
Coingestants: Tamoxifen, citrate flax
seed oil, taurine, and multivitamin
supplements
Amount of ingested clenbuterol
unknown; attempted to self-manage
symptoms with inhaled albuterol prior
to presenting to emergency services
Reported 30 mg ingestion of clenbuterol
2 hours prior to presenting to
emergency services
Amount of ingested clenbuterol
unknown
Intermittent anabolic steroid use over
last 3 years, including intramuscular
depot injections of testosterone,
propionate, cypionate, and enanthate
and oral methandrostenolone and
stanozolol
Reported finishing 2-week cycle of
taking oral clenbuterol (Spiropent:
20 mg; 1 tablet twice daily for 2 days
alternated with 2-day break)
Clinical presentation Management
Palpitations; shortness of breath 30 Atrial fibrillation persisted for
minutes post ingestion 48 hours until elective
Tachycardia, hypokalemia cardioversion to sinus rhythm
Myocardial ischemia supported by
elevated troponins and ECG revealing
supraventricular tachycardia with
ventricular rate of 254
Sudden onset of shortness of breath; Normal sinus rhythm resumed by
“heart racing” beginning 90 minutes 15 hours
prior, chest pain, N/V, tremor, and 3 months: Normal exercise
diaphoresis tolerance with no ECG
Hypokalemia, hyperglycemia abnormalities
ECG: Sinus tachycardia with T-wave
inversions, elevated troponin
ECHO: mild left ventricular hypertrophy
with normal ejection fraction (60%)
Palpitations (“heart was racing right out Resolved in less than 48 hours,
of his chest”), N/V, diaphoresis doing “well” and remaining
Initial ECG: sinus tachycardia with physically active at 1-year
evidence of inferolateral ischemia follow-up
Hypokalemia, hyperglycemia, elevated
troponin, depressed
thyroid-stimulating hormone (TSH)
Dull, central chest pain of 3-hour Reported as asymptomatic 2
duration; reported tremors, weeks after discharge
palpitations, and nervousness over last
2 weeks
Myocardial infarct indicated by ECG
ST-segment elevation and elevated
troponin; mechanism suspected to be
coronary spasm
Presented with stabbing retrosternal Chest pain and heart rate resolved
chest pain reported as intermittent over “several hours”
tachycardic, febrile, elevated One month: normal exercise test;
troponins remained asymptomatic
Final diagnosis of “reperfused non-Q MI
with possible coronary artery spasm”

These patients may not view use of clenbuterol as drug abuse
or present as the stereotype of illicit drug abusers, but may
present as healthy athletic low-risk patients. For example,
one patient in our case series rationalized illegal use of clen-
buterol “to get buff” rather than for recreational purposes.
This trend is not limited to bodybuilders and extreme fitness
enthusiasts. An Internet search of “clenbuterol” will generate
numerous advertisements disguised as “educational informa-
tion” (25). Cases 3, 6, and 13 and the mother of case 8 had all
obtained the clenbuterol for weight loss purposes rather than
muscle building and may illustrate an emerging trend with
the mainstream public. The cases presented in this report and
the published reports involved healthy and fit individuals un-
der age 30 years (Table 2). However, this should not preclude
the possibility of encountering cases involving older adults,
particularly females. It would not be unreasonable to surmise
that any target of weight loss marketing with Internet access
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is susceptible to the appeal of clenbuterol. Although a major-
ity of the literature on clenbuterol overdose involves tainted
drugs of abuse, the majority of cases reported to poison cen-
ters do not involve street drugs.
These individuals abusing clenbuterol may overestimate
their “knowledge,” which is often acquired anecdotally with-
out full understanding of risks. Additionally frequent coad-
ministration of additional agents such as anabolic steroids or
thyroid hormones adds to the risk of serious cardiotoxicity.
Two patients reported in our case series were concomitantly
abusing agents including anabolic steroids, estrogen antago-
nists, liothyronine, caffeine, as well as alcoholic beverages.
The reported doses used among these patients significantly
exceed the therapeutic range of 20 to 40 μg twice daily indi-
cated for asthma; in several of our cases exceeding the dose
by several orders of magnitude (26). One patient had a blood
clenbuterol level of 2.983 ng/mL following the ingestion of
an estimated 4500 μg, which is approximately 100 times the
recommended dose. This serum concentration is in the range
reported from patients with clenbuterol-contaminated heroin.
In a report of clenbuterol in heroin deaths, postmortem blood
clenbuterol levels ranged from 6.3 to 76 ng/mL (22). In a se-
ries of clenbuterol-contaminated heroin, serum clenbuterol
levels were reported in 2 patients: 2.4 and 6 ng/mL, respec-
tively (23).
Clinical effects from clenbuterol were primarily cardio-
vascular and persisted greater than 24 hours in the 3 patients
requiring inpatient management. One patient sustained elec-
trocardiograph conduction disturbances within 3 hours of
ingesting 3000 μg of clenbuterol alone. Two patients in-
gesting clenbuterol with other agents presented with evi-
dence of myocardial injury. Clenbuterol toxicity can include
supraventricular tachycardia, pulmonary edema, myocardial
infarction, elevated troponin and CPK-Mb, ECG changes
including ST-wave changes, chest pain, palpitations, wide
pulse pressure, muscle spasm, hyperreflexia, elevated CPK,
rhabdomyolysis, headache, anxiety, agitation, vomiting, hy-
CASE STUDY 311
pokalemia, and mydriasis (4, 21, 23, 27–29). These clini-
cal effects, including myocardial injury and infarction, have
occurred in otherwise healthy patients with normal coro-
nary arteriograms (28, 29). Several possible mechanisms for
the ischemic injury have been suggested, including coronary
artery vasospasm, microvascular endothelial injury, and de-
mand ischemia due to prolonged metabolic demand on the
myocardium (13, 28, 29). Given that clenbuterol use is ex-
tending into the mainstream public, index of suspicion should
not be solely limited to those with extreme bodybuilding ap-
pearances. Patients and families are often poor historians
unable to give an accurate medication history. Thus, when
obtaining medication histories, it is important to ascertain all
medication use, including “natural” substances and “training
aids.”
Treatment for clenbuterol toxicity has not been clearly
defined. Additionally, use of anabolic steroid and thyroid
hormone complicates diagnosis and management due to an
independent risk of myocyte toxicity, ventricular arrhyth-
mias, myocardial infarction, and cardiomyopathy (29). Man-
agement decisions should be individualized to the patient.
In general, goals of management include stabilizing vital
signs (hypertension, tachycardia) and symptomatic treat-
ment of anxiety, tremor, or agitation. These goals may be
met through a combination of intravenous (IV) fluids, oxy-
gen, β-antagonists, and benzodiazepines. In cases of car-
diac ischemia, aspirin may be warranted. Treatment with
β-antagonists (esmolol, metoprolol, labetalol) proved suc-
cessful in our cases and in published reports and is recom-
mended for patients with persistent tachycardia and hyper-
tension (4, 13, 23, 30, 31). Hypokalemia is frequently present
due to the β 2 -agonist–induced intracellular shift of potassium
and replacement therapy is generally not required.
These cases illustrate the hidden dangers of clenbuterol
abuse among bodybuilders, fitness enthusiasts, and those
seeking a drug for weight loss. These patients do not fit
the prototype of a narcotic or amphetamine abuser and may
present as “fit and healthy.” An increasing number of patients
who are abusing clenbuterol are presenting to emergency de-
partments with adverse or overdose effects.
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