Clinical Toxicology

ISSN: 1556-3650 (Print) 1556-9519 (Online) Journal homepage: http://www.tandfonline.com/loi/ictx20

Acute pancreatitis secondary to the use of the

anabolic steroid trenbolone acetate

Vidhya Kumar, Danny Issa, George Smallfield & Doumit Bouhaidar

To cite this article: Vidhya Kumar, Danny Issa, George Smallfield & Doumit Bouhaidar (2018):
Acute pancreatitis secondary to the use of the anabolic steroid trenbolone acetate, Clinical
Toxicology, DOI: 10.1080/15563650.2018.1491983

To link to this article: https://doi.org/10.1080/15563650.2018.1491983

Published online: 12 Aug 2018.

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CLINICAL TOXICOLOGY
https://doi.org/10.1080/15563650.2018.1491983

TEACHING CASE

Acute pancreatitis secondary to the use of the anabolic steroid

trenbolone acetate
Vidhya Kumara, Danny Issab, George Smallfieldb and Doumit Bouhaidarb
a
Virginia Commonwealth University School of Medicine, Richmond, VA, USA; bDivision of Gastroenterology, Hepatology and Nutrition,
Virginia Commonwealth University, Richmond, VA, USA

ABSTRACT ARTICLE HISTORY

Background: The use of performance-enhancing drugs has increased dramatically in the last decade Received 16 March 2018
with high prevalence reported among the young athlete population. Many of these drugs contain ana- Revised 14 June 2018
bolic steroids and may carry potential significant side effects and health risks. We report a case of ana- Accepted 18 June 2018
bolic steroid-induced acute pancreatitis (AP) that recurred after the reuse of the same drug by the
KEYWORDS
patient, confirming the causative relationship. Acute pancreatitis; anabolic
Case report: A 24 year-old male presented with severe epigastric pain. His past medical history was steroids; drug-induced
significant for two hospitalizations during the last year with AP. During his hospital admissions, exten- pancreatitis; trenbo-
sive workup was performed ruling out the common and uncommon causes of AP. Upon further press- lone acetate
ing, the patient admitted to a history of past and current anabolic steroid use for athletic performance
enhancement. He began this use four years ago and most recently started using trenbolone acetate
(TA). The correlation between the timing of the anabolic steroids administration and the attacks of AP,
along with ruling out other causes, confirmed TA as the cause of pancreatitis.
Discussion: The side effects associated with the use of these increasingly prevalent drugs are difficult
to study in clinical trials due to the unethical nature of their consumption. In addition, these medica-
tions are difficult to study due to the varied usage cycles and patterns, unknown origin and source, as
well as often high dose ingestion. Physicians and body builders need to be aware of the possible ser-
ious consequences of their use.

Background bodybuilder community for muscle growth. Supply of anabolic

steroids are easily found on online sources without a prescrip-
Acute pancreatitis (AP) is the third most common inpatient
tion [8] and supplied by unregulated international pharmacies
gastrointestinal diagnosis and a serious medical problem
with disclaimers that consumers are subject to local laws. In
that can lead to significant morbidity and mortality [1]. The
addition to online access, many athletes have obtained the
etiology of AP ranges from gallstones and excessive alcohol
steroids from friends, gym members or training partners
use, which represents approximately 70% of cases, to less
[9,10]. Our patient was a 24-year-old male who presented
common causes such as trauma, hypercalcemia, hypertrigly-
with AP. He had suffered three previous episodes of recurrent
ceridemia, autoimmune, post-ERCP and drugs [2–4].
Drug-induced pancreatitis (DIP) is rare, with a reported inci- AP following administration of TA - the re-challenge resulting
dence of 0.1–2% of all causes of AP [5]. The mechanism of in AP each time. Other case reports link anabolic steroids to
injury is dependent on the medication-specific characteristics AP [10,11], such as a case involving androgenic anabolic ste-
and not completely understood. The diagnosis of DIP, such as roids such as “Guerilla Warfare” which contains Trenaavar,
other medication-induced conditions, is almost always clinic- Promagnon and Ment Dione, and an additional case with
ally based and difficult to confirm [6]. This is particularly the chronic use of methandrostenolone (Dianabol). Treatment in
case when the origin of DIP is unknown and linked to illicit both of these cases consisted of supportive care, including
drugs. Excluding all other causes of pancreatitis implies the intravenous fluid resuscitation, appropriate pain management,
diagnosis of DIP. Causality assessment scales can be used to and pancreatic rest with slow introduction of oral nutri-
categorize the strength of the relationship between the tion [10,11].
adverse event and the medication. When re-challenge with
the drug causes a similar clinical picture, diagnosis is affirmed.
Case presentation
We report a case of AP induced by an anabolic steroid,
trenbolone acetate (TA). TA is licensed in the United States as A 24-year-old male police officer with past medical history of
a growth promoter in the live stock industry [7], but not anxiety and depression presented to the emergency room
licensed for human use and is frequently used illegally in the with severe epigastric and right upper quadrant abdominal

CONTACT Danny Issa [email protected] Gastroenterology and Hepatology, MCV Box 980341, Richmond, VA 23298-0341, USA
Senior author
ß 2018 Informa UK Limited, trading as Taylor & Francis Group
2 V. KUMAR ET AL.

pain. The patient had previously felt well until five months hypertriglyceridemia, hypercalcemia, toxins, trauma, infec-
ago. He initially presented to an outside hospital emergency tions, autoimmune conditions and medications [13,14]. Drug-
department where his lipase was elevated to >3000 units/L induced pancreatitis is rare, although a multitude of drugs
(normal range 73–393 units/L). Otherwise, his laboratory have been implicated in cases of AP. Previously documented
evaluation was unremarkable including a normal alanine associations of drug-induced AP include thiazides, Vinca alka-
transaminase (ALT) at 31 (normal range 12–78), aspartate loids, didanosine, azathioprine and others [13].
transaminase (AST) at 18 (normal range 15–27) and alkaline The use of performance-enhancing drugs (PED) has
phosphatase at 41 units/L. The patient denied any recent increased dramatically in the US within the last decade with
alcohol consumption or binge-drinking episodes in the past high prevalence reported among the young and athlete
two years. Serum alcohol on admission at the outside institu- population. This abuse is estimated to comprise 1% of the
tion was undetectable (<10 mg/dL). The patient was man- American male population [15]. PED use is increasing among
aged conservatively and discharged home. amateur body builders, becoming widely accessible through
He returned to the outside institution for recurrent intract- the internet and local body building facilities [16]. Many PED
able abdominal pain two weeks later and underwent a more contain anabolic steroids and may carry potential significant
extensive evaluation. Magnetic resonance cholangiopancreatog- side effects. Along with the desired effects of increased
raphy (MRCP) and computerized tomography (CT) of abdomen muscle mass, multiple adverse events have been docu-
and pelvis did not demonstrate bile duct dilatation, evidence of mented including testicular atrophy, gynecomastia, acne,
choledocolithiasis or pancreas divisum. Endoscopic ultrasound liver injury, kidney dysfunction [17], as well as myocardial
showed minimal stranding and diffuse mild enlargement of the infarction [18,19] (Table 1). Our case presents AP as another
pancreatic head, biliary sludge, and non-dilated common bile potential side effect of anabolic steroids use, specifically the
duct with no filling defect. HIDA scan revealed benign biliary product TA. The mechanism of this complication is unknown.
sludge. Eventually, ERCP with sphincterotomy and biliary stent- The assessment of causality is of particular significance
ing was performed, after which the patient underwent a chole- when reporting new adverse drug reactions (ADR). Multiple
cystectomy for the benign biliary sludge. tools have been developed to aid in this assessment. The
The patient was admitted to our institution for the first WHO causality assessment system lays important weight on
time (sixth overall admission) with recurrent severe epigastric positive re-challenge information in order to consider a drug
pain. His physical exam revealed an athletic male with epigas- “certain”; as opposed to other categories of probable/likely,
tric tenderness to palpation. Known causes of AP were again possible, unlikely and conditional/unclassified. Naranjo ADR
excluded as extensive workup was unrevealing, including nor- probability scale is one of the most widely used causality
mal triglycerides, IgG4 levels, HIV, cystic fibrosis screen and assessment tools, which consists of a simple 10-item ques-
repeat MRI/MRCP imaging. Subsequently, the patient admitted tionnaire and classifies the event into similar categories used
to past and current anabolic steroid use for athletic perform- in the WHO system [21]. More recently developed scales,
ance enhancement. He began this use four years ago during such as the Liverpool Causality Assessment Tool (LCAT), use
college and he experimented with multiple steroids over this similar concepts of timing, de-challenge, plausibility and re-
four year course, including Winstrol (Stanozolol), challenge and may offer better inter-rater reliability [22].
DecaDurabolic (NandroloneDecanoate), Equipose and New tools have been developed to assess for causality in the
Methyltrienolone (MT). Most recently and prior to his initial case of new fatal psychoactive substances use. The toxicol-
presentation, he self-reported starting to use TA, a very potent ogy significance score (TSS), described by Elliott et al., helps
anabolic steroid, which the patient referred to as “the most experienced toxicologists to classify suspected psychoactive
powerful steroid out there”, and reported acquiring TA from
substance fatalities into four groups of significance: low,
the internet, and injecting at his local gym. He stopped taking
medium, high and unclassified [23]. As for our patient, the
this drug during hospitalizations but restarted it shortly after-
wards and increased the doses to 400 mcg/week injection Table 1. Potential adverse events to the use of anabolic steroids (Snyder
until he developed symptoms of AP again. Confirmatory drug 2018) [20].
analysis was not available at the institution and attempts to Cardiovascular
secure the patient’s supply of TA were unsuccessful. He Coronary heart disease, myocardial infarction, cardiomyopathy, hemostasis/
coagulation abnormalities, dyslipidemia, hypertension
denied use of additional dietary supplements as a part of his Infection (as a result of unsafe injecting practices)
regimen. The correlation between the timing of steroids HIV, hepatitis B and C, MRSA
administration and the clinical attacks, along with excluding Contaminated products, including medications and illicit drugs
Musculoskeletal
other causes, confirms TA as the cause of his pancreatitis by Tendon rupture
the World Health Organization (WHO) classification [12]. His Neuropsychiatric
condition resolved with conservative management and with- Major mood disorders, aggression, violence, dependence
Men (reproductive)
drawal of drugs. Hypogonadism (following withdrawal), gynecomastia, acne,
prostate cancer
Women (reproductive)
Discussion Acne, virilization including hirsutism, deepening of voice, and clitoromegaly,
irregular menses
The most common causes for AP in adults are cholelithiasis Hepatic (with oral 17-alpha-alkylated androgens)
Cholestasis, peliosis hepatis, hepatic neoplasms
and excessive alcohol intake, but other etiologies include
 CLINICAL TOXICOLOGY 3

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