Dig Dis Sci (2009) 54:11441146

DOI 10.1007/s10620-008-0457-x

CASE REPORT

Severe Cholestasis and Renal Failure Associated with the Use of

the Designer Steroid SuperdrolTM (MethasteronTM): A Case Report
and Literature Review
John Nasr Jawad Ahmad

Received: 28 November 2007 / Accepted: 16 July 2008 / Published online: 22 August 2008
Springer Science+Business Media, LLC 2008

Abbreviations
AAS Androgenic/anabolic steroids
OTC Over the counter

Introduction
The use of over the counter (OTC) nutritional supplements
is widespread among amateur bodybuilders. Reports suggest that up to 30% of people who train regularly with
weights use androgenic/anabolic steroids (AAS) and that a
significant percentage of male high school students use
AAS, not just for muscle gain but also to improve their
physical appearance [1, 2]. The use of AAS is associated
with a variety of potential liver injuries including toxic
hepatitis and cholestasis [3, 4] but is often under-reported
because of its clandestine use. Renal toxicity with the use
of AAS has recently been demonstrated, which was
thought to be related to IgA nephropathy [5]. We report a
case of liver and renal injury secondary to a nutritional
supplement called SuperdrolTM, with the anabolic steroidmethasteronTM as its active ingredient.

Case Report
A 42-year-old Caucasian male with no known past medical
history presented with a 4-week history of jaundice, diffuse
J. Nasr
Department of Internal Medicine, University of Pittsburgh,
Pittsburgh, PA 15213, USA
J. Ahmad (&)
Division of Gastroenterology, Hepatology & Nutrition,
University of Pittsburgh, Pittsburgh, PA 15213, USA
e-mail: ahmadj@msx.upmc.edu

123

pruritus, and dark urine with a 20-pound weight loss.

Approximately 7 weeks prior to the onset of his symptoms,
the patient had started using a nutritional supplement for
bodybuilders called SuperdrolTM. He consumed 100 tablets
of SuperdrolTM, taking two tablets each day. He did not
exceed the maximal suggested dose of 126 tablets. Four
days after he stopped the SuperdrolTM, the patient noticed
scleral icterus and jaundice. Three days later, he started
experiencing diffuse pruritus. There was no history of
alcohol, recreational drugs, or tobacco use, and no family
history of liver or kidney disease. There was no prior history
of nutritional supplement use prior to this course of SuperdrolTM although he was taking multivitamin and protein
milkshakes. He was not taking any prescription medication.
Upon physical examination, his vital signs were stable.
He had scleral icterus and jaundice but no other stigmata of
chronic liver disease. His cardiovascular and respiratory
systems were normal. His abdominal examination demonstrated a soft, non-tender abdomen without evidence of
ascites or hepatosplenomegaly.
At presentation, laboratory parameters revealed a total
bilirubin of 41.2 mg/dl (normal 0.31.5), an AST of
63 IU/l (normal 1040), ALT of 98 IU/l (normal 1040),
alkaline phosphatase of 353 IU/l (normal 40125), and
total protein of 8.1 g/dl (normal 6.37.7). Serology for
viral hepatitis was essentially negative including hepatitis
A-IgM antibody, hepatitis B core-IgM antibody, hepatitis
B surface antigen, hepatitis B core-IgG antibody, hepatitis C antibody, as well as hepatitis C RNA, and hepatitis
B DNA by polymerase chain reaction. His hepatitis B
surface antibody was positive at a high titer from prior
vaccination. Hemoglobin, white cell count, and platelets
were normal. Serum ceruloplasmin and serum alpha-1
antitrypsin levels, smooth muscle, antinuclear, and antiLKM antibodies were normal. Electrolytes were normal

Dig Dis Sci (2009) 54:11441146

Fig. 2 Liver biopsy showing panlobular hepatocanalicular cholestasis with formation of inspissated canalicular bile plugs (arrows ).
(Hematoxylin and Eosin, 9400)
45
40

Total bilirubin (mg/dl)

but his creatinine was elevated at 3.6 mg/dl (normal 0.5

1.4) and his BUN was 43 mg/dl (normal 520). Urinalysis showed bland urine sediment without red cells or
casts and a 24-hour urine collection was significant for
1,005 mg protein (normal 42225). Ultrasound demonstrated no renal obstruction with bilateral echogenic
kidneys. MRI showed a normal liver and biliary tree. A
presumptive diagnosis of drug-induced liver and kidney
injury was made. The patient was admitted for 4 days
and discharged on oral ursodeoxycholic acid at 600 mg
twice daily and hydroxyzine 25 mg as required for pruritus. Upon discharge, the patient had a bilirubin of
42.1 mg/dl and creatinine of 4.2 mg/dl.
The patient was readmitted a second time a week later
for intractable pruritus and was discharged on naltrexone.
At that time, his creatinine had fallen to 2.3 mg/dl and
bilirubin 34.3 g/dl. After a month, the patient remained
jaundiced with minimal improvement in his bilirubin
and cholestatic liver enzymes but his renal function had
essentially normalized. A liver biopsy was performed
demonstrating hepatocyte regeneration and lobular activity with marked hepatocanalicular cholestasis, bile
ductular reaction with neutrophilic cholangiolitis and
focal early bridging fibrosis suggestive of a drug-induced
cholestatic injury (Figs. 1, 2). Two weeks later, the
patients pruritus had significantly improved with normalization of his kidney function and bilirubin had
improved to 8 mg/dl with a normal alkaline phosphatase.
There was continued gradual improvement and 4 months
after his initial presentation his bilirubin normalized.
Figures 3 and 4 demonstrate the trends in his bilirubin
and creatinine.

1145

35
30
25
20
15
10
5
0
0

10

14

21

28

42

49

63

77

91

112

Days after initial presentation

Fig. 3 Graph demonstrating trend in total bilirubin over time

Serum creatinine (mg/dl)

4.5
4
3.5
3
2.5
2
1.5
1
0.5
0
0

10

14

21

28

42

49

77

Days after initial presentation

Fig. 4 Graph demonstrating trend in serum creatinine over time

Discussion

Fig. 1 Liver biopsy showing irregular fibrous expansion of portal

tracts with mild inflammatory infiltrate and bile ductular reaction. The
inflammatory infiltrate is composed of lymphocytes and some
neutrophils (Hematoxylin and Eosin, 9200)

Self-administration of AAS to increase muscular strength

and lean body mass is a widespread practice, even though
the indiscriminate use of such drugs may constitute a serious health risk [6]. AAS are synthetic derivatives of

123

1146

testosterone that can be chemically altered to enhance either

anabolic or androgenic effects. When used in therapeutic
doses they have been used to treat testicular failure, wasting
syndromes, victims of severe burns, and some hematological conditions such as aplastic anemia [79]. However,
when used for athletic performance, the doses used can be
far in excess of normal physiologic levels and this presumably explains the increase in toxic effects [10]. The
hepatotoxicity of AAS typically manifests as cholestasis but
predominant hepatocellular injury, peliosis hepatis and
hepatic adenomas have also been reported [3, 7, 1113].
The liver biopsy in the current case was characteristic of the
usual type of injury seen with AAS with mild lobular
inflammation but marked canalicular cholestasis. The
mechanism of liver injury is unclear but recovery after
cessation of therapy almost always occurs [14].
The patient was started on ursodeoxycholic acid empirically because of the degree of cholestasis and we doubt
whether this accelerated the improvement in his bilirubin.
The rapid drop in bilirubin after day 28 may reflect the
improvement in renal function and hence enhanced bilirubin
excretion. The 1012 weeks that elapsed for normalization
of his bilirubin is consistent with other reports of the length of
time necessary for spontaneous resolution of AAS associated
liver injury.
Renal toxicity with AAS has only been reported once
previously [5] and was associated with changes of IgA
nephropathy on kidney biopsy. We did not biopsy our
patient as his renal function improved spontaneously in 10
14 days after his initial presentation, and the urine sediment did not reveal hematuria. Presumably, the cause of
renal dysfunction was drug-related.
SuperdrolTM is an over the counter (OTC) nutritional
supplement that is available freely over the Internet from a
variety of different distributors. Its active ingredient is methasteronTM (2a-17a0dimethyl-5a-androst-3-one), which is
advertised as definitely not a prohormone: it is a very active
form of a designer supplement that is also highly anabolic.
[15]. Most suppliers mention minimal side effects, and give
testimonials from users that describe muscle gain and very few
side-effects. The standard Food and Drug Administration
(FDA) label for supplements is used on Internet sites: The
products and the claims made about specific products on or
through this site have not been evaluated by the FDA. They are
not approved to diagnose, treat, cure or prevent disease. The
information provided on this site is for informational purposes
only and is not intended as a substitute for advice from your
physician or other health care professional or any information
contained on or in any product label or packaging. Despite
this warning, AAS continue to be used by amateur weight
trainers and particularly adolescents [1, 2]. This case highlights the potential hepatotoxicity and renal toxicity of these
agents but numerous other effects including psychological

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Dig Dis Sci (2009) 54:11441146

changes, decreased sperm count, and adverse lipid profiles

have been seen [16]. The lack of federal regulation of OTC
nutritional supplements means that physicians need to be
vigilant in suspecting the use of AAS, particularly in young
male patients presenting with unexplained elevated liver
injury tests and even renal dysfunction.

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