CASE REPORT
Severe Cholestasis and Renal Failure Associated with the Use ofthe Designer Steroid SuperdrolTM (MethasteronTM): A Case Reportand Literature Review
John Nasr Æ 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 sug-
gest 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 steroid-
methasteronTM 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
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 Su-
perdrolTM 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 dem-
onstrated 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 0.3–1.5), an AST of
63 IU/l (normal 10–40), ALT of 98 IU/l (normal 10–40),
alkaline phosphatase of 353 IU/l (normal 40–125), and
total protein of 8.1 g/dl (normal 6.3–7.7). 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, hepa-
titis 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 anti-
LKM antibodies were normal. Electrolytes were normal
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: [email protected]
123
Dig Dis Sci (2009) 54:1144–1146
DOI 10.1007/s10620-008-0457-x
but his creatinine was elevated at 3.6 mg/dl (normal 0.5–
1.4) and his BUN was 43 mg/dl (normal 5–20). Urinal-
ysis showed bland urine sediment without red cells or
casts and a 24-hour urine collection was significant for
1,005 mg protein (normal 42–225). Ultrasound demon-
strated 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 pru-
ritus. 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 activ-
ity 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
patient’s pruritus had significantly improved with nor-
malization 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.
Discussion
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 seri-
ous health risk [6]. AAS are synthetic derivatives of
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)
Fig. 2 Liver biopsy showing panlobular hepatocanalicular cholesta-
sis with formation of inspissated canalicular bile plugs (arrows ).
(Hematoxylin and Eosin, 9400)
0
5
10
15
20
25
30
35
40
45
0 1 3 10 14 21 28 42 49 63 77 91 112
Days after initial presentation
To
tal b
iliru
bin
(m
g/d
l)
Fig. 3 Graph demonstrating trend in total bilirubin over time
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
0 1 3 10 21 42
Days after initial presentation
Ser
um
cre
atin
ine
(mg
/dl)
77492814
Fig. 4 Graph demonstrating trend in serum creatinine over time
Dig Dis Sci (2009) 54:1144–1146 1145
123
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 hematolog-
ical conditions such as aplastic anemia [7–9]. However,
when used for athletic performance, the doses used can be
far in excess of normal physiologic levels and this pre-
sumably 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, 11–13].
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 empiri-
cally 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 10–12 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 sedi-
ment 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 meth-
asteronTM (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 high-
lights the potential hepatotoxicity and renal toxicity of these
agents but numerous other effects including psychological
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.
References
1. Parkinson AB, Evans NA. Anabolic androgenic steroids: a survey
of 500 users. Med Sci Sports Exerc. 2006;38:644–651. doi:
10.1249/01.mss.0000210194.56834.5d.
2. Handelsman DJ, Gupta L. Prevalence and risk factors for ana-
bolic-androgenic steroid abuse in Australian high school students.
Int J Androl. 1997;20:159–164. doi:10.1046/j.1365-2605.1997.
d01-285.x.
3. Stimac D, Milic S, Dintinjana RD, Kovac D, Ristic S. Androgenic/
anabolic steroid-induced toxic hepatitis. J Clin Gastroenterol.2002;35:350–352. doi:10.1097/00004836-200210000-00013.
4. Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in
athletes. Sports Med. 2004;34:513–554. doi:10.2165/00007256-
200434080-00003.
5. Jasiurkowski B, Raj J, Wisinger D, Carlson R, Zou L, Nadir A.
Cholestatic jaundice and IgA nephropathy induced by OTC
muscle building agent superdrol. Am J Gastroenterol. 2006;101:
2659–2662.
6. Maravelias C, Dona A, Stefanidou M, et al. Adverse effects of
anabolic steroids in athletes. A constant threat. Toxicol Lett.2005;158:167–175. doi:10.1016/j.toxlet.2005.06.005.
7. Sanchez-Osorio M, Duarte-Rojo A, Martinez-Benitez B, Torre A,
Uribe M. Anabolic-androgenic steroids and liver injury. Liver Int.
2007; Epub ahead of print.
8. Orr R, Fiatorone Singh M. The anabolic androgenic steroid
oxandrolone in the treatment of wasting and catabolic disorders:
review of efficacy and safety. Drugs. 2004;64:725–750. doi:
10.2165/00003495-200464070-00004.
9. Murphy KD, Thomas S, Mlcak RP, Chinkes DL, Klein GL,
Herndon DN. Effects of long-term oxandrolone administration in
severely burned children. Surgery. 2004;136:219–224. doi:
10.1016/j.surg.2004.04.022.
10. Hall RC, Hall RC. Abuse of supraphysiologic doses of anabolic
steroids. South Med J. 2005;98:550–555. doi:10.1097/01.SMJ.
0000157531.04472.B2.
11. Bagheri SA, Boyer JL. Peliosis hepatis associated with andro-
genic-anabolic steroid therapy. A severe form of hepatic injury.
Ann Intern Med. 1974;81:610–618.
12. Socas L, Zumbado M, Perez-Luzardo O, Ramos A, Perez C,
Hernandez JR. Hepatocellular adenomas associated with anabolic
androgenic steroid abuse in bodybuilders: a report of two cases
and a review of the literature. Br J Sports Med. 2005;39:e27. doi:
10.1136/bjsm.2004.013599.
13. Carrasco D, Prieto M, Pallardo L, et al. Multiple hepatic adenomas
after long-term therapy with testosterone enanthate. Review of the
literature. J Hepatol. 1985;1:573–578. doi:10.1016/S0168-8278
(85)80001-5.
14. Gurakar A, Caraceni P, Fagiuoli S, Van Thiel DH. Androgenic/
anabolic steroid-induced cholestasis: a review with four addi-
tional case reports. J Okla State Med Assoc. 1994;87:399–404.
15. http://www.worldclassnutrition.com/superdrol.html.
16. Bonetti A, Tirelli F, Catapano A, Dazzi D, Dei Cas A, Solito F,
et al. Side effects of anabolic androgenic steroids abuse. Int JSports Med. 2007; Epub ahead of print.
1146 Dig Dis Sci (2009) 54:1144–1146
123
Top Related