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: ahmadj@msx.upmc.edu

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

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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.

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