60 Clinical Sciences

Multi-Organ Dysfunction in Bodybuilding Possibly

Caused by Prolonged Hypercalcemia due to Multi-
Substance Abuse: Case Report and Review of
Literature

Authors C. N. Schäfer1, H. Guldager1, H. L. Jørgensen2

1
Affiliations Hospital Zealand South/Nykøbing F Hospital, Department of Anesthesiology, Nykøbing F, Denmark
2
Bispebjerg Hospital, Department of Clinical Biochemistry, København, Denmark

Key words Abstract the patient developed signs of multi-organ dys-

●▶ bodybuilding ▼ function, including pancreatitis, hemorrhagic

Downloaded by: East Carolina University. Copyrighted material.

●▶ substance abuse
A 26-year-old male bodybuilder was admitted to gastritis, nephropathy with temporary anuria,
●▶ site-enhancement oils
the surgical department of a Danish community and respiratory insufficiency, and was trans-
●▶ anabolic steroids
hospital for hematemesis. During the clinical ferred to the ICU. After manometric monitor-
●▶ hypervitaminosis

●▶ vitamin D interview, he revealed that he had recently fin- ing on the patient’s upper arms proved difficult,
●▶ vitamin A ished a course of anabolic steroids and erythro- invasive blood pressure monitoring was used
●▶ erythropoietin poietin. The patient also had a previous history and revealed that the patient was in a state of
●▶ hypercalcemia of infections and chronic ulcers due to paraf- hypertensive crisis. This case of multi-organ
●▶ pancreatitis
fin-oil injections in both upper arms one year dysfunction was possibly caused by multi-sub-
●▶ nephropathy
before. Over the course of the next few hours, stance-induced hypercalcemia.
●▶ hypertension

Introduction metabolism in relation to anabolic steroid con-

accepted after revision
September 06, 2010
Bibliography
DOI http://dx.doi.org/
10.1055/s-0030-1267200
Published online:
November 11, 2010
Int J Sports Med 2011; 32:
60–65 © Georg Thieme
Verlag KG Stuttgart · New York
ISSN 0172-4622
Correspondence
Christopher Niels Schäfer
Hospital Zealand South
Department of Anesthesiology
Nykøbing F Hospital
4800 Nykøbing F
Denmark
Tel.: + 45/22/77 59 77
Fax: + 45/56/51 57 61
schaefer@dadlnet.dk
▼ sumption [8, 18]. In addition, anabolic steroids
The increasing tendency towards poly-pharma-
cological abuse in bodybuilding makes it chal-
lenging to provide timely treatment and diagnosis
of the medical emergencies that are related to
the bodybuilder subculture. Bodybuilding
patients are often reluctant to seek medical sup-
port for various late and end-stage conditions
because they fear legal sanctions. In addition,
these types of patients only reveal part of their
long history of multi-substance abuse [22], which
might contain several anabolic steroids and a
wide range of illegally provided and produced
supplemental drugs and substances, including
other anabolic hormones, antiestrogens, pain-
killers, anti-inflammatory drugs, high-dose vita-
mins, and food-supplements with additives of
unknown quality and origin.
The majority of the current knowledge concern-
ing anabolic steroid abuse has come from case
reports and investigations of low evidence,
although an increased mortality is documented
[32]. Reports on the side effects of anabolic ster-
oids are controversial [17, 39], and some of these
effects are thought to be reversible [42]. Several
investigations have reported adverse liver condi-
tions [33], parenchymal, even malignant abnor-
malities, and changes in lipid and glucose
have been associated with cardiac hypertrophy/
decompensation [34] and arrhythmias [3].
Hypertension that affects the vascular endothe-
lium [36] and the adrenal glands [28] is a com-
mon side effect of anabolic steroid abuse, in
addition to erythropoiesis, which increases the
risk of cardiac and cerebral thrombo-embolic
events.
The renal disturbances typically observed in the
bodybuilding subculture are reported to range
from habitually elevated creatinine levels to seri-
ous renal impairment and failure [16, 28] and
have been explained by exertional rhabdomyoly-
sis [38] or the intake of food supplements, such
as creatine, vitamin A, D and even anabolic ster-
oids [19, 24, 30, 40].
We speculate whether the possible link between
many of these side effects might be the influence
of androgen steroids, vitamin A, vitamin D, and
supplemental calcium on calcium homeostasis
resulting in both intra and extracellular hyper-
calcemia [6]. We base our calcium hypothesis on
several experimental studies employing cell cul-
tures, which have shown that anabolic steroids
increase calcium intracellular transport and cal-
cium concentration [13, 14]. Observational stud-
ies of weightlifters have demonstrated that

Schäfer CN et al. Multi-Organ Dysfunction in Bodybuilding Possibly … Int J Sports Med 2011; 32: 60–65

androgens can cause an access build up of calcium in bone and
muscle tissue due to bone matrix augmentation [25, 29] and
muscular fibre hypertrophy. Whereas the excessive intake of
vitamin D and calcium in bodybuilder subculture does not need
to be discussed, excessive vitamin A ingestion can cause hyper-
calcemia due to an overweight of bone resorption by increasing
osteoclastic activity and impairing osteogenesis, showing char-
acteristic symptoms of bone pain and tenderness and also results
in osteomalaci, cortical thickening, periostal calcification, and
osteoporosis [11]. The most frequent cause is intended or acci-
dental intake of high-doses of vitamin A from nutritional sup-
plements [1]. But bodybuilders might also be treated with
retinoic acids, which are vitamin A derivatives, for anabolic ster-
oid-induced acne [2]. Furthermore hypercalcemia might be
aggravated by a preexisting unknown renal insufficiency [7].
Case Report
▼ forced diuresis. On day 4, the patient was transferred to the ICU
A 26-year-old bodybuilder was admitted to the surgical depart-
ment of a Danish community hospital for hematemesis and
abdominal pain, which prevented all oral intake for 3 days. The
patient remembered a slow onset of the aforementioned condi-
tions over several days and had also suffered from chronic reflux
and pyrosis for several months prior to admission. In addition,
the patient had taken 2 annual injection-cycles of oxymeth-
olone, DECA, testosterone, epitestosterone, and erythropoietin.
The patient denied the intake of other substances but had an
oral intake of up to 7 liters of water per day. The patient was
under the impression that anabolic steroids retained fluid in the
body; however, he exhibited diuresis with nocturia (7–10 times
per night). The patient had no other complaints concerning his
health but had contacted the surgical department of a nearby
community hospital twice; once for an infection of the right
thigh caused by steroid injections and once for perforating skin
necrosis on both upper arms caused by intramuscular injections
of paraffin oil, which had been terminated 1 year before
(●▶ Fig. 1).
Fig. 1 This Magnetic Resonance scan was conducted when the patient
was treated for the complications associated with his oil injections [MR
Siemens Avanto, 1.5 Tesla, axial T1-weighted TSE sequences (TS 8 mm,
TR 796 msecs)]. This scan depicts multiple variable-sized areas in the
sub cutis, biceps, and triceps musculature that are consistent with a
greasy material, which could possibly be paraffin. Thickened subcutane-
ous retinacula indicate reactive fibrous changes, which also include the
neurovascular bundle.
Schäfer CN et al. Multi-Organ Dysfunction in Bodybuilding Possibly … Int J Sports Med 2011; 32: 60–65
Clinical Sciences 61
The arterial puncture of the patient drawn on admission showed
a compensated metabolic lactic acidosis pH of 7.36 (7.35–7.45)
and an se-lactate level of 3.7 mmol/L (0.5–1.6 mmol/L). The
patient also exhibited an elevated lactate dehydrogenase, a total
calcium, an ionized calium and a pancreatic amylase, which pos-
sibly indicated hypercalcemia-induced pancreatitis (● ▶ Table 1).
Gallstone-related pancreatitis was ruled out because ALAT,
bilirubin, and alkaline phosphatase levels were normal. An
abdominal Computer Tomography (CT) scan on day 2 confirmed
an edematous pancreas and substantial ascites (● ▶ Fig. 2).
Because the patient’s paralytic ilius did not improve, a gastros-
copy was performed on day 2 and showed a hemorrhagic gastri-
tis, which was treated with an acid pump inhibitor.
Even though the elevated hemoglobin and potassium were inter-
preted as dehydration and treated with aggressive intravenous
rehydration, the patient developed signs of renal failure that
progressed to anuria. Furthermore, the patient exhibited ele-
vated creatinine and carbamide levels that did not respond to
for closer surveillance and intensive treatment. In depth investi-
gation revealed no cause. A timed urine collection (day 5)
Downloaded by: East Carolina University. Copyrighted material.
showed a normal clearance. The abdominal CT scan (day 2),
ultrasound of the renal system (day 3 and 9), renography (day 7),
and renal scintigraphy (day 9) found normal renal parenchyma,
3 concrements situated in the calyces, pelvic dilatation, and
slightly delayed urinary flow from the left kidney, although both
kidneys exhibited an equal functional distribution (44 % left vs.
56 % right). Rhabdomyolysis was ruled out due to normal
myoglobin, creatine kinase, and phosphate levels.
Frequent hemodynamic monitoring in the ICU with a blood
pressure cuff was difficult and impractical, because the patient
had large disfigured upper arms and therefore was discontin-
ued. To our surprise invasive blood pressure monitoring facili-
tated by radial artery cannulation revealed, that the patient had
a blood pressure much higher than normal (260/125 vs. a nor-
mal 190/100) (● ▶ Fig. 3). Therefore, the patient was considered
to be in a hypertensive crisis, and his blood pressure was nor-
malized using labetalole and nitroglycerin infusions. Bedside
echocardiography (days 4 and 10) showed an enlarged left ven-
tricle (a posterior wall thickness of 2 cm) with chronic circum-
ferential, apical, and non-compaction-type hypertrophy, as well
as enlarged septal and inferior papillary muscles. Ejection Frac-
tion was estimated to range from 55 to 60 %. The absence of car-
diac complaints, a normal ECG, and marginally elevated troponin
T level of 0.08 μg/L (0.0–0.03 μg/L) excluded myocardial ischemia.
During his stay in the ICU, the patient developed pleural effusion
with infiltrative changes that required supplemental oxygen,
which were confirmed by a chest X-ray. The patient was treated
with cefuroxime (750 mg × 3 i. v.) because of leucocytosis and a
delayed CRP increase (day 6) to 205 μg/L (0–8 μg/L) was inter-
preted as pneumonia.
Frequent blood testing indicated that the patient suffered from
massive fibrinolysis with elevated D-dimer, INR, APTT, fibrino-
gen and low antithrombin throughout his hospital stay, suggest-
ing one or several thrombo-embolic events, which could not be
detected. The abdominal CT scan (day 2) and a Doppler ultra-
sound examination of the abdominal vessels (day 6) could not
confirm a thrombo-embolic event.
The patient’s confession of his steroid injection cycle led to sup-
plemental investigations for anabolic steroid-related adverse
effects. We detected changes in lipid and glucose metabolism.
Although morning glucose levels were slightly elevated, glyco-
62 Clinical Sciences

Day 1 2 5 12 Reference Table 1 Blood and urine testing

during admission.
hemoglobin 19.5* 19.8* 11.6* 12.6* 13–16.6 g/dL
thrombocytes 374 328 687* 145–390 109/L
INR 1 1.2 1.5* 1.1 0.8 – 1.3
fibrinogen 16.7* 6.5–13.5 μmol/L
APTT 39* 26–38 s
antithrombin 0.74 0.8–1.2 K units/L
D-dimer 4* 0–0.5 mg/L
creatinine 203* 342* 288* 114* 60–100 μmol/L
carbamide 5.6 10.7* 12.5* 3.3 3.2–8.1 mmol/L
potassium 5.2* 6.1* 3.7 4.1 3.6–4.6 mmol
sodium 139 134 131* 141 137–145 mmol/L
creatinine kinase 45* 50–400 units/L
troponin T 0.07* 0–0.03 μg/L
myoglobin 47 28–72 μg/L
LDH 405* 464* 363* 283* 105–205 units/L
ALAT 24 21 39 59 10–70 units/L
alkaline phosphatase 107* 105* 49 82 35–105 units/L
amylase 899* 967* 238* 53 10–65 units/L
CRP 26* 125* 159* 13 0–8 mg/L
leukocytes 31.2* 30.6* 16.2* 3.5–8.8 109/L
calcium total 3.16* 2.19 2.15–2.51 mmol/L

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calcium ionized 1.56* 1.37* 1.17–1.34 mmol/L
paratyroid hormone 1.1* 1.6–6.9 pmol/L
cholesterol 1.7 2.9–6.1 mmol/L
HDL 0.2* 0.8–2.1 mmol/L
VLDL 0.4
triglyceride 0.8 0.5–2.6 mmol/L
glucose 9.1* 6.9 7.8* 5–7.2 mmol/L
Hb1Ac 5.3 3.4 – 6.1 %
pH 7.36 7.38 7.35–7.45
lactate 3.7* 2.1* 0.5–1.6 mmol/L
U-vanillic mandelic acid 42.8* 5–35 μmol/d
U-clearance 86 72–168 ml/hr
The results on other days were omitted
* Blood samples out of range

sylated hemoglobin was normal at 5.3 % (3.4–6.1 %) [8]. The

Fig. 2 A CT scan on
day 2 without contrast
(CT Philips Brilliance
16P, 173 Gy) depicted
an edematous-inflamed
pancreas and substantial
ascites.
patient’s cholesterol status was normal, but High Density Cho-
lesterol was low 0.2 mmol (0.8–2.1 mmol/L) [17]. His adrenal
gland function (Vanillic mandelic acid and adrenergic metabo-
lite levels after a timed urine collection) was observed to be
elevated; however, this finding was considered to be insignifi-
cant. Evidence of chronic hypercalcemia was based on low para-
thyroid hormone level. Unfortunately, serum vitamin D levels
were not evaluated because the patient had denied taking other
supplements. No further investigations concerning his erythro-
poietin abuse were undertaken, hematocrit was not evaluated.
After the patient was transferred to the medical department
(day 9), he was discharged (day 12) and provided with 3 antihy-
pertensive medications and a planned follow-up, which he did
not attend.

Discussion
▼
This case report presents a bodybuilder with multi-organ dys-
function that involved the pancreas, kidneys, lungs, heart, and
fibrinolytic system. The patient admitted to being on a cycle of
anabolic steroids, erythropoietin, and intensive training.
We could rule out gallstone related pancreatitis in relation to
liver function and did not observe signs of rhabdomyolysis. We
interpret the patient’s slightly changed lipid and glucose metab-

Schäfer CN et al. Multi-Organ Dysfunction in Bodybuilding Possibly … Int J Sports Med 2011; 32: 60–65
 Clinical Sciences 63

300 Fig. 3 This schematic shows the blood-pressure

Invasive blood pressure
measurements of the patient during the admis-
Highest systolic BP sion. Treatment of the hypertensive crisis started
250 on day 3. A discrepancy in systolic blood pressure
Mean systolic BP
is seen which indicates limited compressibility
Lowest systolic BP
around the upper arm vessels.
200 Mean diastolic BP
Pulse
mmHg

150 External blood pressure

Systolic BP
100 Diastolic BP
Pulse

50
Invasive
blood pressure
0
1 2 3 4 5 6 7 8 9 10 11 12
days of admission

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Fig. 4 This schematic shows the possible
Anabolic Steroids
mechanisms (white boxes) between anabolic
steroids/erythropoietin/food supplements (dark
Muscle hypertrophia grey boxes) and the multi-organ dysfunction (grey
Increased bone density
boxes) observed in our case.
Foodsupplements
Hospitalization Vitamin A/retinoic acid
Adrenal Anorexia Inactivity Vitamin D
gland effect Immobilization Calcium
Training

Bone-/Mucledystrophia Erythropoietin
(Rhabdomyolysis,
Fluid- Myoglobinaemia Osteoporosis)
retention Polycytaemia

Vasoconstrict- Hyper- Thrombo-

Thrombocyte-
Hypertension ion/increased calcaemia embolic event
activation
SVR

Polydipsia
Enzyme-
Hyper- activation
Polyuria gastraemia

Pancreatitis
Nephropathy ATIN Gastritis
Glomerulonephritis Reflux
Interstial nephritis GI dysmotility Ascites
Pleural effusion
Creatine-
phospate Nephrocalcinosis Vomiting
Respiratory
Insufficiency
Anuria Oliguria Dehydration

olism as a stress response related to his severe condition but it
could also be explained by use of anabolic steroids. In addition,
primary hyperparathyroidism was excluded because the par-
athyroid hormone was suppressed by elevated calcium levels.
The observed cardiomyopathy is compatible with the reported
abuse of anabolic steroids but could also be explained by
untreated hypertension. The observed high hemoglobin level
was initially explained by the use of erythropoietin but was later
assumed to have been caused by dehydration. Thus, we con-
cluded that this case could be possibly explained by primary
hypercalcemia related to the patient’s substance abuse and
Daher et al. [9] reported 2 similar cases of hypercalcemia that
were associated with anabolic steroids, vitamin D, and calcium
supplementation. In addition, Titan et al. [41] identified one
case of hypercalcemia, that appeared to result from combined
vitamins A and D intoxication, and in one case similar to ours
presenting pancreatitis, Samaha et al. [37] identified a hypercal-
cemia solely induced by anabolic steroids.
Like other authors, we feel confident about presenting the
observed multi-organ dysfunction as a result of chronic hyper-
calcemia, which was most likely caused by several contributing
factors (●
▶ Fig. 4). We can also identify additional factors, which

training cycle. can explain all findings in our case. Hypercalcemia associated
with immobilization and renal failure has been documented in

Schäfer CN et al. Multi-Organ Dysfunction in Bodybuilding Possibly … Int J Sports Med 2011; 32: 60–65
64 Clinical Sciences
the literature and can develop within a few days [26]. Calcium
release from damaged muscle fibers contributes to the develop-
ment of renal failure in rhabdomyolysis [4]. Furthermore, one or
several thrombi-embolic events can be explained by hypercal-
cemia. The use of erythropoietin in disseminated chronic cancer
is associated with a high frequency of thrombi-embolic compli-
cations [12] and hypercalcemia contributes to thrombocyte-
activated hypercoagulopathy [21].
Our patient exhibited all of the classical signs of primary hyper-
calcemia in the month prior to admission [5]. He had experi-
enced upper gastrointestinal symptoms, gastritis, reflux and
vomiting [35]. The patient’s water intake was consistent with
polydipsia and polyuria in relation to hypercalcemia.
We speculate that the patient’s chronic renal deficiency was
caused by the unreported, unconfirmed, and perhaps even acci-
dental intake of supplemental vitamin A, D and calcium. Increased
vitamin A, D and calcium intake could explain prolonged hyper-
calcemia and secondary hypertension, which was then exagger-
ated by a mild rhabdomyolysis caused by the increased amount of
training. We have to conclude that the patient’s calcium metabo-
lism was in a fragile balance that was maintained by his excessive
fluid intake. Gastritis, vomiting, and insufficient fluid and food
intake prior to the patient’s admission caused dehydration and
prevented essential renal clearance; this, in turn, resulted in an
increase in serum calcium, which led to an activation of pancre-
atic enzymes. The resultant pancreatitis then provoked massive
vomiting and abdominal discomfort, which contributed to fur-
ther increase the already persistent hypercalcemia.
Intramuscular injections with site-enhancement oils (SEOs) are
a relatively unknown form of substance abuse in the bodybuilder
subculture [10, 15, 20, 23, 27, 31]. We conclude that reactive
fibrosis in the upper arms complicated brachial arterial com-
pression, which made external blood pressure monitoring diffi-
cult and could explain the discrepancy between typical
non-invasively measured blood pressures and the invasively
measured blood pressure observed in this case.
This is the first investigation that has reported on the impact of
previous SEO abuse on the diagnosis and treatment of an acute
medical condition. The chronic changes in both of the patient’s
upper arms due to previous SEO abuse could have caused the med-
ical staff to overlook the patient’s hypertensive crisis, which could
have contributed to a deterioration of the patient’s condition.
Conclusion
▼ ney injury due to anabolic steroid and vitamin supplement abuse:
We report multi-substance-induced hypercalcemia as a possible
cause of multi-organ dysfunction. We present evidence that
raises questions about whether changes in calcium metabolism
may play a central role in the development of the reported
adverse effects related to the abuse of anabolic steroids and sup-
plements. We hope that further attention to and research about
whether our hypothesis about calcium homeostasis might lead
to a better understanding of short- and long-term adverse effects
of multi-substance abuse in bodybuilding.
The established evidence concerning the medical implications of
anabolic steroid abuse should be interpreted with caution. The
focus should remain on the obvious causes of the critical medical
conditions encountered in bodybuilders so that a correct diagno-
sis can be achieved and proper treatment can be provided. The
course of our investigation was influenced by the expectation of
finding the typical reported adverse effects of anabolic steroids
Schäfer CN et al. Multi-Organ Dysfunction in Bodybuilding Possibly … Int J Sports Med 2011; 32: 60–65
and erythropoietin, which left us without a clear diagnostic strat-
egy. Thus, we failed to evaluate the possibility of vitamin A and D
intoxication. A critical review of the blood samples, including
evaluation of serum levels for vitamin A and D, in combination
with a stringent search for the possible cause of the observed pan-
creatitis, could have resulted in a more straightforward treatment
of the observed nephropathy and pancreatitis. We recommend a
thorough evaluation and monitoring of calcium metabolism for
bodybuilders who seek assistance from the health care system.
Greater attention should be paid to the possible supplemental
intake of vitamin A, vitamin D, and calcium.
Funding/Conflicting Interests : Funding: None received.
No conflicting interests.
The patient’s informed consent was obtained.
●▶ Fig. 1 has been previously published in references [23] and
[20].
Acknowledgement
▼
Downloaded by: East Carolina University. Copyrighted material.
We thank the Department of Radiology Nykøbing F and Næstved
Hospital for their kind permission to publish the clinical pictures
in (●
▶ Fig. 1, 2).
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