|Year : 2018 | Volume
| Issue : 1 | Page : 38-40
Anabolic Steroid Abuse in Gym Enthusiasts – An Under-Recognized Cause of Cerebral Venous Thrombosis
Geeta A Khwaja, Abhilekh Srivastava, Aviraj Deshmukh, Neera Chaudhry
Department of Neurology, GB Pant Hospital, New Delhi, India
|Date of Web Publication||27-Mar-2018|
Department of Neurology, GB Pant Hospital, Jawaharlal Nehru Marg, New Delhi - 110002
Source of Support: None, Conflict of Interest: None
Anabolic steroid use is constantly increasing, especially among athletes and gym enthusiasts. Of the many dangers of this rampant drug abuse is a hypercoagulable state predisposing to cerebral venous thrombosis (CVT). Androgen abuse for bodybuilding or increasing muscle mass is an under-recognized cause of CVT in young males. We report one such case, which highlights that awareness regarding the dangers of androgen abuse needs to be propagated, and a careful history of androgen abuse is mandatory in young adults presenting with CVT.
Keywords: CVT, gym enthusiasts, steroid abuse
|How to cite this article:|
Khwaja GA, Srivastava A, Deshmukh A, Chaudhry N. Anabolic Steroid Abuse in Gym Enthusiasts – An Under-Recognized Cause of Cerebral Venous Thrombosis. MAMC J Med Sci 2018;4:38-40
|How to cite this URL:|
Khwaja GA, Srivastava A, Deshmukh A, Chaudhry N. Anabolic Steroid Abuse in Gym Enthusiasts – An Under-Recognized Cause of Cerebral Venous Thrombosis. MAMC J Med Sci [serial online] 2018 [cited 2020 Jan 20];4:38-40. Available from: http://www.mamcjms.in/text.asp?2018/4/1/38/228654
| Introduction|| |
The clinical manifestations and cause of cerebral venous thrombosis (CVT) are variable, and the prognosis depends on the underlying cause. Androgen abuse for bodybuilding or increasing muscle mass is an under-recognized cause of CVT in young males. We report a case of stanozolol- and human chorionic gonadotropin (HCG)-induced CVT.
| Case Presentation|| |
A 23-year-old male presented to us with a 5-day history of headache and vomiting followed by increasing drowsiness and an acute confusional state of 1-day duration. The headache was bitemporal, severe, throbbing, continuous, and associated with photophobia and vomiting for 4–5 times per day. There was no history of fever, seizures, or any focal weakness. His history revealed that he had joined a gym 3 months back. For the last 1 month, besides exercising, he was also taking tablet stanozolol at the dose of 10 mg three times a day for bodybuilding. One day prior to the onset of his symptoms, he had also received a single intramuscular injection of HCG at the dose of 5000 IU.
On examination, the patient was conscious but drowsy, irritable, and not oriented to time, place, or person. Except for the presence of bilateral papilledema, all the cranial nerves were intact. There were no signs of meningeal irritation or any evidence of motor or sensory deficit.
On laboratory evaluation, including hemogram, blood counts, erythrocyte sedimentation rate (ESR) test, and routine blood chemistry including blood sugar, liver function tests (LFT), kidney function tests (KFT), and serum electrolyte levels were normal. Blood examination was negative for venereal disease research laboratory (VDRL), human immunodeficiency virus (HIV), hepatitis B surface antigen, and antibodies to hepatitis C virus. Workup for vasculitic profile was negative for antinuclear antibody (ANA), double stranded deoxyribonucleic acid (dSDNA), perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCA), cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA), and rheumatoid arthritis (RA) factor. Serum homocysteine levels were normal, and antiphospholipid antibody (APLA) test was negative. There was no evidence of protein C or protein S deficiency or factor V Leidin mutation. The results of electrocardiogram (ECG) and X-ray chest were normal. Magnetic resonance imaging (MRI) brain revealed a prominent hemorrhagic infarct in the left temporal lobe on T1, T2, and gradient response echo (GRE) sequences, whereas magnetic resonance venography (MRV) showed a thrombus in the left transverse sinus [Figure 1].
|Figure 1: (a) Axial T2-weighted sections showing heterogenous hyperintensities in the left temporoparietal region; (b) DWI showing hyperintensity in the same area suggestive of acute infarct; (c) GRE sequence showing evidence of blooming suggestive of hemorrhagic infarct; (d) MR venography showing a thrombosed left transverse sinus. DWI, diffusion weighted imaging; MR, magnetic resonance|
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On the basis of the history and MRI features, a diagnosis of CVT was made. Because extensive investigations did not reveal any other known cause of CVT, a possibility of stanozolol- and HCG-induced CVT was entertained. The patient was started on low-molecular-weight heparin (Enoxaparin, 0.6 ml subcutaneous injection, two times a day) along with mannitol and frusemide for the management of raised intracranial pressure. His headache was relieved, and he became fully conscious, alert, and ambulatory within 10 days of starting therapy.
| Discussion|| |
Cerebral venous sinus thrombosis (CVT) is a disease with a wide spectrum of nonspecific clinical signs and symptoms that include headache, focal neurological deficits, seizures, and coma. Our patient presented with an acute confusional state and features suggesting raised intracranial pressure in the form of headache and vomiting with bilateral papilledema in the setting of a left transverse sinus thrombosis.
The cause of CVT can be multifactorial. The common predisposing factors include elevated homocysteine levels, alcoholism, contraceptive pills, pregnancy, puerperium, coagulopathies, and intracranial infections. In our case, however, CVT was precipitated by the use of anabolic androgen steroids used for the purpose of bodybuilding and increasing muscle mass.
Anabolic androgenic steroids (AASs) have many potential clinical uses. They are often prescribed in patients with burns, postoperative patients, and patients with cachexia related to HIV, hepatic or renal failure, chronic obstructive pulmonary disease, and some types of cancer. However, as was the case with our patient, AASs are also used and abused by gym enthusiasts and athletes to enhance their physique or physical performance. Exogenous AAS exposure in males activates a negative feedback with the shutdown of the hypothalamic–pituitary–gonadal axis and decreased endogenous production of testosterone and testicular atrophy. In males, HCG helps restore and maintain testosterone production in the testes by mimicking leutinizing hormone (LH) and triggering the production and release of testosterone. HCG is, thus, commonly used during and after steroid cycles to maintain and restore testicular size and normal testosterone production. Our patient also received oral stanozolol for around 1 month followed by an injection of HCG before developing CVT. In the world of performance-enhancing drugs, AAS and HCG are included in the sports’ illegal drug list. Athletes’ self-prescribing habits are usually excessive, and it is very common for the AAS abuser to “stack” drugs, or to use multiple drugs at the same time. The surveys of weightlifters have documented the concurrent use of multiple drugs, employed in a cyclic fashion for 12–16 weeks; the dose used is typically 2–8 times higher than the therapeutic dose range. These factors, coupled with decreased medical surveillance, place the AAS abuser at high risk for serious complications.
The anabolic activity of testosterone and its derivatives is primarily manifested in its myotrophic actions, which result in greater muscle mass and strength. This has led to a widespread use of androgenic anabolic steroids by athletes at all levels. Testosterone, however, also regulates and impacts homeostasis in a complex dualistic manner. It exerts a profibrinolytic and anticoagulatory effect by lowering fibrinogen and plasminogen activator inhibitor-1. By decreasing cycloxygenase activity, however, it exerts a proaggregatory effect on platelets, especially in high doses. Androgens may also predispose to thrombosis by increasing collagen and other fibrous proteins in the arterial vascular tissues and skin. They may also increase the levels of procoagulant factors such as factors VIII and IX, which in turn may shift the balance toward a net prothrombotic state. According to currently available data, the proaggregatory effect of testosterone and other synthetic androgens is a more reliable theory for the development of CVT.
Some of the commonly used AASs include dianabol, oxandrolone, nandrolone, oxymetholone, metolonone, trembolone, danazol, and stanozolol. Stanozolol, which was used by our patient, is a highly active oral AAS derived from dihydrotestosterone with a high binding affinity for the androgen receptors. HCG is used to induce ovulation in women with infertility, and thrombosembolism is a known complication of HCG therapy. Increased blood viscosity and a hypercoagulable state characterized by an increase in fibrinogen and reduction in AT III concentration is the most probable mechanism for this complication.
Several reports of CVT following AAS abuse in bodybuilders can be found in literature. Venous sinus thrombosis in a healthy young male using androgens for bodybuilding was first reported by Jaillard et al. in 1994. Shimada et al. reported CVT in a 27-year-old man using high-dose anabolic steroids. In another case report by Sveinsson and Herrman, a bodybuilder developed CVT within 1 month of starting anabolic androgens (AAs) (dianabol 20 mg/day). Sahraian et al. have reported a patient in whom CVT developed within 5 months of starting nandrolone decanoate at the dose of 25 mg once or twice a week. Our patient developed CVT within 1 month of stating stanozolol, followed by HCG. Juhl et al. observed severe hyperhomocysteinemia with concomitant arterial and venous thrombosis in a bodybuilder abusing anabolic steroids.In CVT, the clinical outcome is highly variable and depends on the underlying cause. The patients may either recover completely or develop severe and lasting neurological deficits. Our patient showed a good response to therapy with complete recovery on a 3-month follow-up.
| Conclusion|| |
Androgen use may be a frequent but hidden and underestimated cause of CVT in gym enthusiasts and athletes. The mechanism of CVT following exogenous androgen usage is not completely understood, but androgens may increase coagulation factors or platelet activity and cause arterial or venous thrombosis. Our case highlights that awareness regarding the dangers of androgen abuse needs to be propagated, and a careful history of androgen abuse is mandatory in young adults presenting with CVT.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Basaria S, Wahlstrom JT, Dobs AS. Clinical review 138: Anabolic-androgenic steroid therapy in the treatment of chronic diseases. J Clin Endocrinol Metab 2001;86:5108-17.
Ramasamy R, Armstrong JM, Lipshultz LI. Preserving fertility in the hypogonadal patient: An update. Asian J Androl 2015;17:197-200.
] [Full text]
Anderson RA, Ludlam CA, Wu FC. Haemostatic effects of supraphysiological levels of testosterone in normal men. Thromb Haemost 1995;74:693-7.
Wu FC, Von Eckardstein A. Androgens and coronary artery disease. Endocr Rev 2003;24:183-217.
Lowe GD. Anabolic steroids and fibrinolysis. Wien Med Wochenschr 1993;143:383-5.
Kumar P, Sait SF, Sharma A, Kumar M. Ovarian hyperstimulation syndrome. J Hum Reprod Sci 2011;4:70-5.
] [Full text]
Jaillard AS, Hommel M, Mallaret M. Venous sinus thrombosis associated with androgens in a healthy young man. Stroke 1994;25:212-3.
Shimada Y, Yoritaka A, Tanaka Y, Miyamoto N, Ueno Y, Hattori N et al.
Cerebral infarction in a young man using high-dose anabolic steroids. J Stroke Cerebrovasc Dis 2012;21:906.e9-11.
Sveinsson O, Herrman L. Cortical venous thrombosis following exogenous androgen use for bodybuilding. BMJ Case Rep 2013;2013. bcr2012008638. doi:10.1136/bcr-2013-008638
Sahraian MA, Mottamedi M, Azimi AR, Moghimi B. Androgen-induced cerebral venous sinus thrombosis in a young body builder: Case report. BMC Neurol 2004;4:22.
Juhl S, Shorsh K, Videbaek H, Binzer MN. [Concomitant arterial and venous thrombosis in a body builder with severe hyperhomocysteinemia and abuse of anabolic steroids]. Ugeskr Laeger 2004;166:3508-9.