Acta Neurol Belg DOI 10.1007/s13760-014-0378-8
LETTER TO THE EDITOR
Hypertensive encephalopathy associated with anabolic– androgenic steroids used for bodybuilding Bengt Edvardsson
Received: 28 September 2014 / Accepted: 6 October 2014 Ó Belgian Neurological Society 2014
Hypertensive encephalopathy (HE) is one of the possible causes of posterior reversible encephalopathy syndrome (PRES). PRES is a clinicoradiological entity. It is characterized by severe headache, seizures, visual disturbances, alteration in consciousness, nausea and vomiting [1]. Since the initial report, PRES is now associated with many medical conditions. Hypertension is nearly always present in patients with PRES. The clinical presentation of HE/ PRES may be nonspecific [2]. Magnetic resonance imaging (MRI) is the preferred imaging method used to detect PRES. In cases of drug-induced PRES, particularly in young persons, the diagnosis can be missed. HE/PRES in the setting of anabolic–androgenic steroids (AAS) use has not earlier been reported. I describe a 20-year-old man who developed HE/PRES associated with AAS used for bodybuilding. A 20-year-old man presented with severe headache. He had been using AAS (methandrostenolone 25 mg/day and methenolone enanthate 300 mg/week) for about 3 months for the purpose of bodybuilding. Blood pressure had been monitored earlier and he had been normotensive. There was no history of headache or other diseases. He took no medication besides AAS. The headache was followed by nausea, vomiting, visual disturbances and confusion. On presentation in the emergency department he was sleepy, but arousable. General physical and neurologic examination was normal. Fundoscopic examination was normal. He B. Edvardsson (&) Department of Clinical Sciences, Lund University, Skane University Hospital, Lund 221 85, Sweden e-mail: [email protected] B. Edvardsson Department of Neurology, Skane University Hospital, Lund, Sweden
had a blood pressure of 190/100 mmHg. Plasma testosterone was very low 1.2 and 1.7 nmol/L (normal range 8–30 nmol/L) indicating exogenous androgen use. Computer tomography/angiography of the brain was normal. Repeated blood pressure monitoring displayed marked hypertension. The blood pressure was aggressively treated with intravenous drugs. AAS use was stopped. Extensive investigations were ordered to exclude cerebral infection/ inflammation, ischemic stroke, vasculitis and cerebral venous thrombosis. An electroencephalogram showed diffuse slowing indicating an encephalopathy. Cerebrospinal fluid examination was normal apart from a high pressure of 35 mmH2O. A brain MRI displayed an increased signal in the cortex/white matter on images throughout the parietal, occipital, and frontal lobes. No contrast enhancement was seen and diffusion weighted imaging showed no signs of ischemia (Fig. 1a). The MRI findings were consistent with posterior reversible encephalopathy syndrome due to severe acute hypertension. Repeated cerebral angiographies displayed no signs of vasospasm. All serological tests were normal. Oral antihypertensive treatment continued. Other secondary causes of hypertension were excluded. The patient was discharged after 5 weeks. An MRI after 3 months displayed marked regression of the abnormalities (Fig. 1b). At follow-up after 6 months and 1 year he felt well. His blood pressure remained normal after discontinuation of AAS/antihypertensives. The case study highlights a patient with HE/PRES in the setting of AAS use. The patient had no earlier known hypertension and he recovered completely after discontinuation of AAS. Consequently, HE/PRES induced by AAS was the only rational cause of HE/PRES in this case. Different medications are linked to PRES and are a common cause of the condition. There are now reported an extensive number of toxic agents known to be associated to
123
Acta Neurol Belg Fig. 1 MRI brain T2/FLAIR displaying increased T2 signal in the cortex/white matter throughout the parietal, occipital and frontal lobes consistent with PRES (a). A MRI after 3 months displayed marked regression of the abnormalities (b)
PRES [2]. For example, the immunosuppressive agents cyclosporine A and tacrolimus (FK 506) have been linked to PRES in many reports [1]. Abuse of AAS is estimated to be common both in athletes and in nonathletes. AAS abuse in sportsmen has been associated with direct cardiovascular effects such as myocardial changes and indirect cardiovascular effects such as abnormal plasma lipoprotein, alterations in blood pressure, cardiac arrhythmia and myocardial infarction [3]. The connection between AAS abuse and blood pressure is not clear. Some studies have not observed any link [3]. An association between AAS abuse and hypertension has been found in other studies [3]. When a link is observed the underlying mechanism is likely to be the renal retention of sodium from AAS [3]. Blood pressure response to AAS abuse normally displays a dose–response relation [3]. Very high blood pressures (as high as 195/110 mmHg) have been noted in relation to the use of AAS in fit sportspersons with no other identifiable cause [3]. The effects of AAS abuse on blood pressure can persist for long periods [4]. Interestingly, in young and healthy persons HE/PRES may occur at blood pressure levels as low as 160/100 mmHg [5], as in this case. HE/PRES is usually reversible through control of blood pressure or removal of the underlying cause [1].
123
HE/PRES can occur in the setting of AAS use. Patients on AAS should have regular monitoring of blood pressure. AAS use is probably common in certain groups. Consequently, in young people presenting with hypertension and, as might be the case, a resulting PRES, AAS should be considered a possible underlying cause. Conflict of interest interest.
The author declares that he has no conflict of
Informed consent from human subject
Yes.
References 1. Hinchey J, Chaves C, Appignani B et al (1996) A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494–500 2. Lamy C, Oppenheim C, Mas JL (2014) Posterior reversible encephalopathy syndrome. Handb Clin Neurol 121:1687–1701 3. Achar S, Rostamian A, Narayan SM (2010) Cardiac and metabolic effects of anabolic–androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. Am J Cardiol 106:893–901 4. Lenders JW, Demacker PN, Vos JA et al (1988) Deleterious effects of anabolic steroids on serum lipoproteins, blood pressure, and liver function in amateur bodybuilders. Int J Sports Med 9:19–23 5. Manning L, Robinson TG, Anderson CS (2014) Control of blood pressure in hypertensive neurological emergencies. Curr Hypertens Rep 16:436
LETTER TO THE EDITOR
Hypertensive encephalopathy associated with anabolic– androgenic steroids used for bodybuilding Bengt Edvardsson
Received: 28 September 2014 / Accepted: 6 October 2014 Ó Belgian Neurological Society 2014
Hypertensive encephalopathy (HE) is one of the possible causes of posterior reversible encephalopathy syndrome (PRES). PRES is a clinicoradiological entity. It is characterized by severe headache, seizures, visual disturbances, alteration in consciousness, nausea and vomiting [1]. Since the initial report, PRES is now associated with many medical conditions. Hypertension is nearly always present in patients with PRES. The clinical presentation of HE/ PRES may be nonspecific [2]. Magnetic resonance imaging (MRI) is the preferred imaging method used to detect PRES. In cases of drug-induced PRES, particularly in young persons, the diagnosis can be missed. HE/PRES in the setting of anabolic–androgenic steroids (AAS) use has not earlier been reported. I describe a 20-year-old man who developed HE/PRES associated with AAS used for bodybuilding. A 20-year-old man presented with severe headache. He had been using AAS (methandrostenolone 25 mg/day and methenolone enanthate 300 mg/week) for about 3 months for the purpose of bodybuilding. Blood pressure had been monitored earlier and he had been normotensive. There was no history of headache or other diseases. He took no medication besides AAS. The headache was followed by nausea, vomiting, visual disturbances and confusion. On presentation in the emergency department he was sleepy, but arousable. General physical and neurologic examination was normal. Fundoscopic examination was normal. He B. Edvardsson (&) Department of Clinical Sciences, Lund University, Skane University Hospital, Lund 221 85, Sweden e-mail: [email protected] B. Edvardsson Department of Neurology, Skane University Hospital, Lund, Sweden
had a blood pressure of 190/100 mmHg. Plasma testosterone was very low 1.2 and 1.7 nmol/L (normal range 8–30 nmol/L) indicating exogenous androgen use. Computer tomography/angiography of the brain was normal. Repeated blood pressure monitoring displayed marked hypertension. The blood pressure was aggressively treated with intravenous drugs. AAS use was stopped. Extensive investigations were ordered to exclude cerebral infection/ inflammation, ischemic stroke, vasculitis and cerebral venous thrombosis. An electroencephalogram showed diffuse slowing indicating an encephalopathy. Cerebrospinal fluid examination was normal apart from a high pressure of 35 mmH2O. A brain MRI displayed an increased signal in the cortex/white matter on images throughout the parietal, occipital, and frontal lobes. No contrast enhancement was seen and diffusion weighted imaging showed no signs of ischemia (Fig. 1a). The MRI findings were consistent with posterior reversible encephalopathy syndrome due to severe acute hypertension. Repeated cerebral angiographies displayed no signs of vasospasm. All serological tests were normal. Oral antihypertensive treatment continued. Other secondary causes of hypertension were excluded. The patient was discharged after 5 weeks. An MRI after 3 months displayed marked regression of the abnormalities (Fig. 1b). At follow-up after 6 months and 1 year he felt well. His blood pressure remained normal after discontinuation of AAS/antihypertensives. The case study highlights a patient with HE/PRES in the setting of AAS use. The patient had no earlier known hypertension and he recovered completely after discontinuation of AAS. Consequently, HE/PRES induced by AAS was the only rational cause of HE/PRES in this case. Different medications are linked to PRES and are a common cause of the condition. There are now reported an extensive number of toxic agents known to be associated to
123
Acta Neurol Belg Fig. 1 MRI brain T2/FLAIR displaying increased T2 signal in the cortex/white matter throughout the parietal, occipital and frontal lobes consistent with PRES (a). A MRI after 3 months displayed marked regression of the abnormalities (b)
PRES [2]. For example, the immunosuppressive agents cyclosporine A and tacrolimus (FK 506) have been linked to PRES in many reports [1]. Abuse of AAS is estimated to be common both in athletes and in nonathletes. AAS abuse in sportsmen has been associated with direct cardiovascular effects such as myocardial changes and indirect cardiovascular effects such as abnormal plasma lipoprotein, alterations in blood pressure, cardiac arrhythmia and myocardial infarction [3]. The connection between AAS abuse and blood pressure is not clear. Some studies have not observed any link [3]. An association between AAS abuse and hypertension has been found in other studies [3]. When a link is observed the underlying mechanism is likely to be the renal retention of sodium from AAS [3]. Blood pressure response to AAS abuse normally displays a dose–response relation [3]. Very high blood pressures (as high as 195/110 mmHg) have been noted in relation to the use of AAS in fit sportspersons with no other identifiable cause [3]. The effects of AAS abuse on blood pressure can persist for long periods [4]. Interestingly, in young and healthy persons HE/PRES may occur at blood pressure levels as low as 160/100 mmHg [5], as in this case. HE/PRES is usually reversible through control of blood pressure or removal of the underlying cause [1].
123
HE/PRES can occur in the setting of AAS use. Patients on AAS should have regular monitoring of blood pressure. AAS use is probably common in certain groups. Consequently, in young people presenting with hypertension and, as might be the case, a resulting PRES, AAS should be considered a possible underlying cause. Conflict of interest interest.
The author declares that he has no conflict of
Informed consent from human subject
Yes.
References 1. Hinchey J, Chaves C, Appignani B et al (1996) A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494–500 2. Lamy C, Oppenheim C, Mas JL (2014) Posterior reversible encephalopathy syndrome. Handb Clin Neurol 121:1687–1701 3. Achar S, Rostamian A, Narayan SM (2010) Cardiac and metabolic effects of anabolic–androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. Am J Cardiol 106:893–901 4. Lenders JW, Demacker PN, Vos JA et al (1988) Deleterious effects of anabolic steroids on serum lipoproteins, blood pressure, and liver function in amateur bodybuilders. Int J Sports Med 9:19–23 5. Manning L, Robinson TG, Anderson CS (2014) Control of blood pressure in hypertensive neurological emergencies. Curr Hypertens Rep 16:436
