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Bluelight Crew
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Here's another case-study recently published of a guy using AAS who had a thrombosis, but this time it led to a stroke (clot in the brain) rather than a heart attack.
The cause was, as before, likely to be polycythemia (too many red blood cells/thick blood), which is an almost inevitable consequence of prolonged AAS use.
This guy was not a bodybuilder, he smoked 20 cigarettes/day (increasing his risk factors), and his likely ignorance of what he was doing is the type that gives many AAS using bodybuilders a bad reputation. As they state in the report:
This kind of casual use of AAS, though prevalent, is never advisable because it encourages men to trivialise their use and also therefore the potential side-effects.
If we sometimes seem harsh critiquing cycles or the reason for starting one, bear in mind that it's because we're thinking of the risk-reward ratio and taking a necessarily cautious, harm-reduction approach. We don't want you to have a heart attack or die!
Don't be this guy. Research what you're doing. If you eventually decide to embark on chemical enhancement, make sure you're using AAS effectively and for a less ephemeral reason than just a week at the beach.
If you're not aware of sensible practices like venesection or blood donation, taking low-dose aspirin, reducing stimulant intake on cycle etc, etc, etc, then you're probably not yet ready.
*****
[h=4]Anabolic androgenic steroids, an easily forgotten cause of polycythaemia and cerebral infarction[/h]
[h=3]Abstract[/h]Excessive anabolic androgenic steroids (both exogenous and endogenous) are known causes of polycythaemia and ischaemic cardiovascular events. Despite this, they are commonly forgotten in the workup of patients. We report a case of exogenous anabolic androgenic steroid-induced polycythaemia and stroke and explore possible pitfalls for clinicians.
Polycythaemia, an elevation in concentration of haemoglobin, can result from increased red cell mass or reduced plasma volume. Increased red cell mass can be caused by numerous primary (bone marrow) and secondary causes.[1] In some patients, polycythaemia can cause thrombosis due, in part, to hyperviscosity of blood.[2] Accurate diagnosis of the underlying cause is important for optimal management of patients. Identification of secondary causes, such as smoking, increased erythropoietin and high affinity haemoglobins, are critical for patient management and education. Increased levels of anabolic androgenic steroids (AAS) are another known cause of polycythaemia, but are easily forgotten in the workup of patients with polycythaemia. AAS can be either endogenous, such as testosterone, or exogenous in the form of drugs with structural and functional similarities to testosterone. We hereby present the case of a 36-year-old male who presented for follow up at our clinic.
On examination, he was noted to have left homonymous haemianopia, mild (4+) left-sided weakness in his upper limbs and ataxia in his left upper limb. Brain magnetic resonance imaging showed an extensive region of acute infarction in the right posterior cerebral artery territory (Fig. 1A, red arrow). Magnetic resonance angiography scan revealed an ongoing occlusion in his right posterior cerebral artery (Fig. 1B, green arrow). He had a past history of previous intravenous (heroin), and inhaled (marijuana) drug use although he denied any active illicit drug use at time of admission. He was not taking any prescribed medication. He was admitted for further investigation, rehabilitation and commenced on aspirin and atorvastatin.
Figure 1. (A) Diffusion-weighted image showing acute cerebral infarction in the right posterior cerebral artery territory that involved the medial occipital and posterior temporal lobes, hippocampus and thalamus.
(B) Magnetic resonance angiography showing occlusion of the right posterior cerebral artery
Further investigation revealed raised haemoglobin at 200 g/L (reference range: 130?180) with a haematocrit of 0.61 (reference range: 0.38?0.54). His white cell count was raised at 14.8 × 109/L (reference range: 4.0?11.0) with a mild neutrophilia (11.3 × 109/L; reference range: 2.0?8.0) and monocytosis (1.1 × 109/L; reference range: 0.2?1.0). His platelets were within the normal range at 260 × 109/L (reference range: 150?450). A blood film revealed no abnormal morphology in any lineage. Whilst he smoked 20 cigarettes a day and had a raised carboxyhaemoglobin 2.3% (reference range: <2%), he was not considered likely to have a clear secondary cause for polycythaemia. On presumption of a possible myeloproliferative neoplasm precipitating his cerebral infarction, he was venesected on days 1 and 3 of admission (440 mL of blood on each day) with a corresponding fall in haemoglobin (172 g/L) and haematocrit (0.52). Abnormalities in white cell indices resolved over first 2 days of admission. Further investigation for an underlying cause, including JAK2 mutation testing (including exon 12 testing) and BCR-ABL PCR were negative. A serum erythropoietin level was normal at 6.4 U/L (reference range: 2.5?18.5). A thrombophilia screen, including protein C levels, protein S levels, antithrombin levels, factor V Leiden mutation, prothrombin gene mutation and a lupus anticoagulant screen were all negative. Computed tomography angiogram revealed no structural abnormalities, stenosis or dissection of the vertebral arteries. Transthoracic echocardiogram and 24-h Holter monitoring failed to reveal a clear source of thrombus. He was eventually discharged on day 7 post-admission after making a full neurological recovery with plans for 2 weekly venesection and ongoing haematological follow up and investigation.
He was reviewed in our clinic as an outpatient and on detailed secondary screening, he once again denied recent use of illicit drugs; however, he did admit to the use of AAS for 3 months prior to the cerebral infarction in an attempt to improve his aesthetics. He disclosed using both injectable (nandrolone decanoate) and oral (methandrostenolone/danabol) anabolic steroids sourced from outside the healthcare setting. Testosterone, LH and FSH levels were not checked during his admission as a result of multiple factors. First, the patient did not consider AAS an illicit drug and hence failed to disclose this information. Second, treating clinicians failed to exclude specifically exogenous AAS as a possible cause as the patient did not meet the stereotypical image of an exogenous AAS user, with normal muscle mass and an estimated body mass index of 23 kg/m2. The patient was counselled to avoid use of AAS and his venesection ceased. He has been monitored clinically with his haemoglobin remaining within normal range for 2 months follow up.
[h=3]Discussion[/h]
Supra-physiological levels of AAS can increase muscle mass, fat-free mass and strength when combined with strength training leading to its widely publicised use in elite athletes.[3] The rates of illegal consumption of AAS in the general population are difficult to ascertain with estimates ranging 1?7% in non-elite athletes. These numbers suggest that AAS use may, in fact, be more common in general society than in elite sport.[4, 5]
Some groups in society are documented to have higher consumption of AAS, such as body builders, weight lifters and prison populations.[6] Similarly, men consistently use anabolic steroids at higher rates than their female counterparts.[5] With this knowledge, clinicians may be prejudiced as to which patients they consider exogenous AAS use as a possible cause for their patient's medical problems. It is clear that the use of AAS has spread beyond elite athletes with some evidence that its use is now commonly linked with poor body image particularly in young men.[7]
Excessively elevated androgen levels (either endogenous or exogenous) can have many adverse effects, including changes in endocrine function, psychiatric disturbances and changes in lipid profiles.[8] Pertinent to our case, high levels of androgens can cause polycythaemia, as well as changes to cardiac structure and function, which can lead to sudden cardiac death.[1, 9] Less commonly reported are cerebrovascular ischaemic events.[10, 11] The exact mechanism by which testosterone leads to polycythaemia remains incompletely understood, although recent evidence suggests AAS reduce hepcidin and stimulate erythropoiesis by recalibrating the erythropoietin set point.[12, 13] In addition, testosterone has been shown to stabilise telomeres in bone marrow progenitors, which may play a role in increased red cell production.[14]
Given the relative prevalence of illegal AAS use, it is important that clinicians consider both endogenous and exogenous AAS as a possible cause in all patients, regardless of body size or physical appearance. Importantly, evidence suggests that education can reduce illegal AAS use in adolescent males.[15] Therefore medical professionals could play a critical role in education and prevention from the potentially serious adverse effects of exogenous AAS administration.
The cause was, as before, likely to be polycythemia (too many red blood cells/thick blood), which is an almost inevitable consequence of prolonged AAS use.
This guy was not a bodybuilder, he smoked 20 cigarettes/day (increasing his risk factors), and his likely ignorance of what he was doing is the type that gives many AAS using bodybuilders a bad reputation. As they state in the report:
This kind of casual use of AAS, though prevalent, is never advisable because it encourages men to trivialise their use and also therefore the potential side-effects.
If we sometimes seem harsh critiquing cycles or the reason for starting one, bear in mind that it's because we're thinking of the risk-reward ratio and taking a necessarily cautious, harm-reduction approach. We don't want you to have a heart attack or die!
Don't be this guy. Research what you're doing. If you eventually decide to embark on chemical enhancement, make sure you're using AAS effectively and for a less ephemeral reason than just a week at the beach.
If you're not aware of sensible practices like venesection or blood donation, taking low-dose aspirin, reducing stimulant intake on cycle etc, etc, etc, then you're probably not yet ready.
*****
[h=4]Anabolic androgenic steroids, an easily forgotten cause of polycythaemia and cerebral infarction[/h]
- M. S. Y. Low
- S. Vilcassim
- P. Fedele
- G. Grigoriadis
[h=3]Abstract[/h]Excessive anabolic androgenic steroids (both exogenous and endogenous) are known causes of polycythaemia and ischaemic cardiovascular events. Despite this, they are commonly forgotten in the workup of patients. We report a case of exogenous anabolic androgenic steroid-induced polycythaemia and stroke and explore possible pitfalls for clinicians.
Polycythaemia, an elevation in concentration of haemoglobin, can result from increased red cell mass or reduced plasma volume. Increased red cell mass can be caused by numerous primary (bone marrow) and secondary causes.[1] In some patients, polycythaemia can cause thrombosis due, in part, to hyperviscosity of blood.[2] Accurate diagnosis of the underlying cause is important for optimal management of patients. Identification of secondary causes, such as smoking, increased erythropoietin and high affinity haemoglobins, are critical for patient management and education. Increased levels of anabolic androgenic steroids (AAS) are another known cause of polycythaemia, but are easily forgotten in the workup of patients with polycythaemia. AAS can be either endogenous, such as testosterone, or exogenous in the form of drugs with structural and functional similarities to testosterone. We hereby present the case of a 36-year-old male who presented for follow up at our clinic.
On examination, he was noted to have left homonymous haemianopia, mild (4+) left-sided weakness in his upper limbs and ataxia in his left upper limb. Brain magnetic resonance imaging showed an extensive region of acute infarction in the right posterior cerebral artery territory (Fig. 1A, red arrow). Magnetic resonance angiography scan revealed an ongoing occlusion in his right posterior cerebral artery (Fig. 1B, green arrow). He had a past history of previous intravenous (heroin), and inhaled (marijuana) drug use although he denied any active illicit drug use at time of admission. He was not taking any prescribed medication. He was admitted for further investigation, rehabilitation and commenced on aspirin and atorvastatin.
Figure 1. (A) Diffusion-weighted image showing acute cerebral infarction in the right posterior cerebral artery territory that involved the medial occipital and posterior temporal lobes, hippocampus and thalamus.
(B) Magnetic resonance angiography showing occlusion of the right posterior cerebral artery
Further investigation revealed raised haemoglobin at 200 g/L (reference range: 130?180) with a haematocrit of 0.61 (reference range: 0.38?0.54). His white cell count was raised at 14.8 × 109/L (reference range: 4.0?11.0) with a mild neutrophilia (11.3 × 109/L; reference range: 2.0?8.0) and monocytosis (1.1 × 109/L; reference range: 0.2?1.0). His platelets were within the normal range at 260 × 109/L (reference range: 150?450). A blood film revealed no abnormal morphology in any lineage. Whilst he smoked 20 cigarettes a day and had a raised carboxyhaemoglobin 2.3% (reference range: <2%), he was not considered likely to have a clear secondary cause for polycythaemia. On presumption of a possible myeloproliferative neoplasm precipitating his cerebral infarction, he was venesected on days 1 and 3 of admission (440 mL of blood on each day) with a corresponding fall in haemoglobin (172 g/L) and haematocrit (0.52). Abnormalities in white cell indices resolved over first 2 days of admission. Further investigation for an underlying cause, including JAK2 mutation testing (including exon 12 testing) and BCR-ABL PCR were negative. A serum erythropoietin level was normal at 6.4 U/L (reference range: 2.5?18.5). A thrombophilia screen, including protein C levels, protein S levels, antithrombin levels, factor V Leiden mutation, prothrombin gene mutation and a lupus anticoagulant screen were all negative. Computed tomography angiogram revealed no structural abnormalities, stenosis or dissection of the vertebral arteries. Transthoracic echocardiogram and 24-h Holter monitoring failed to reveal a clear source of thrombus. He was eventually discharged on day 7 post-admission after making a full neurological recovery with plans for 2 weekly venesection and ongoing haematological follow up and investigation.
He was reviewed in our clinic as an outpatient and on detailed secondary screening, he once again denied recent use of illicit drugs; however, he did admit to the use of AAS for 3 months prior to the cerebral infarction in an attempt to improve his aesthetics. He disclosed using both injectable (nandrolone decanoate) and oral (methandrostenolone/danabol) anabolic steroids sourced from outside the healthcare setting. Testosterone, LH and FSH levels were not checked during his admission as a result of multiple factors. First, the patient did not consider AAS an illicit drug and hence failed to disclose this information. Second, treating clinicians failed to exclude specifically exogenous AAS as a possible cause as the patient did not meet the stereotypical image of an exogenous AAS user, with normal muscle mass and an estimated body mass index of 23 kg/m2. The patient was counselled to avoid use of AAS and his venesection ceased. He has been monitored clinically with his haemoglobin remaining within normal range for 2 months follow up.
[h=3]Discussion[/h]
Supra-physiological levels of AAS can increase muscle mass, fat-free mass and strength when combined with strength training leading to its widely publicised use in elite athletes.[3] The rates of illegal consumption of AAS in the general population are difficult to ascertain with estimates ranging 1?7% in non-elite athletes. These numbers suggest that AAS use may, in fact, be more common in general society than in elite sport.[4, 5]
Some groups in society are documented to have higher consumption of AAS, such as body builders, weight lifters and prison populations.[6] Similarly, men consistently use anabolic steroids at higher rates than their female counterparts.[5] With this knowledge, clinicians may be prejudiced as to which patients they consider exogenous AAS use as a possible cause for their patient's medical problems. It is clear that the use of AAS has spread beyond elite athletes with some evidence that its use is now commonly linked with poor body image particularly in young men.[7]
Excessively elevated androgen levels (either endogenous or exogenous) can have many adverse effects, including changes in endocrine function, psychiatric disturbances and changes in lipid profiles.[8] Pertinent to our case, high levels of androgens can cause polycythaemia, as well as changes to cardiac structure and function, which can lead to sudden cardiac death.[1, 9] Less commonly reported are cerebrovascular ischaemic events.[10, 11] The exact mechanism by which testosterone leads to polycythaemia remains incompletely understood, although recent evidence suggests AAS reduce hepcidin and stimulate erythropoiesis by recalibrating the erythropoietin set point.[12, 13] In addition, testosterone has been shown to stabilise telomeres in bone marrow progenitors, which may play a role in increased red cell production.[14]
Given the relative prevalence of illegal AAS use, it is important that clinicians consider both endogenous and exogenous AAS as a possible cause in all patients, regardless of body size or physical appearance. Importantly, evidence suggests that education can reduce illegal AAS use in adolescent males.[15] Therefore medical professionals could play a critical role in education and prevention from the potentially serious adverse effects of exogenous AAS administration.
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