Anabolic steroid–induced hypogonadism: diagnosis and treatment

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Fertil Steril. 2014 Mar 14.
Anabolic steroid–induced hypogonadism: diagnosis and treatment Anabolic steroid–induced hypogonadism: diagnosis and treatment
Cyrus D. Rahnema, B.S.a, Larry I. Lipshultz, M.D.b, Lindsey E. Crosnoe, B.S.a, Jason R. Kovac, M.D., Ph.D.b, Edward D. Kim, M.D.


Objective To develop an understanding of hypogonadal men with a history of anabolic-androgenic steroid (AAS) use and to outline recommendations for management.

Design Review of published literature and expert opinions. Intended as a meta-analysis, but no quality studies met the inclusion criteria.

Setting Not applicable.

Patient(s) Men seeking treatment for symptomatic hypogonadism who have used nonprescribed AAS.

Intervention(s) History and physical examination followed by medical intervention if necessary.

Main Outcome Measures(s) Serum testosterone and gonadotropin levels, symptoms, and fertility restoration.

Result(s) Symptomatic hypogonadism is a potential consequence of AAS use and may depend on dose, duration, and type of AAS used. Complete endocrine and metabolic assessment should be conducted. Management strategies for anabolic steroid–associated hypogonadism (ASIH) include judicious use of testosterone replacement therapy, hCG, and selective estrogen receptor modulators.

Conclusion(s) Although complications of AAS use are variable and patient specific, they can be successfully managed. Treatment of ASIH depends on the type and duration of AAS use. Specific details regarding a patient's AAS cycle are important in medical management.

 

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I want to bump this study because it's important. While it contains nothing groundbreaking for Meso members who are familiar with Dr. Scally's approach to PCT, it IS significant because the research might finally be moving in Scally's direction and this study confirms what he's been saying for a long time, ie, AIH can and should be be treated medically and that more study is needed.

Fertil Steril. 2014 Mar 14.
Anabolic steroid–induced hypogonadism: diagnosis and treatment Anabolic steroid–induced hypogonadism: diagnosis and treatment
Cyrus D. Rahnema, B.S.a, Larry I. Lipshultz, M.D.b, Lindsey E. Crosnoe, B.S.a, Jason R. Kovac, M.D., Ph.D.b, Edward D. Kim, M.D.


Objective To develop an understanding of hypogonadal men with a history of anabolic-androgenic steroid (AAS) use and to outline recommendations for management.

Design Review of published literature and expert opinions. Intended as a meta-analysis, but no quality studies met the inclusion criteria.

Setting Not applicable.

Patient(s) Men seeking treatment for symptomatic hypogonadism who have used nonprescribed AAS.

Intervention(s) History and physical examination followed by medical intervention if necessary.

Main Outcome Measures(s) Serum testosterone and gonadotropin levels, symptoms, and fertility restoration.

Result(s) Symptomatic hypogonadism is a potential consequence of AAS use and may depend on dose, duration, and type of AAS used. Complete endocrine and metabolic assessment should be conducted. Management strategies for anabolic steroid–associated hypogonadism (ASIH) include judicious use of testosterone replacement therapy, hCG, and selective estrogen receptor modulators.

Conclusion(s) Although complications of AAS use are variable and patient specific, they can be successfully managed. Treatment of ASIH depends on the type and duration of AAS use. Specific details regarding a patient's AAS cycle are important in medical management.

 

[Mike Oxbig]

I'd imagine it's still going to take quite a few more years for AIH treatment to become the norm but it's definitely a step in the right direction. You have to start somewhere I suppose.

 

[Millard]

It's about time. Dr. Scally was saying this 15+ years ago. Researchers are finally coming around to saying the same thing. Dr. Scally is definitely a trailblazer!

 

[Dr JIM]

It's about time. Dr. Scally was saying this 15+ years ago. Researchers are finally coming around to saying the same thing. Dr. Sally is definitely a trailblazer![/QUOTE]

Agreed but just where has OUR trailblazer been?

We all need his input on occasion, IMO!
JIM

 

[TheGuy85]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360778/pdf/postmedj00085-0047.pdf think this is from 1998.

 

[Sugar12]

That article was fucking scary. The guy was completely impotent and had only needed to shave once in four months. Crazy though that he had a full recovery without needing anything drastic. The article was a great read.

Question related to this: What do you think contributes more to shutdown: cycle length or dosage?

To be honest I have never used HCG in the past and have always recovered normally with a SERM and AI...Though admittedly it sometimes took longer.

This article is making me think about the future: I have never done more than 12 weeks, but was looking to go 16 next - with low dosages (350mg test, 300mg tren). Makes me a little fearful though after reading it.

 

[Dr JIM]

Although none of this is surprising it's always nice to have evidence which supports intuitive thought, IMO!

 

[TheGuy85]

Yeah that article from 98' was based on a 17 year old bodybuilder. God knows how long he had been running gear. They brought him back though.

 

[Michael Scally MD]

Full-Text Attached

There are NO case studies. It is wrong in many places, but at least on the map a bit more.

 

[Michael Scally MD]

Nangia AK. Anabolic steroid abuse: a paradox of manliness. Fertil Steril. http://www.fertstert.org/article/S0015-0282(14)00187-3/fulltext (Elsevier)

The study by Rahnema et al. in this issue of the Journal has highlighted a surprising issue in the understanding of anabolic androgen steroid (AAS) use in that no quality studies on the subject met inclusion criteria to perform a meta-analysis. A systematic review of the literature over a 48-year period from 1965 to 2013 and of expert opinion was performed.

This systematic review provided an educational insight into the behavior of AAS abusers and the side effects, including infertility, with subsequent management including the ironic anabolic steroid–induced hypogonadism (ASIH).

The dilemma that always exists for providers is whether treating such patients, and the sudden or later hypogonadism, is feeding into their abuse/dependent personality versus a liberal and nonjudgmental belief that these men need help with their physical symptoms and signs. Rahnema et al. proposed an example of a ‘‘recovery’’ protocol for such men.

…

The only analogous studies to investigate the recovery from AAS are the trials that have used T as a male contraceptive agent. The largest and longest study by Gu et al. in 2009 demonstrated that after a loading dose of 1,000 mg of T IM and 500 mg once a month for 30 months, the median recovery time for sperm production to the patient's baseline after cessation of the treatment alone was 182 days. All but two of 729 patients recovered spermatogenesis by 15 months.

…

With multiple different AAS regimens being used and variable durations and cycles of treatment, the exact recovery from AAS is not known. A prospective study of different real world AAS regimens and recovery would be difficult to conduct in a structured and ethical manner since these are controlled drugs that are obtained illicitly from a number of questionable sources of variable quality and given in doses that are much higher than are considered safe. Trials of different recovery medication protocols and subsequent expert opinion may remain the only methods to study the treatment of these men after AAS abuse.

 

[Millard]

The dilemma that always exists for providers is whether treating such patients, and the sudden or later hypogonadism, is feeding into their abuse/dependent personality versus a liberal and nonjudgmental belief that these men need help with their physical symptoms and signs. Rahnema et al. proposed an example of a ‘‘recovery’’ protocol for such men.

Why does this seem to be a "dilemma" only when it comes to steroid users? There is never a dilemma when it comes to treating smokers or sedentary individuals with poor dietary habits, etc.

 

[Michael Scally MD]

In 2001, when Hep C was not a curable disease as it is today, those infected were still recommended to be treated despite ongoing drug use!!! AAS are the most politicized group of drugs in history.

Davis GL, Rodrigue JR. Treatment of Chronic Hepatitis C in Active Drug Users. New England Journal of Medicine 2001;345(3):215-7. MMS: Error

 

[TheGuy85]

I am sure you are already aware of this but the witch hunts against doctors prescribing controlled substances has gotten way out of control in the United States. Doctors are afraid to prescribe any controlled substances and this had led to inadequate healthcare practices and ineffective treatments for patients. Narcotic pain relievers have become extremely difficult, if not, almost impossible to get in many states. When other forms of pain relievers fail to work doctors refer them to pain management where they may have to wait up to 6 months to get an appointment. So a person who is legitimately in pain has to wait half a year to possibly experience some relief. The same thing is now happening to psychiatrists, they are now terrified to prescribe controlled substances, especially schedule II's. I believe this stems from the abuse of stimulant ADHD medications among minors. A lot of doctors have flat out refused to prescribe any type of controlled substances because they fear losing their practice.

The ethical thing to do is to treat a patient's symptoms and improve their quality of life (even if that requires prescribing them "habit forming" drugs). Even if the patient could potentially be a drug abuser seeking out prescription drugs (which a doctor can't determine unless the patient flat out admits it), wouldn't it be safer for them to use prescription drugs versus illicit street drugs? All the crack down on prescription narcotic pain killers has done is increase heroin use (along with crime) and has further placed a burden on patients suffering from chronic pain that are seeking relief.

 

[Michael Scally MD]

Anabolic Steroid Induced Hypogonadism Set Up [AAS/PCT Cycle Fail]

In the recent article on ASIH, they included a table of an example AAS/PCT Cycle. Anabolic steroid–induced hypogonadism: diagnosis and treatment

I did not find any appreciable commentary and IMO they should have, at a minimum, mentioned that this was a set up for ASIH. But, one wonders if they even realize that fact.

This is the most common error in AAS use that leads to a failed PCT (ASIH). While the oral will be long gone, the total AAS load on the last pin is ONE GRAM. And, this in the long-acting esters – Testosterone Cypionate (TC) & Nandrolone Decanoate (ND). This is of some import if they expect to fit this into their recommendation for treatment.

Those familiar with the half-lifes as well as the suppressive effects of ND will recognize that the AAS will not be cleared enough from the body for the HPTA to be in a state for functionality/restoration. The article would have been markedly improved if they discussed this point. JMHO

 

[Millard]

Anabolic Steroid Induced Hypogonadism Set Up [AAS/PCT Cycle Fail]

In the recent article on ASIH, they included a table of an example AAS/PCT Cycle. Anabolic steroid–induced hypogonadism: diagnosis and treatment

I did not find any appreciable commentary and IMO they should have, at a minimum, mentioned that this was a set up for ASIH. But, one wonders if they even realize that fact.

This is the most common error in AAS use that leads to a failed PCT (ASIH). While the oral will be long gone, the total AAS load on the last pin is ONE GRAM. And, this in the long-acting esters – Testosterone Cypionate (TC) & Nandrolone Decanoate (ND). This is of some import if they expect to fit this into their recommendation for treatment.

Those familiar with the half-lifes as well as the suppressive effects of ND will recognize that the AAS will not be cleared enough from the body for the HPTA to be in a state for functionality/restoration. The article would have been markedly improved if they discussed this point. JMHO

What other reason is there for including an example of something done incorrectly unless it's for the express purpose of discussing it? It's concerning if even researchers don't question bro-science

 

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Anabolic Steroid Induced Hypogonadism Set Up [AAS/PCT Cycle Fail]



I did not find any appreciable commentary and IMO they should have, at a minimum, mentioned that this was a set up for ASIH. But, one wonders if they even realize that fact.

I think it's a pretty safe assumption they DON"T.

Their recommendation for restoration:

For the severely symptomatic patients, a 4-week tapered course of transdermal or injectable TRT may provide immediate symptom improvement. Simultaneous administration of a SERM (such as clomiphene citrate, 25 mg every other day) will interact at the hypothalamus causing stimulation of LH and ultimately increase intratesticular T

After 4 weeks of treatment with TRT and/or a SERM, repeated hormone panels should be obtained. If the patient has had either a poor gonadotropin response or a poor T response, the authors commence a 4-week course of hCG (1,000–3,000 IU, 3 times per week) while continuing daily treatment with a SERM at the initial starting dose


​

By following their recommendations, what are the chances the patient will have a "good" gonadotropin response?

 

[whodatnation]

This is why this place is the best on the internet. While many people could very well be mislead by reading these articles , if they used google and it pulled them up , we are blessed here to have people who have the best knowledge for pct on the internet.

I want to give a personal thanks to Millard , Dr. Scally , Dr. Jim and Bill Roberts for their efforts in raising awareness and sharing their knowledge. The knowledge I have gained here is priceless.

 

[Michael Scally MD]

Comments on ASIH Diagnostic and Treatment Recommendations
And, there are plenty. But, hey, they are only decades BEHIND!

[from the recent report “Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril.” Anabolic steroid–induced hypogonadism: diagnosis and treatment ]

Initial testing typically consists of a hormonal panel (LH, FSH, E2, T, free T, SHBG, and PRL), complete blood cell count, lipid profile, prostate-specific antigen, and a comprehensive metabolic profile.

Common post-cycle complaints include depressive mood alterations, fatigue, lethargy, insomnia, and decreased libido, and any such symptoms should be addressed. Physical examination should include height, weight, blood pressure, and body mass index, and common signs consistent with AAS use, such as acne, gynecomastia, testicular atrophy, skin striations, and alopecia should be noted if present.

For AAS users seeking treatment and assistance in permanently discontinuing AAS, certain steps should be taken. Following establishment of a nonjudgmental, healthy, and trusting physician-patient relationship, the patient should be counseled to discontinue all AAS as well as any self-administered ancillary drugs and supplements.

For the severely symptomatic patients, a 4-week tapered course of transdermal or injectable TRT may provide immediate symptom improvement.

Simultaneous administration of a SERM (such as clomiphene citrate, 25 mg every other day) will interact at the hypothalamus causing stimulation of LH and ultimately increase intratesticular T.

For patients with ASIH-induced gynecomastia, 20 mg tamoxifen daily will block the breast estrogen receptors and stimulate HPG axis recovery.

After 4 weeks of treatment with TRT and/or a SERM, repeated hormone panels should be obtained.

If the patient has had either a poor gonadotropin response or a poor T response, the authors commence a 4-week course of hCG (1,000–3,000 IU, 3 times per week) while continuing daily treatment with a SERM at the initial starting dose.

If a patient develops gynecomastia while on hCG, tamoxifen (10 mg b.i.d.) or anastrazole may be commenced.

After 8 weeks of hCG and adjunctive treatment, hormone levels should once again be assessed.

At this point, if the total serum T remains low and the patient continues to be symptomatic, primary testicular failure is likely.

These patients will require a longer duration of TRT to avoid permanent ASIH.

If appropriately increased serum T and gonadotropin levels are observed, the SERM may be reduced to 50% of its starting dose at 10 weeks of treatment and continued through weeks 12–16 or until target serum T level is achieved.

Recovery of hormonal function may be limited in men with testicular failure, and close monitoring is recommended.