Anabolic Steroids & Liver [GI]

[Dr JIM]

Sorry but who KNOWS what you had fella.

Ya think maybe just maybe some pretty significant advancements has occurred in the past SEVENTY YEARS.

Heck effective treatment for BACTERIAL infections was not available until the 1940s with the discover of Pen. In fact Viruses were not considered communicable infectious agents until the EARLY 1900"s!

 

[Marcus]

Sorry but who KNOWS what you had fella.

Ya think maybe just maybe some pretty significant advancements has occurred in the past SEVENTY YEARS.

Heck effective treatment for BACTERIAL infections was not available until the 1940s with the discover of Pen. In fact Viruses were not considered communicable infectious agents until the EARLY 1900"s!

I'm confused dr Jim... Are you saying a similar panel back in the 1960's cannot determine whether some has hepatitis? Or that TX for it has advanced so much since his original results? Or what?

 

[Dr JIM]

had hepatitus in late 20's in the hospital in isolation for a week.now 69 and this is my latest test results

View attachment 29163

I'm somewhat confused also bc either the testing was done when the OP was in his "late 20s" and if he is now 69, the testing would have been conducted some 40-50 YEARS ago which would be roughly 1965.

If such is the case, there should be no doubt the accuracy (sensitivity and specificity) of viral testing in the 1960's PALES IN COMPARISON TO CONTEMPORARY TECHNOLOGY!

I'd have to determine when the SPECIFIC viral antigens and antibodies panels in use today were established as the standard, and how the existing standard compared to it's predecessors, IF THERE WAS ONE>

The antigens I'm referring are actually virlal proteins that arise when the virus is lysed by WBC's! We are talking about some pretty SMALL SHIT mate, most of it requiring direct detection via electron microscopy or indirect detection via specific antibody screens.

Consequently I suspect the significance of these viral proteins and/or our ability to ascertain their presence was VERY unlikely to be noted prior to the 1980s !

 

[Marcus]

I'm somewhat confused also bc either the testing was done when the OP was in his "late 20s" and if he is now 69, the testing would have been conducted some 40-50 YEARS ago which would be roughly 1965.

If such is the case, there should be no doubt the accuracy (sensitivity and specificity) of viral testing in the 1960's PALES IN COMPARISON TO CONTEMPORARY TECHNOLOGY!

I'd have to determine when the SPECIFIC viral antigens and antibodies panels in use today were established as the standard, and how the existing standard compared to it's predecessors, IF THERE WAS ONE>

The antigens I'm referring are actually virlal proteins that arise when the virus is lysed by WBC's! We are talking about some pretty SMALL SHIT mate, most of it requiring direct detection via electron microscopy or indirect detection via specific antibody screens.

Consequently I suspect the significance of these viral proteins and/or our ability to ascertain their presence was VERY unlikely to be noted prior to the 1980s !

Hmmmm, interesting. Never knew that, although it does make sense when thought through. So you believe it could most likely be a false-positive in the original test due to whatever limitations the technology of the time had?

@MR10X were you having any symptoms associated with hepatitis? Regardless, congrats on your results man!! I'm sure that means so much to you

 

[MR10X]

It was in the late 70's when i contracted the hepatitis.I wasn't using any drugs was married with 2 kids.I started peeing dark urine,eyes were a little yellow and i was feeling weak i went to my primary and as i sat across the doc looked at me and said i need to go to the hospital right now...he didn't even have to do any tests to know i had it.I don't remember how they treated it but they put me in isolation for almost a week,kept doing blood work till my blood count was back to normal or close to it. i started dong AAS in my early 30's,i did a small amount of orals for a little while but eventually quit using then all together.I have done over 30 cycles most were not high doses untill a few years ago where i did a few at 1500mg a week for 8 weeks at the time.i have had by blood work done every year for the past 4 years and my liver and kidney function has always come back normal when off AAS,i never had blood work done while on....had complete heart check up last year and everything is fine,no enlarged heart or other problems. Had prostrate cancer in 2012 and had seed implants and 25 external radiation treatments. so far my PSA tests has been low last test was 0.30....

 

[heady muscle]

http://www.anabolic.org/anabolic-steroid-hepatotoxicity-and-liver-protectants/

 

[Michael Scally MD]

Mody A, White D, Kanwal F, Garcia JM. Relevance of low testosterone to non-alcoholic fatty liver disease. Cardiovasc Endocrinol. 2015;4(3):83-9. http://journals.lww.com/cardiovascu...ce_of_low_testosterone_to_nonalcoholic.3.aspx
Non-alcoholic fatty liver disease (NAFLD) is a condition where there is excess accumulation of triglycerides in the liver in the absence of excess alcohol consumption.

It ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which can progress to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC).

NAFLD, one of the most common causes of chronic liver disease in Western populations, is the hepatic component of the metabolic syndrome (MetS) and is associated with increased visceral adipose tissue (VAT), insulin resistance, and dyslipidemia.

Studies have also shown that testosterone deficiency is associated with increased VAT and insulin resistance in males while hyperandrogenemia has been associated with increased risk of insulin resistance and VAT in females.

Thus, the aims of this review are to discuss the available experimental and epidemiological data evaluating the association between testosterone and NAFLD, to discuss the potential clinical relevance of these data, and to identify gaps in the literature.

 

[Michael Scally MD]

Sinclair M, Grossmann M, Angus PW, et al. Low testosterone is a better predictor of mortality than sarcopenia in men with advanced liver disease. J Gastroenterol Hepatol. http://onlinelibrary.wiley.com/doi/10.1111/jgh.13182/abstract

INTRODUCTION: Both sarcopenia and low serum testosterone have been associated with increased mortality in men with cirrhosis. It is not known how these variables interact.

METHODS: We conducted a retrospective longitudinal cohort study of 145 men referred for liver transplant evaluation between 2005 and 2012. Baseline demographics included hormone profile and MELD score. Baseline computerised tomography was reformatted to calculate skeletal muscle area at L4 using validated, Tomovision software-based methodology. The primary outcome was time to death or liver transplantation.

RESULTS: Median testosterone was low at 6.2 nmol/L (ref 10-27.6 nmol/L) as was muscle mass at 48.0 cm2 /m2 (ref >52.4 cm2 /m2 ). Muscle mass correlated with both serum testosterone (tau = 0.132, p = 0.019) and MELD score (tau = -0.155, p = 0.007).

In separate multivariable models, both sarcopenia (HR 1.05, p = 0.04) and low testosterone (HR 1.08, p = 0.01) were significantly associated with mortality independent of MELD score. When the variables MELD score, muscle area and testosterone were entered into a single model, low testosterone but not sarcopenia remained significantly predictive of mortality (HR 1.07, p = 0.02; HR 1.04, p = 0.09 respectively).

CONCLUSION: Low testosterone and sarcopenia are both associated with increased mortality in men with advanced liver disease and may identify patients at high risk of mortality that would be missed by the MELD score alone. Low testosterone appears to be a better predictor of mortality than sarcopenia and is a simpler test to improve the prognostic value of the MELD score. Interventional trials are required to determine whether low testosterone and sarcopenia are markers or mediators of mortality in this population. This article is protected by copyright. All rights reserved.

 

[Michael Scally MD]

[Open Access] Samieinasab MR, Shahraki MR, Samieinasab F, Najafi S. Influence of nandrolone decanoate administration on serum lipids and liver enzymes in rats. ARYA Atheroscler 2015;11(4):256-60. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4593662/

BACKGROUND: Anabolic-androgenic steroids have been associated with several side effects range. This experimental study was conducted to evaluate the effects of nandrolone decanoate (ND, an anabolic steroid) on lipid profile and liver enzymes in rats in Iran.

METHODS: Forty adult male and female of Wistar strain rats were randomly assigned to four groups of 10 animals each: male control, female control, ND-male treated (15 mg/kg b.w./day), and ND-female treated (15 mg/kg b.w./day). Serum concentrations of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured in all studied groups.

RESULTS: Treating rats with ND (case group) resulted in a significant elevation of TC (69.4 +/- 8.7), TG (101.6 +/- 32.9) and ALT (72.2 +/- 13.8) and significant reduction of LDL (6.4 +/- 2.6) and AST (138.7 +/- 19.4) as compared to control group in female rats. ND supplementation (case group) significantly increased TC (64.4 +/- 6.2), AST (255.0 +/- 32.0), and ALT (84.3 +/- 3.8) in comparison with the control group in male rats.

CONCLUSION: Overall, our result indicated that the ND use can cause a negative effect on lipid profile and liver enzyme in rats.

 

[DedLift]

I would ask a question of you but answering questions doesn't seem to be your strong point. I do appreciate the very informative articles, however. Thanks

 

[Michael Scally MD]

“He was [using] 1500 mg of testosterone/nandrolone, via intramuscular injection, per week for 3 months. 3 weeks prior to the presentation, he abruptly decreased the dose to 500 mg/week.”

Cavanagh Y, Shah N, Thomas AB, Gupta A. Multiple Intussusceptions Associated with Polycythemia in an Anabolic Steroid Abuser, A Case Report and Literature Review. Ann Med Health Sci Res 2015;5(5):368-72. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594352/

Intussusceptions are generally associated with mechanical lead points or localized inflammation that function as foci for intestinal telescoping.

We present the case of a patient whose abuse of anabolic steroids resulted in the development of multiple simultaneous intussusceptions. Our patient had no additional identifiable risk factors for intussusception.

Consistent with previous reports, corticosteroid induced polycythemia and its consequent hyperviscosity led to intravascular sludging and mesenteric ischemia with associated bowel wall thickening. The localized intestinal induration then served as mechanical foci for intussusception.

Due to the illicit nature of anabolic androgenic steroid (AAS) abuse, the physiologic effects of supraphysiologic doses are sparsely reported and poorly understood. The scope of AAS abuse and its consequences are likely under-reported and under-recognized within the medical community.

Our case presented a unique diagnostic and therapeutic challenge with which we aim to increasing awareness and clinical suspicion for AAS among healthcare personnel.

 

[DedLift]

I'm learning a lot from your posts and truly appreciate all the time and effort you've put into educating us. I haven't done any aas but wanted to educate myself a lot more so I can at the very least make an informed decision. I'm unable to take anything liver toxic. Contracted hep c about 10 years ago and have yet to be treated as my insurance company (highmark) balked at the cost.

 

[Michael Scally MD]

Schwingel PA, Cotrim HP, dos Santos CrR, et al. Recreational Anabolic-Androgenic Steroid Use Associated With Liver Injuries Among Brazilian Young Men. Substance Use & Misuse 2015:1-9. http://www.tandfonline.com/doi/full/10.3109/10826084.2015.1018550

Background: The recreational use of anabolic-androgenic steroids (AAS) has reached alarming levels among healthy people. However, several complications have been related to consumption of these drugs, including liver disorders.

Objective: To evaluate the prevalence of liver injuries in young Brazilian recreational AAS users. Methods: Between February/2007 and May/2012 asymptomatic bodybuilders who were ≥18 years old and reported AAS use for ≥6 months were enrolled. All had clinical evaluations, abdominal ultrasound (AUS), and blood tests.

Results: 182 individuals were included in the study. The median age (interquartile range) was 26.0 years (22.0–30.0) and all were male.

Elevated liver enzyme levels were observed in 38.5% (n = 70) of AAS users, and creatine phosphokinase was normal in 27.1% (n = 19) of them. Hepatic steatosis was observed by AUS in 12.1% of the sample. One individual had focal nodular hyperplasia and another had hepatocellular adenoma. One case each of hepatitis B and C virus infection was found.

A diagnosis of toxic liver injury was suggested in 23 (12.6%) AAS users without a history of alcohol or other medications/drugs consumption, or evidence of other liver diseases.

Conclusions/Importance: Young Brazilian recreational AAS users presented a wide spectrum of liver injuries that included hepatotoxicity, fatty liver, and liver neoplasm. They also presented risk factors for liver diseases such as alcohol consumption and hepatitis B and C virus infection. The results suggest that the risk of AAS use for the liver may be greater than the esthetic benefits, and demonstrate the importance of screening AAS users for liver injuries.

 

[Michael Scally MD]

Schwingel PA, Zoppi CuC, Cotrim HP. The Influence of Concomitant Use of Alcohol, Tobacco, Cocaine, and Anabolic Steroids on Lipid Profiles of Brazilian Recreational Bodybuilders. Substance Use & Misuse 2014;49(9):1115-25.
http://www.tandfonline.com/doi/full/10.3109/10826084.2014.903753

Anabolic-androgenic steroids (AAS) are used to enhance physical performance and/or appearance. The aim of this study was to evaluate the influence of the concomitant use of alcohol, tobacco, cocaine, and AAS on blood lipid profiles of 145 asymptomatic male bodybuilders from the Northeast region of Brazil. Interviews, clinical exams, and serological evaluations were performed on all participants between 2007 and 2009. All subjects’ self-reported use of testosterone or its derivatives, 118 individuals reported alcohol intake, 27-reported cigarette smoking, and 33 confirmed cocaine use. Four subjects were users of all drugs at the same time. Higher levels of total cholesterol and LDL-cholesterol were observed among concomitant users of alcohol, tobacco, cocaine, and AAS. The study's limitations are noted.


Schwingel PA, Cotrim HP, Salles BR, et al. Anabolic-androgenic steroids: a possible new risk factor of toxicant-associated fatty liver disease. Liver International 2011;31(3):348-53. http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02346.x/abstract

Background: Industrial toxin and drugs have been associated with non-alcoholic fatty liver disease (NAFLD); in these cases, the disease has been termed toxicant-associated steatohepatitis (TASH).

Aim: This study hypothesizes that the use of anabolic-androgenic steroids (AAS) could also be a risk factor to TASH or better toxicant-associated fatty liver disease (TAFLD) development.

Methodology: Case–control study including 180 non-competitive recreational male bodybuilders from August/2007 to March/2009. Ninety-five had a history of intramuscular AAS use (cases; G1) and 85 were non-users (controls; G2). They underwent a clinical evaluation and abdominal ultrasound, and their blood levels of aminotransferases, creatine phosphokinase (CPK), lipids, glucose and insulin were measured. TAFLD criteria: history of AAS use >2 years; presence of hepatic steatosis on ultrasound and/or aminotransferase alterations with normal CPK levels; exclusion of ethanol intake ≥20 g/day or use of other drugs; and exclusion of obesity, dyslipidaemia, diabetes and other liver diseases. Homeostasis model assessment for insulin resistance ≥3 was considered insulin resistant. Independent t-test, odds ratio (OR) and 95% confidence intervals (95% CI) were calculated.

Results: All cases were asymptomatic. Clinical and laboratorial data were similar in G1 and G2 (P>0.05). TAFLD criteria were observed in 12.6% of the G1 cases and 2.4% of controls had criteria compliant with non-alcoholic fatty liver related to metabolic conditions. OR was 6.0 (95% CI: 1.3–27.6).

Conclusions: These results suggest that AAS could be a possible new risk factor for TAFLD. In this type of fatty liver disease, the individuals had a low body fat mass and they did not present insulin resistance.

 

[Michael Scally MD]

[N-acetylcysteine (NAC)] Antioxidants Can Increase Melanoma Metastasis In Mice

Antioxidants are found in a variety of foods and dietary supplements and are frequently used with the goal of preventing cancer, but mounting evidence suggests that they may not be as beneficial as once thought.

Clinical studies have shown mixed or no benefits, and other works demonstrated that antioxidants may accelerate the progression of lung cancer.

Now, Le Gal et al. discovered that some common antioxidants increase the rate of melanoma cell migration and invasion and increase metastasis in a mouse model.

These are early findings, and additional work will be required to confirm the generalizability of this observation.

Nevertheless, the results suggest a need for caution in the use of antioxidants, especially for patients with existing cancer.

Le Gal K, Ibrahim MX, Wiel C, et al. Antioxidants can increase melanoma metastasis in mice. Science Translational Medicine 2015;7(308):308re8-re8. http://stm.sciencemag.org/content/7/308/308re8

Antioxidants in the diet and supplements are widely used to protect against cancer, but clinical trials with antioxidants do not support this concept.

Some trials show that antioxidants actually increase cancer risk and a study in mice showed that antioxidants accelerate the progression of primary lung tumors.

However, little is known about the impact of antioxidant supplementation on the progression of other types of cancer, including malignant melanoma.

We show that administration of N-acetylcysteine (NAC) increases lymph node metastases in an endogenous mouse model of malignant melanoma but has no impact on the number and size of primary tumors.

Similarly, NAC and the soluble vitamin E analog Trolox markedly increased the migration and invasive properties of human malignant melanoma cells but did not affect their proliferation.

Both antioxidants increased the ratio between reduced and oxidized glutathione in melanoma cells and in lymph node metastases, and the increased migration depended on new glutathione synthesis.

Furthermore, both NAC and Trolox increased the activation of the small guanosine triphosphatase (GTPase) RHOA, and blocking downstream RHOA signaling abolished antioxidant-induced migration.

These results demonstrate that antioxidants and the glutathione system play a previously unappreciated role in malignant melanoma progression.

 

[Michael Scally MD]

[1923] Severe and Prolonged Jaundice Associated with Body Building Supplements (BBS): Review of 44 Cases from the Drug-Induced Liver Injury Network (DILIN)
http://onlinelibrary.wiley.com/doi/10.1002/hep.28237/full

Background & Aim: The use of body building supplements (BBS) containing anabolic steroids (AS) continues to rise despite efforts to curtail their availability. We sought to characterize the clinical features and outcomes of presumed AS-induced jaundice in patients taking BBS prospectively enrolled in the DILIN.

Methods: 44 (5%) out of 847 cases of liver injury attributed to drug or herbal dietary supplements enrolled between Sept 2004 and March 2013 were attributed solely to BBS. The presence of various natural and synthetic androgens in consumed products was quantified by LC/MS compared with 18 known standards with an average assay sensitivity [limit of quantitation] ~ 38 fmoles/mg of product. Liver biopsies were interpreted by the study hepatopathologist without clinical information.

Results: All 44 were men, ages 21 to 59 (mean = 32) years with 81% self-identified as Caucasian and the remainder African-American. 2 subjects had chronic HCV infection. The BBS products were used for body building and purported to contain various AS with different chemical structures and commercial names. All were were taken orally in otherwise healthy males.

Median latency to onset was 1.8 (range 0.4 to 14) months, but the exact dates of starting and stopping were not always available. All 44 cases were jaundiced and symptomatic at presentation and 43 patients had pruritus that was frequently severe, prolonged and debilitating.

Initial median bilirubin was 9.8 mg/dL, ALT 168 U/L, Alk P 111 U/L and INR 1. Subsequently, median ALT fell steadily, while Alk P and bilirubin levels increased 2-3 fold before falling. Peak median bilirubin in first 6 months was 25.8 (range 7.3- 63).

64% were hospitalized and 18% had evidence of hepatic dysfunction (e.g. elevated INR). Liver biopsy in 22 patients reviewed revealed canalicular cholestasis often with only mild portal and lobular inflammation, in contrast to the classic “bland cholestasis” often described in association with AS.

Symptomatic hepatic failure was not observed and no patient died or required liver transplantation.

Seven of the 44 patients (16%) had creatinine elevation > 1.5 mg/dL during their episode which trended down as the bilirubin improved.

Of 14 BBS products available for analysis, 71% had identifiable AS along with other non-defined steroid containing compounds.

Conclusion: Jaundice associated with BBS containing AS is a distinct clinical syndrome marked by severe and prolonged cholestasis in previously healthy men but which did not lead to hepatic failure or chronic liver injury in this study. AS were often identified in BBS despite efforts to limit their availability.

 

[Michael Scally MD]

[842] Low Serum Testosterone Predicts Outcome in Men with Cirrhosis Independent of the MELD Score
http://onlinelibrary.wiley.com/doi/10.1002/hep.28219/full

Background: Low serum testosterone has been independently associated with mortality in a retrospective study of men with advanced liver disease. This study aims to prospectively explore the relationship between low testosterone and outcome in a large cohort of men with cirrhosis

Methods: We conducted a prospective observational study at a single centre. All men with cirrhosis were invited to undergo baseline sex hormone profile screening during outpatient consultations. Standard parameters including MELD score and Child Pugh Score were also documented at baseline. Patients were then followed for 12 months to assess the composite end-point of mortality or liver transplantation. Secondary outcomes include mortality, transplantation, hospitalisation and fracture.

Results: 203 men with cirrhosis were enrolled between April 2013 and March 2014. The median age was 55 years [50, 64], Child Pugh score was 6 [5, 9] MELD score was 10 [8, 15].

The median total testosterone level was 17.6nmol/L [8.55, 25.35] (normal 10-27.6nmol/L) and 28.1% of men had low total testosterone. During the 12 month follow-up period 27 patients died and 12 patients received a liver transplant.

Median serum testosterone was lower in men who died than those who did not (3.20nmo-l/L [1.05; 12.6] versus 18.1 nmol/L [10.6; 26.0], p < 0.001. Median MELD score was 18 [15.5; 22.5] in those who died versus 9 [7; 13] in those who remained alive, p < 0.001.

On multivariable analysis incorporating both MELD score and total testosterone, testosterone was significantly associated with the composite endpoint of death or transplant (HR 0.95, [0.91, 0.99], p = 0.023), as was MELD score (HR 1.29, [1.19, 1.36), p < 0.001).

Total testosterone by itself confers a 13% risk increase per 1 nmol/l decrease, however adjusting for MELD reduces the independent influence of testosterone to a 5.2% increase in risk of the composite endpoint for every 1 nmol/l decrease in testosterone.

Conclusion: Low serum testosterone is associated with an increased risk of death or transplantation independent of the MELD score in men with cirrhosis. This represents an objective biomarker that may be able to assist in the prediction of prognosis.

 

[Payne]

What sort of complications are we talking here say we cycle for about 3 years with sane dosages. There isn't really any information on the long term effects of AAS. I believe orals should be avoided but what about test only cycles. Tren seems to be unsafe.

Some say that orals are safer. I don't know why, just prefer injection anyway.

 

[Michael Scally MD]

Popular Rochdale bodybuilder Dean Wharmby died as a 'direct cause' of taking steroids, inquest hears
Popular Rochdale bodybuilder Dean Wharmby died as a 'direct cause' of taking steroids, inquest hears

A popular body builder died as a ‘direct cause’ of taking steroids, an inquest heard.

Dean Wharmby’s misuse of anabolic steroids caused his death from liver cancer on July 19 this year, coroner Lisa Hashmi ruled.

The inquest was told fitness fan Dean, 39, of Brookland Street, from Rochdale’s Buersil area, first developed health problems in 2010, when multiple tumours were found in his liver.

The fitness enthusiast, who had been taking steroids for several years, later developed liver cancer with the drugs cited as the ‘direct cause’ of his death by Mrs Hashmi.

 

[hankmoody]

Very informative thread! thank you!