Anabolic Steroids & Liver [GI]

[Dr JIM]

Yeah, but as far as I can tell both are referring to AAS side effects:

"They demonstrate a rare and not widely known about, but potentially fatal adverse effect of AAS, now becoming prevalent with the high use of these drugs."

IOW, it is a rare side effect in users of AAS.

And it is a prevalent side effect in users of AAS.

They do say "high use" of AAS.

 

[Dr JIM]

I agree @Millard Baker the authors wrongly imply the prevalence of HCC is higher in AAS users than the general population, and reflects a common causal bias in case reports of this nature.

The fact is although NINE case reports have linked HCC to AAS abuse the number required, using HCC and Hep-C data, to assess risk alone would approximate several hundred.

I can’t imagine we will ever know bc HCC is not only rare but slow growing

A study designed to assess HCC/ASS prevalence would span at least ten years, require thousands of chronic users, who are willing to accurately log their consumption and follow up on no less than an annual basis,

Regards
Jim

 

[Michael Scally MD]

A male in his 30s with recent legal trouble and potential pending job loss purposefully stepped in front of a train and received multiple blunt force injuries of the head and trunk. The manner of death was certified as suicide.

This paper presents the death of a known professional bodybuilder with pancreatic islet hyperplasia identified upon histologic examination of the pancreas. Based upon information available in the medical literature (i.e., how common AAS usage is and the associated of AAS use and pancreatic islet hyperplasia), the most likely source of the pancreatic islet hyperplasia in this case was the use of AAS. Further exploration of this potential association in a larger case series would be prudent, as islet hyperplasia could provide a more reliable and specific histologic marker of AAS use than would cardiac hypertrophy or the other described cardiac effects.


Weinand J, Kemp WL. Pancreatic Islet Hyperplasia: A Potential Marker for Anabolic-Androgenic Steroid Use. Academic forensic pathology 2018;8:777-85. SAGE Journals: Your gateway to world-class research journals

It has been estimated that up to four million Americans have used anabolic-androgenic steroids (AAS) to increase muscle mass - either for improved athletic performance, enhanced personal appearance, or both.

While the pathologic effects of supra-physiologic doses of AAS have been well-described for some organ systems, such as the cardiovascular system, the effects on other organ systems are less well-described; for example, there is a dearth of knowledge in the medical literature regarding the effects of recreational use of AAS on the islet cells of the endocrine pancreas.

As pancreatic islet hyperplasia has previously been described in the literature in a group of patients receiving long-term AAS treatment for Fanconi anemia, it is reasonable to suggest that the use of AAS by bodybuilders could produce the same (or similar) histologic changes.

We present A case that offers support for the association of anabolic-androgenic steroid use and pancreatic islet hyperplasia.

 

[88general88]

These Pro-Hormones have been known for a long time as being very harsh on the liver, and the body in general. Sure they are easily accessible and pretty cheap, but there is a price to pay. I stopped all forms of orals long ago and have never looked back. My blood tests have thanked me ever since.

Actually, they maybe easier to get hands on, but as far as price wise. The majority of the time they end up me much more expensive then AAS

 

[Michael Scally MD]

[OA] Histologically Proven Hepatic Steatosis Associates with Lower Testosterone Levels in Men with Obesity

Men with obesity often present with low testosterone (T) and sex hormone-binding globulin (SHBG) levels. Several mechanisms for this have been proposed, but as SHBG is secreted by hepatocytes and sex steroids undergo hepatic metabolization, this study investigates whether severity and histological components of nonalcoholic fatty liver disease (NAFLD) are associated with sex steroid levels in obese men.

This cross-sectional study included 80 obese men (age: 46 ± 11 years; body mass index: 42.2 ± 5.5 kg m−2). Serum levels of total T and estradiol (E2) were measured using liquid chromatography coupled with tandem mass spectroscopy (LC/MS-MS) and SHBG and gonadotropins by immunoassay. Liver biopsies were evaluated using Steatosis, Activity, and Fibrosis scoring.

Participants with steatohepatitis had similar median (1stquartile–3rd quartile) total T levels (7.6 [5.0–11.0] nmol l−1 vs 8.2 [7.2–10.9] nmol l−1; P = 0.147), lower calculated free T (cFT) levels (148.9 [122.9–188.8] pmol l−1 vs 199.5 [157.3–237.6] pmol l−1; P = 0.006), and higher free E2/T ratios (10.0 [6.4–13.9] x10-3 vs 7.1 [5.7–10.7] x10-3;

Van de Velde F, Bekaert M, Hoorens A, Geerts A, T'Sjoen G, Fiers T, Kaufman JM, Van Nieuwenhove Y, Lapauw B. Histologically proven hepatic steatosis associates with lower testosterone levels in men with obesity. Asian J Androl [Epub ahead of print] [cited 2019 Jul 5]. Available from: http://www.ajandrology.com/preprintarticle.asp?id=262150

 

[Michael Scally MD]

Drug-Induced Liver Injury — Types and Phenotypes

The liver has a range of responses to drug-induced injury, with a number of phenotypes. In addition, idiosyncratic reactions may occur as a consequence of both direct drug action and indirect drug effects. Antibiotics are the most common cause of drug-induced liver injury.

Hoofnagle JH, Björnsson ES. Drug-Induced Liver Injury — Types and Phenotypes. New England Journal of Medicine 2019;381:264-73. https://doi.org/10.1056/NEJMra1816149

 

[Michael Scally MD]

[OA] Anabolic Steroid Toxicity

Androgenic-anabolic steroids (AAS) are widely missed worldwide as performance-enhancing agents. The use of AAS started in competitive sports and spread to non-competitive athletes. The World Anti-Doping Agency banned AAS since the 1950s and has continued adding new methods and new variations of AAS. Currently, the CDC estimates that the majority of AAS users are adolescent males.

The hypothalamus is the integrating center for the reproductive axis (HPG). It receives signals from the amygdala, olfactory, and visual cortex. Gonadotropin-releasing hormone (GnRH) then gets released into a venous portal system which carries it to adenohypophysis of the pituitary gland.

In addition to signals from the CNS, humoral factors from the testes also play a role in modulating the release of GnRH. Gonadotropin-releasing hormone release is pulsatile, seasonal, and circadian. Levels of GnRH are highest during spring and in the morning with peaks occurring every 90 to 120 minutes.

Once released, GnRH acts on the pituitary gland and promotes the production and release of luteinizing hormone (LH) and to a lesser extent, follicle stimulating hormone (FSH). Luteinizing hormone, in turn, acts on Leydig cells in the testes, which are the site of production of most of the endogenous androgens.

Androgen production also occurs in the adrenal cortex and the conversion of androstenedione peripherally. Testosterone, in turn, inhibits the production of GnRH in the hypothalamus.

Testosterone is a 19-carbon steroid and is the most potent endogenous androgen. As such, it is the basis of most AAS. Addition of various functional groups to this basic 19-carbon structure changes androgenic, anabolic, and toxicity profiles of AAS.

…

Middlebrook I, Schoener B. Anabolic Steroid Toxicity. [Updated 2019 Jun 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: Anabolic Steroid Toxicity - StatPearls - NCBI Bookshelf

 

[Michael Scally MD]

[OA] Role of Anabolic Agents in Colorectal Carcinogenesis: Myths and Realities

Colorectal cancer (CRC) is one of the four leading causes of cancerrelated mortality worldwide. Even though over the past few decades the global scientific community has made tremendous efforts to understand this entity, many questions remain to be raised on this issue and even more to be answered.

Epidemiological findings have unveiled numerous environmental and genetic risk factors, each one contributing to a certain degree to the final account of new CRC cases. Moreover, different trends have been revealed regarding the age of onset of CRC between the two sexes.

That, in addition to newly introduced therapeutic approaches for various diseases based on androgens, antiandrogens and anabolic hormones has raised some concerns regarding their possible carcinogenic effects or their synergistic potential with other substances/risk factors, predisposing the individual to CRC.

Notably, despite the intense research on experimental settings and population studies, the conclusions regarding the majority of anabolic substances are ambiguous. Some of these indicate the carcinogenic properties of testosterone, dihydrotestosterone (DHT), growth hormone and insulinlike growth factor (IGF) and others, demonstrating their neutral nature or even their protective one, as in the case of vitamin D.

Thus, the synergistic nature of anabolic substances with other CRC risk factors (such as type 2 diabetes mellitus, metabolic syndrome and smoking) has emerged, suggesting a more holistic approach.

Krasanakis T, Nikolouzakis TK, Sgantzos M, et al. Role of anabolic agents in colorectal carcinogenesis: Myths and realities (Review). Oncology reports 2019. Role of anabolic agents in colorectal carcinogenesis: Myths and realities (Review)

 

[Michael Scally MD]

[OA] Spontaneous Haemorrhage of Hepatic Adenoma in A Patient Addicted to Anabolic Steroids

This case report describes a patient with a nearly fatal spontaneous haemorrhage of a hepatic adenoma that occurred in association with anabolic androgenic steroid (AAS) use. The patient was addicted to AAS and had been using exceptionally high dosages as well as growth hormone. After cessation of AAS use, testosterone replacement therapy was started to prevent post-AAS hypogonadism and consequent relapse.

Smit DL, Nuijens JH, de Ronde W. Spontaneous haemorrhage of hepatic adenoma in a patient addicted to anabolic steroids. The Netherlands journal of medicine 2019;77:261-3. Article: Spontaneous haemorrhage of hepatic adenoma in a patient addicted to anabolic steroids (full text) - September 2019 - NJM

 

[Michael Scally MD]

Hepatocellular Carcinomas [HCC] and Hepatocellular Adenomas [HCA] in Non-cirrhotic Patients: What You See May Not Be Enough

Case 1. A previously healthy 16-year-old man was initially evaluated in the emergency department for traumatic injuries following a high-impact motor vehicle accident. He was a bodybuilder who used anabolic steroids.

He denied abdominal or back pain. His physical examination was significant for a palpable liver edge. Routine laboratory tests including liver function tests were unremarkable. A computed tomographic (CT) scan showed an unsuspected mass in the right lobe of the liver.

He underwent partial hepatectomy; the resected surgical specimen showed a well-differentiated hepatocellular carcinoma. The tumor was confined to the liver with no vascular invasion or regional lymph node involvement.

The patient and his guardian decided against undergoing chemotherapy. The patient is being followed up by the pediatric oncology service, to monitor for possible tumor progression, with periodic surveillance by imaging with MRI.

Patients with fatty liver disease, anabolic steroid use, and several rare congenital and inherited metabolic disorders are also more likely to develop HCC.

First reported in 1965, non-cirrhotic HCC also occurs when anabolic steroids are used to build muscle mass; as in case 1, these drugs have a high first-pass metabolism in the liver and can cause significant liver toxicity, including intrahepatic structural changes of cholestasis, and both benign and malignant tumors.

In the literature, there are several case reports of patients developing HCC while being treated with androgenic steroids for the anemia of Fanconi’s syndrome, but fewer cases reports in patients using anabolic steroids to increase muscle mass.

Ling C, Khalid S, Martin D, Hanson J, Castresana D, McCarthy D. HCCs and HCAs in Non-cirrhotic Patients: What You See May Not Be Enough. Digestive diseases and sciences 2019. https://link.springer.com/article/10.1007%2Fs10620-019-05920-z

 

[Michael Scally MD]

Drug-induced Liver Injury Secondary to Herbal and Dietary Supplements

The use of herbal and dietary supplements (HDS) is increasing in the United States and worldwide. Its significant association with liver injury has become a concern, particularly because rates of hepatotoxicity caused by HDS are increasing.

There are variety of HDS available, ranging from multi-ingredient substances, to anabolic steroids for bodybuilding purposes, to individual ingredients for purposes of supplementing a diet.

This article reviews the impact of liver injury cause by HDS and explores the hepatotoxic potential of such products and their individual ingredients.

Zheng E, Sandhu N, Navarro V. Drug-induced Liver Injury Secondary to Herbal and Dietary Supplements. Clinics in liver disease 2020;24:141-55. Drug-induced Liver Injury Secondary to Herbal and Dietary Supplements - ScienceDirect

 

[Old]

Possible clinical cure in a high percentage of cases of liver cirrhosis with a treatment based on high doses of testosterone and vitamin B 1 [Possible clinical cure in a high percentage of cases of liver cirrhosis with a treatment based on high doses of testosterone and vitamin B 1 ]. - PubMed - NCBI

This treatment protocol is old – 1964 and earlier, starting in 1943. However if you look up current treatment, you will not find results this good. It would be interesting to know if this is still in use, at least in Italy where this was done. Some patients were advanced and in a coma yet survived due to the treatment.

As for the dosage, they use TP at 700mg/wk for 2 weeks alternating at 350mg/wk for 2 weeks. Treatment continues well over 3 years with the later dosing after "clinical cure" of 175 mg/wk. Same amounts for women as men though sometimes using DHT instead of T to reduce virilization issues.

It works by breaking down the cirrhosis into smaller amounts allowing the liver to start functioning normally.

Some excerpts:

A therapeutic regimen for hepatic cirrhosis based on administration of large doses of testosterone propionate plus thiamine has led to “clinical cure” in 60 percent of 700 cases. Clinical signs of the disease have disappeared and biochemical values have returned to normal. Therapy is continued at least three years after clinical symptoms disappear. The rationale of this method of treatment includes the theory that a deficiency of hyaluronidase activity in the liver may be responsible for the enormous growth of connective tissues.

The essential point of our method of treatment is the intramuscular administration of large doses of testosterone (50 to 100 mg daily or EOD) and of thiamine (50 mg two or three times a week). All the androgenic hormones and testosterone derivatives have anticirrhotic activity. We have had the best results with testosterone propionate.
We have adopted the following treatment, which can be modified in individual cases:
1st and 2nd weeks: 50mg of TP EOD; 100 mg of B1 twice a week.
3rd and 4th weeks: 50 mg of TP every day; 100 mg of B1 twice a week.
5th and 6th week: 100 mg of TP EOD; 50 mg of B1 twice a week.
7th and 8th weeks: 100 mg of TP every day; 50 mg of B1 twice a week.
9th and 10th weeks: 100mg of TP EOD; 500 mg of B1 twice a week.
In succeeding weeks, 100 mg of TP is given intramuscularly every day for two weeks then EOD for two weeks. This four week cycle is repeated thereafter. Thiamine (50 mg intramuscularly twice a week) should be continue for the duration of the treatment period.

Once clinical cure has been achieved, it is difficult to decide when to discontinue therapy. ... Therapy should not be interrupted if complications arise. It must be continue, along with treatment which is directed against the complications.

Our observations allow us the state the testosterone treatment must be continue for at least three years following clinical cure in order to prevent a relapse. When clinical cure has been achieved, one should continue to give TP for two to three months in alternating course of 100 mg daily for two weeks and 100 mg EOD for two weeks. Thereafter, dosage can be reduced. Beginning three months after clinical cure, the following schedule can be followed in most cases:
3rd and 4th months (after clinical cure): 100 mg TP EOD; 50 mg B1 twice a week
4th through 36 months (or longer): 50 mg TP EOD; 25 mg B1 twice a week.

 

[Michael Scally MD]

Spectrum of Drug Induced Liver Injury Caused by Anabolic Androgenic Steroids Abuse

Purpose of Review - Potent anabolic androgenic steroids (AAS) are often illegally present in commercially available body building supplements (BBS) and may cause drug induced liver injury (DILI) with different phenotypes.

Recent Findings - AAS induced DILI typically presents with a prolonged cholestatic liver injury with pruritus and a typical enzyme pattern of elevated transaminases that rapidly fall as alkaline phosphatase slowly increases. Liver biopsy reveals bland cholestasis that usually does not have chronic sequalae. Pathophysiology is unknown and genetic variants in genes associated with cholestatic syndromes were observed in a minority of patients. Chemical analysis of BBS have identified controlled AAS, which were not documented on the label.

Summary - More frequent use of BBS in males to enhance physical performance is predicted to increase the incidence of cholestatic DILI. The typical presentation of AAS induced liver injury in an at risk populations should prompt careful assessment of BBS exposure.

Takyar V, Stolz A. Spectrum of Drug Induced Liver Injury Caused by Anabolic Androgenic Steroids Abuse. Current Hepatology Reports 2019. Spectrum of Drug Induced Liver Injury Caused by Anabolic Androgenic Steroids Abuse

 

[Michael Scally MD]

[OA] Severe and Protracted Cholestasis in 44 Young Men Taking Bodybuilding Supplements: Assessment of Genetic, Clinical and Chemical Risk Factors

Background Bodybuilding supplements can cause a profound cholestatic syndrome.

Aim To describe the drug-Induced liver injury network's experience with liver injury due to bodybuilding supplements.

Methods Liver injury pattern, severity and outcomes, potential genetic associations, and exposure to anabolic steroids by product analysis were analysed in prospectively enrolled subjects with bodybuilding supplement-induced liver injury with causality scores of probable or higher.

Results Forty-four males (mean age 33 years) developed liver injury with a median latency of 73 days. Forty-one per cent presented with hepatocellular pattern of liver injury as defined by the R > 5 ([Fold elevation of ALT] ÷ [Fold elevation of Alk Phos] (mean, range = 6.4, 0.5-31.4, n = 42) despite all presenting with clinical features of cholestatic liver injury (100% with jaundice and 84% with pruritus).

Liver biopsy (59% of subjects) demonstrated a mild hepatitis and profound cholestasis in most without bile duct injury, loss or fibrosis. Seventy-one per cent were hospitalised, and none died or required liver transplantation. In some, chemical analysis revealed anabolic steroid controlled substances not listed on the label.

No enrichment of genetic variants associated with cholestatic syndromes was found, although mutations in ABCB11 (present in up to 20%) were significantly different than in ethnically matched controls.

Conclusions Patients with bodybuilding supplements liver injury uniformly presented with cholestatic injury, which slowly resolved. The ingested products often contained anabolic steroids not identified on the label, and no enrichment in genetic variants was found, indicating a need for additional studies.

Stolz A, Navarro V, Hayashi PH, et al. Severe and protracted cholestasis in 44 young men taking bodybuilding supplements: assessment of genetic, clinical and chemical risk factors. Alimentary Pharmacology & Therapeutics 2019;49:1195-204. https://doi.org/10.1111/apt.15211

 

[Michael Scally MD]

Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes.

Anabolic-androgenic steroids are testosterone derivatives, used by body-builders to increase muscle mass. Epistane (EPI) is an orally administered 17α-alkylated testosterone derivative with 2a-3a epithio ring. We identified four individuals who, after EPI consumption, developed long-lasting cholestasis.

The bile acid (BA) profile of three patients was characterized, as well the molecular mechanisms involved in this pathology. The serum BA pool was increased from 14 to 61-fold, basically on account of primary conjugated BA (cholic acid (CA) conjugates), whereas secondary BA were very low.

In in vitro experiments with cultured human hepatocytes, EPI caused the accumulation of glycoCA in the medium. Moreover, as low as 0.01 μM EPI upregulated the expression of key BA synthesis genes (CYP7A1, by 65% and CYP8B1, by 67%) and BA transporters (NTCP, OSTA and BSEP), and downregulated FGF19. EPI increased the uptake/accumulation of a fluorescent BA analogue in hepatocytes by 50-70%.

Results also evidenced, that 40 μM EPI trans-activated the nuclear receptors LXR and PXR. More importantly, 0.01 μM EPI activated AR in hepatocytes, leading to an increase in the expression of CYP8B1. In samples from a human liver bank, we proved that the expression of AR was positively correlated with that of CYP8B1 in men.

Taken together, we conclude that EPI could cause cholestasis by inducing BA synthesis and favouring BA accumulation in hepatocytes, at least in part by AR activation. We anticipate that the large phenotypic variability of BA synthesis enzymes and transport genes in man provide a putative explanation for the idiosyncratic nature of EPI-induced cholestasis.

Petrov PD, Fernández-Murga L, Conde I, et al. Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes [published online ahead of print, 2020 Jan 1]. Arch Toxicol. 2020;10.1007/s00204-019-02643-y. Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes

 

[Bigboy727]

Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes.

Anabolic-androgenic steroids are testosterone derivatives, used by body-builders to increase muscle mass. Epistane (EPI) is an orally administered 17α-alkylated testosterone derivative with 2a-3a epithio ring. We identified four individuals who, after EPI consumption, developed long-lasting cholestasis.

The bile acid (BA) profile of three patients was characterized, as well the molecular mechanisms involved in this pathology. The serum BA pool was increased from 14 to 61-fold, basically on account of primary conjugated BA (cholic acid (CA) conjugates), whereas secondary BA were very low.

In in vitro experiments with cultured human hepatocytes, EPI caused the accumulation of glycoCA in the medium. Moreover, as low as 0.01 μM EPI upregulated the expression of key BA synthesis genes (CYP7A1, by 65% and CYP8B1, by 67%) and BA transporters (NTCP, OSTA and BSEP), and downregulated FGF19. EPI increased the uptake/accumulation of a fluorescent BA analogue in hepatocytes by 50-70%.

Results also evidenced, that 40 μM EPI trans-activated the nuclear receptors LXR and PXR. More importantly, 0.01 μM EPI activated AR in hepatocytes, leading to an increase in the expression of CYP8B1. In samples from a human liver bank, we proved that the expression of AR was positively correlated with that of CYP8B1 in men.

Taken together, we conclude that EPI could cause cholestasis by inducing BA synthesis and favouring BA accumulation in hepatocytes, at least in part by AR activation. We anticipate that the large phenotypic variability of BA synthesis enzymes and transport genes in man provide a putative explanation for the idiosyncratic nature of EPI-induced cholestasis.

Petrov PD, Fernández-Murga L, Conde I, et al. Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes [published online ahead of print, 2020 Jan 1]. Arch Toxicol. 2020;10.1007/s00204-019-02643-y. Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes

Well being a commercial Real estate developer this makes complete sense! Thanks for the share!

 

[TheSpectre]

What about sulfasalazine?

 

[Michael Scally MD]

[Mice] Abuse of Androgenic Anabolic Drugs With "Cycling" Induces Hepatic Steatosis

Highlights

· This study is the first to have tested the usefulness of the “Cycling” protocol in the SAA abuse,
· The protocol is simplified to better follow the liver response at stop treatment,
· Our results reports that the use of AAS for a period of 3 months by only a 10 times supra-therapeutic dose is associated with a lot of deleterious effects on liver with peliosis and hepatic inflammations in male,
· Morover, stop treatment showed a very distinguished periportal microvesicular steatosis, thrombosis with a fibro-hyaline organization and loss of structure in different areas.
· Therefore, the periodical cessation of treatment which constitutes a “Cycling” protocol for abusers leads to the accumulation of fat in the liver and increases hepatic distress.

BACKGROUND: The importance of the present study comes from the lack of sufficient information about the reversibility of the potential hepatic histopathological alterations which may result from anabolic androgenic drugs abuse by "Cycling" protocol. So, the aim of this study is to explore the negative effects of Deca-Durabolin abuse in hepatic function and structure during an administration cycle.

METHODS: For our purpose, study was performed on 40 male adult mices. Animals were divided into five groups of 8 animals each treated weekly by Deca-Durabolin (nandrolone decanoate) at 30g/kg of BW during one month (GI); during two months (GII); during three months (GIII); during three months followed by six weeks of treatment discontinuation (GIV) and Control (C). Plasma assay of liver enzymes (ALT and AST) and cytohistological examination to determine the histopathological damage properties of the liver were performed.

RESULTS: Our results showed that the animals supported very well the administrated substance. Our study showed an increase in plasma levels of liver enzymes (ALT and AST) with the duration of treatment accompanied by important degenerative changes in hepatic tissue with peliosis evolution after two months of treatment. These damages worsen again 6 weeks after stopping treatment and ended by the development of hepatic steatosis with increases hepatic distress.

CONCLUSION: These results ported that the use of AAS with "Cycling" may lead to the development of hepatic steatosis before progressing to more serious pathological liver situations in AAS abusers.

Kahal A, Allem R, Zahzeh T, Oulmane S, Tafroukhte Z. Abuse of androgenic anabolic drugs with "Cycling" induces hepatic steatosis in adult male mice. Steroids 2019:108574. Abuse of androgenic anabolic drugs with “Cycling” induces hepatic steatosis in adult male mice - ScienceDirect

 

[Michael Scally MD]

Anabolic Androgenic Steroids Exert A Selective Remodeling of The Plasma Lipidome That Mirrors the Decrease of The De Novo Lipogenesis In The Liver

Introduction - The abuse of anabolic androgenic steroids (AASs) is a source of public concern because of their adverse effects. Supratherapeutic doses of AASs are known to be hepatotoxic and regulate the lipoproteins in plasma by modifying the metabolism of lipids in the liver, which is associated with metabolic diseases. However, the effect of AASs on the profile of lipids in plasma is unknown.

Objectives - To describe the changes in the plasma lipidome exerted by AASs and to discuss these changes in the light of previous research about AASs and de novo lipogenesis in the liver.

Methods - We treated male Wistar rats with supratherapeutic doses of nandrolone decanoate and testosterone undecanoate. Subsequently, we isolated the blood plasma and performed lipidomics analysis by liquid chromatography-high resolution mass spectrometry.

Results - Lipid profiling revealed a decrease of sphingolipids and glycerolipids with palmitic, palmitoleic, stearic, and oleic acids. In addition, lipid profiling revealed an increase in free fatty acids and glycerophospholipids with odd-numbered chain fatty acids and/or arachidonic acid.

Conclusion - The lipid profile presented herein reports the imprint of AASs on the plasma lipidome, which mirrors the downregulation of de novo lipogenesis in the liver. In a broader perspective, this profile will help to understand the influence of androgens on the lipid metabolism in future studies of diseases with dysregulated lipogenesis (e.g. type 2 diabetes, fatty liver disease, and hepatocellular carcinoma).

Balgoma D, Zelleroth S, Grönbladh A, Hallberg M, Pettersson C, Hedeland M. Anabolic androgenic steroids exert a selective remodeling of the plasma lipidome that mirrors the decrease of the de novo lipogenesis in the liver. Metabolomics. 2020;16(1):12. Published 2020 Jan 10. Anabolic androgenic steroids exert a selective remodeling of the plasma lipidome that mirrors the decrease of the de novo lipogenesis in the liver

 

[Michael Scally MD]