Anabolic Steroids & Liver [GI]

[Michael Scally MD]

Liver cysts are commonly found incidentally from imaging scans or at autopsy.

These benign neoplasms vary in size and represent a heterogeneous group of disorders, for which the demographics, risk factors, apparent inciting event, clinical presentation, and outcome are varied.

Complications that can develop from a liver cyst include development of spontaneous hemorrhage, infection, and/or obstruction.

Although the etiology of liver cysts varies, fatal rupture of a hemorrhagic liver cyst due to anabolic steroid use is a rare occurrence.

In fact, there are few reported cases in journal literature.

We report a case of a fatal liver cyst rupture with resultant hemoperitoneum in the presence of anabolic steroid (stanozolol) use.

Hansma P, Diaz FJ, Njiwaji C. Fatal Liver Cyst Rupture Due to Anabolic Steroid Use: A Case Presentation. Am J Forensic Med Pathol. Fatal Liver Cyst Rupture Due to Anabolic Steroid Use: A Case... : The American Journal of Forensic Medicine and Pathology

 

[Michael Scally MD]

McGettigan MJ, Menias CO, Gao ZJ, Mellnick VM, Hara AK. Imaging of Drug-induced Complications in the Gastrointestinal System. Radiographics 2016;36(1):71-87. RSNA Publications Online

Drug-induced injury commonly affects the gastrointestinal and hepatobiliary systems because of the mechanisms of absorption and metabolism.

In pill esophagitis, injury is frequently related to direct contact with the esophageal mucosa, resulting in small superficial ulcers in the mid esophagus.

Nonsteroidal anti-inflammatory drugs can lead to gastrointestinal tract ulcers and small bowel mucosal diaphragms (thin weblike strictures).

Injury to the pancreatic and hepatobiliary systems can manifest as pancreatitis, acute or chronic hepatitis, cholestasis, or steatosis and steatohepatitis (which may progress to cirrhosis).

Various drugs may also insult the hepatic vasculature, resulting in Budd-Chiari and sinusoidal obstructive syndromes.

Focal lesions such as hepatic adenomas may develop after use of oral contraceptives or anabolic steroids.

Ultrasonography, computed tomography, and magnetic resonance imaging can aid in diagnosis of drug-induced injuries and often are necessary to exclude other causes.

 

[Michael Scally MD]

[Open Access] Peliosis Hepatis Presenting with Massive Hepatomegaly in A Patient with Idiopathic Thrombocytopenic Purpura [Not AAS; Nice Review]

Peliosis hepatis is a rare condition that can cause hepatic hemorrhage, rupture, and ultimately liver failure.

Several authors have reported that peliosis hepatis develops in association with chronic wasting disease or prolonged use of anabolic steroids or oral contraceptives.

In this report we describe a case in which discontinuation of [corticosteroid] steroid therapy improved the condition of a patient with peliosis hepatis.

Our patient was a 64-year-old woman with a history of long-term steroid treatment for idiopathic thrombocytopenic purpura.

Her symptoms included abdominal pain and weight loss; the only finding of a physical examination was hepatomegaly.

We performed computed tomography (CT) and magnetic resonance imaging (MRI) of the liver and a liver biopsy.

Based on these findings plus clinical observations, she was diagnosed with peliosis hepatis and her steroid treatment was terminated.

The patient recovered completely 3 months after steroid discontinuation, and remained stable over the following 6 months.

Kim SB, Kim do K, Byun SJ, et al. Peliosis hepatis presenting with massive hepatomegaly in a patient with idiopathic thrombocytopenic purpura. Clin Mol Hepatol 2015;21(4):387-92. http://www.e-cmh.org/upload/CMH_21_4_387_392.pdf

 

[taco33150]

There is no supplement out there worth taking for the liver..from what I get from the docs..

 

[Michael Scally MD]

[Open Access] Severe Cholestasis and Bile Acid Nephropathy From Anabolic Steroids Successfully Treated With Plasmapheresis

A 31-year-old man was admitted to the hospital for mild confusion, severe pruritus, jaundice, and Acute kidney injury (AKI). Sixteen weeks prior to presentation, he started an Herbal and Dietary Supplement (HDS) regimen for weight loss and muscle building.

On average, he consumed 22 capsules per day from 8 different HDS bottles containing at least 80 ingredients, including a cumulative daily dose (104 mg) of anabolic steroids 4-chloro-17αmethyl-andro-4-ene-3,17β-diol (50 mg) and 2α,3αepithio-17αmethyl-51-androstan-17β-ol (54 mg). After reporting fatigue and change in skin color to his local gastroenterologist, HDS was stopped due to suspected drug-induced liver injury.

He was hospitalized for severe jaundice with total bilirubin of 53 mg/dL. Viral, autoimmune, and inherited causes of liver disease were ruled out. Magnetic resonance cholangiopancreatography ruled out biliary tract pathology or obstruction. Liver biopsy showed significant cholestasis and mild intraparenchymal neutrophilic infiltrate in hepatocytes surrounding the central veins with no significant necrosis, bile duct injury, or steatosis.

Supportive care was provided with intravenous (IV) fluids for pre-renal azotemia, while hydroxyzine, cholestyramine, ursodiol, sertraline, naloxone, and topical emollients were sequentially used for pruritus, with minimal relief. He was started on IV solumedrol 30 mg daily with no improvement in jaundice after 11 days.

Over 2 subsequent hospitalizations he continued to have AKI (creatinine 2 mg/dL), persistent jaundice (total bilirubin 46.5 mg/dL), and uncontrolled pruritus. He lost 100 lbs, developed severe insomnia due to pruritus, reported hallucinations, and was re-admitted for concerns of encephalopathy and liver failure. Exam revealed a chronically ill-appearing man with a flat affect, scleral icterus, and pronounced jaundice. He was well-oriented to questions but displayed asterixis.

He had no tender hepatomegaly, but had extensive excoriations on his torso and extremities induced by pruritus. He had temporal wasting and loss of adipose tissue in his arms and abdomen. Laboratory results during his third hospital admission included an albumin level of 4.7 mg/dL and a prothrombin time of 9.5 s.

We highlight the use of plasmapheresis resulting in rapid improvement in cholestatic jaundice with resolution of AKI. Plasmapheresis should be considered in special cases in which there is progressive clinical decline despite supportive care.

Flores A, Nustas R, Nguyen HL, Rahimi RS. Severe Cholestasis and Bile Acid Nephropathy From Anabolic Steroids Successfully Treated With Plasmapheresis. ACG Case Rep J 2016;3(2):133-5. http://acgcasereports.gi.org/2016/01/20/severe-cholestasis-and-bile-acid-nephropathy-from-anabolic-steroids-successfully-treated-with-plasmapheresis/

 

[Dr JIM]

[Open Access] Severe Cholestasis and Bile Acid Nephropathy From Anabolic Steroids Successfully Treated With Plasmapheresis

Supportive care was provided with intravenous (IV) fluids for pre-renal azotemia, while hydroxyzine, cholestyramine, ursodiol, sertraline, naloxone, and topical emollients were sequentially used for pruritus, with minimal relief. He was started on IV solumedrol 30 mg daily with no improvement in jaundice after 11 days.

Flores A, Nustas R, Nguyen HL, Rahimi RS. Severe Cholestasis and Bile Acid Nephropathy From Anabolic Steroids Successfully Treated With Plasmapheresis. ACG Case Rep J 2016;3(2):133-5. http://acgcasereports.gi.org/2016/01/20/severe-cholestasis-and-bile-acid-nephropathy-from-anabolic-steroids-successfully-treated-with-plasmapheresis/

So much for "hepatic supplements" altering the course of this poor fellas Liver Disease

 

[Michael Scally MD]

So much for "hepatic supplements" altering the course of this poor fellas Liver Disease

Could Not Resist!!!

 

[Dr JIM]

Hard not to love them fellas

 

[Daedae90]

So at age 22 I was diagnosed with hepatitis c, I forget which particular genome and all that but I did my first cycle at 23. Tren a winny and test p. I continued to get liver bloods every 6 months. I ran another cycle of the same above mentioned at age 24. Both were 12 week cycles. I'm now 25 and have non detectable viral levels. I haven't drank or used drugs in 4 years, I ate healthy and exercised.

 

[Notits]

So much for "hepatic supplements" altering the course of this poor fellas Liver Disease

I hope the "what liver support sups should i take?" people read this.

 

[Michael Scally MD]

Sinclair M, Gow PJ, Angus PW, et al. High circulating estrone and low testosterone correlate with adverse clinical outcomes in men with advanced liver disease. Liver Int. High circulating estrone and low testosterone correlate with adverse clinical outcomes in men with advanced liver disease - Sinclair - Liver International - Wiley Online Library

BACKGROUND & AIMS: Circulating testosterone is usually reduced in men with cirrhosis but there has not been a comprehensive analysis of androgen status or circulating estrogens. Little is known about associations between circulating sex steroids with aspects of health in this population.

METHODS: We report data from men with cirrhosis and low serum testosterone (<12nmol/L or calculated free testosterone <230pmol/L). Comprehensive circulating sex steroid profiles were measured by liquid chromatography-mass spectrometry and compared with age-matched controls. Relationships between sex hormone levels, severity of liver disease, biochemistry, and clinical outcomes were assessed.

RESULTS: Serum estrone and estradiol were significantly elevated in men with cirrhosis compared to controls (median 869.1pmol/L vs 133.8pmol/L and 166.7pmol/L vs 84.6pmol/L respectively). Serum estrone correlated with MELD score (correl +0.306, p<0.001), and inversely correlated with serum sodium (correl -0.208, p=0.004) and haemoglobin (correl -0.177, p=0.012). No such correlations were observed for estradiol. Serum testosterone levels inversely correlated with MELD score (correl -0.294, p<0.001), and positively with handgrip strength (correl +0.242, p<0.001), physical activity (correl +0.276, p=0.012), haemoglobin (correl +0.282, p<0.001), and serum sodium (+0.344, p<0.001)). Dihydrotestosterone inversely correlated with MELD score (correl -0.225, p=0.002) and shared similar significant relationships to testosterone.

CONCLUSION: Low serum androgens and elevated serum estrone (but not estradiol) are associated with higher MELD and individual adverse health outcomes in cirrhotic cohort of men selected for low testosterone. Serum estrone may be a novel marker of ill health in this population. Whether low androgens are markers or mediators of ill health requires further investigation.

 

[taco33150]

Are there no liver supplements worth taking ?

 

[MythotiK]

Are there no liver supplements worth taking ?

Lots of water!

 

[taco33150]

Lots of water!

I drink a gallon a day before 4pm and when I get home I take two table spoons of lemon juice then with my dinner a half a cup of cranberry juice

 

[Michael Scally MD]

[Open Access] Hepatotoxicity by Dietary Supplements: A Tabular Listing and Clinical Characteristics

Dietary supplements (DS) are extensively consumed worldwide despite unproven efficacy. The true incidence of DS-induced liver injury (DSILI) is unknown but is probably under-diagnosed due to the general belief of safety of these products. Reported cases of herbals and DS-induced liver injury are increasing worldwide.

The aim of this manuscript is to report a tabular listing with a description of DS associated with hepatotoxicity as well as review the phenotype and severity of DSILI.

Natural remedies related to hepatotoxicity can be divided into herbal product-induced liver injury and DS-induced liver injury.

In this article, we describe different DS associated with liver injury, some of them manufactured DS containing several ingredients (Herbalife products, Hydroxycut, LipoKinetix, UCP-1 and OxyELITE) while others have a single ingredient (green tea extract, linoleic acid, usnic acid, 1,3-Dimethylamylamine, vitamin A, Garcinia cambogia and ma huang).

Additional DS containing some of the aforementioned ingredients implicated in liver injury are also covered. We have also included illicit androgenic anabolic steroids for bodybuilding in this work, as they are frequently sold under the denomination of DS despite being conventional drugs.

Garcia-Cortes M, Robles-Diaz M, Ortega-Alonso A, Medina-Caliz I, Andrade RJ. Hepatotoxicity by Dietary Supplements: A Tabular Listing and Clinical Characteristics. Int J Mol Sci 2016;17(4). http://www.mdpi.com/1422-0067/17/4/537/htm

 

[guimaraes.gerson]

I take 3gr vitamin C a day, 400mg silymarin per day, 400 IU vitamin E per day, 10gr fish oil per day, 20 grams flaxseed a day ..... but I recently discovered that I am with hepatic steatosis, what can I do to treat?

 

[Michael Scally MD]

Sarges P, Steinberg JM, Lewis JH. Drug-Induced Liver Injury: Highlights from a Review of the 2015 Literature. Drug Saf. Drug-Induced Liver Injury: Highlights from a Review of the 2015 Literature - Online First - Springer

Numerous publications contributed to the expanding knowledge base about drug-induced liver injury (DILI) in 2015. New findings from the US Drug Induced Liver Injury Network (DILIN) in their most recently updated registry include a 1- to 3-week delay in the appearance of acute DILI from short-course antibiotics such as cefazolin. They corroborated the finding that acute DILI in patients with underlying liver disease was far more severe and potentially fatal than in patients without liver disease. The only drug that seemed to have an increased risk of hepatotoxicity in these patients was azithromycin.

While nearly one in six patients with acute DILI had persistently elevated liver tests at 6 months, and results for 75 % of these patients continued to be abnormal at 12 months, most of these "chronic" injury cases were relatively minor and the result of cholestatic hepatotoxins.

Newly described DILI agents include tolvaptan, as well as some new direct-acting antiviral protease inhibitors for chronic hepatitis C. The latter have been associated with serious acute hepatitis, hyperbilirubinemia, and decompensation. Herbal hepatotoxicity continues to be increasingly reported, although applying causality assessment to these cases can, in fact, be more challenging than with prescription drugs. As important as cases with DILI, the class of PCSK9 inhibitors used to lower low-density lipoprotein (LDL) cholesterol have not been associated with significant liver injury, in contrast with other lipid-lowering agents.

With respect to pharmacologic DILI risk factors, new data show that drugs metabolized by cytochrome P450 enzymes had a nearly four times higher likelihood of causing DILI. Interestingly, high lipophilicity, which was previously felt to be a risk factor for DILI, was not found to be associated, although more study is needed to confirm this observation.

While human leukocyte antigen (HLA) genotypes have been linked to several specific agents, the role of such testing in the general population remains undefined due to the currently low positive and negative predictive values of the available tests.

New DILI biomarkers, specifically microRNA-122 and keratin-18, among others, appear to have the necessary predictive value to determine the prognosis and outcome of patients with paracetamol (acetaminophen [AAP])-induced acute liver failure (ALF), and may be of great benefit in deciding who requires N-acetylcysteine (NAC), and for what duration. Treatment options for other forms of DILI remain limited; no firm conclusions can currently be drawn for the use of NAC in non-AAP ALF.

 

[bigpoppachump]

I take 3gr vitamin C a day, 400mg silymarin per day, 400 IU vitamin E per day, 10gr fish oil per day, 20 grams flaxseed a day ..... but I recently discovered that I am with hepatic steatosis, what can I do to treat?

To treat you need to stop taking all that nonsense and start drinking nothing but water and start preparing and eating nothing but whole natural foods.

I may get some flack about this from our house Dr's but fish oil definitely without a doubt made me feel worse when my liver disease was at it's worse. I started up and stopped with the fish oil multiple times and each time it had the same results on my overall condition. If you google fish oil and liver problems there are articles out there that state that there may be a downside to taking large amounts of fish oil with a compromised liver.

Glutamine was another supplement that had negative effects while having liver disease . There is a lot of info on this posted in many articles online.

 

[Jimmyinkedup]

To treat you need to stop taking all that nonsense and start drinking nothing but water and start preparing and eating nothing but whole natural foods.

I may get some flack about this from our house Dr's but fish oil definitely without a doubt made me feel worse when my liver disease was at it's worse. I started up and stopped with the fish oil multiple times and each time it had the same results on my overall condition. If you google fish oil and liver problems there are articles out there that state that there may be a downside to taking large amounts of fish oil with a compromised liver.

Glutamine was another supplement that had negative effects while having liver disease . There is a lot of info on this posted in many articles online.

So what did you rely on with your bout with liver disease? Plenty of water and a good clean diet? Did you take anything you felt helped in any way? (I apologize if you have covered this). Thanks.

 

[bigpoppachump]

So what did you rely on with your bout with liver disease? Plenty of water and a good clean diet? Did you take anything you felt helped in any way? (I apologize if you have covered this). Thanks.

The only thing that I ever felt that had an effect on the way I felt during a inflammation was Tudca. It may have also been a placebo but I did feel slightly better after day or two when I would resume taking it. I also became more conscious of what I was eating and how much sleep I was getting as well so it may have had more to do with straightening up and flying right more than the actual tudca. The biggest differences came when I dropped all beverages an stuck strictly with water and started preparing all my meals from fresh ingredients instead of fast foods, pre-made meals, and lots of quick fix it's for dinner prep. When you get to reading the ingredients they use for preservatives and spices they begin to sound like chemicals used for industrial purposes more than for ingesting. I've stopped taking the tudca about a month ago and my most recent blood work drawn 10 days ago had my AST and ALT at 18/21 which is downright amazing compared to some of the liver panel test results I've had over the past 4 years and there is no doubt in my mind that the biggest overall contributor to those low numbers was whole natural food and good ol fashioned H2O